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. 2025 Dec 8;36:102642. doi: 10.1016/j.mtbio.2025.102642

A novel metal-organic coordination polymer based on Ru complexes for photoredox catalysis and photodynamic therapy of breast cancer

Shengsheng Cui a,1, Yingbin Wang d,1, Xinni Pan a, Yingao Jiao a, Cheng Cao a, Xinyuan Cui c, Yanfei Fu a, Shujin Lin a, He Li b,⁎, Yanlei Liu a,⁎⁎, You Wang b,⁎⁎⁎
PMCID: PMC12765071  PMID: 41492647

Abstract

This study introduces the synthesis and application of a novel metal-organic coordination polymer for photocatalytic cancer therapy. The material was prepared via coordination between Ru(dcbpy)3Cl2 and manganese ions, forming sheet-like nanostructures with strong visible-light absorption and high photostability. Upon light irradiation, Mn-Ru MOCPs not only produce singlet oxygen via a type II photodynamic pathway but also efficiently catalyze the oxidation of intracellular NADH with a high photocatalytic turnover frequency (TOF) of 175 h−1. Moreover, the material facilitates the photocatalytic reduction of cytochrome c in the presence of NADH, triggering multimodal therapeutic effects including ROS erupt, NADH and ATP depletion, loss of mitochondrial membrane potential, and ultimately apoptosis. Both intracorporeal and extracorporeal experiments exhibited significant light-induced anticancer activity against 4T1 breast cancer cells and xenograft tumor models, with good biocompatibility and tumor-targeting capability.

Keywords: Ru-based metal complexes, Metal-organic coordination polymer, Photodynamic therapy, Photoredox catalysis

Graphical abstract

Image 1

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1. Introduction

Light-driven catalysis represents an influential revolutionary strategy with diverse applications in air/water purification [1], plastic recycling [2], industrial production [3], and energy conversion [4,5]. Inspired by biocatalyst and enzyme mediated biological processes, researchers are exploring this strategy to address one of humanity's most pressing challenges: cancer [6,7]. Photodynamic therapy (PDT), based on photosensitizers (PSs), light and oxygen, has continuously demonstrated promising tumor targeted anti-cancer potential because of its spatiotemporal precision in drug activation for the past few decades [[8], [9], [10]]. As is widely known, PDT involves the transition of the PSs to an excited state under light irradiation. The excited state PSs can generate intracellular reactive oxygen species (ROS) such as superoxide radicals and hydroxyl radicals through electrons transfer with surrounding biomolecules (type Ⅰ pathway) or singlet oxygen (1O2) through energy transfer with intracellular oxygen (type Ⅱ pathway). However, most of the organic PSs used in clinical PDT currently exhibit anticancer activity through oxygen dependent type II pathway, and the application of such PSs is restricted by side effects such as hepatotoxicity and skin photosensitivity [11,12]. In addition, the hypoxic microenvironment in solid tumors will further drastically reduce the therapeutic effect of the organic PSs which through oxygen dependent type II pathway PDT. Therefore, developing a new generation of PSs that can work even at low oxygen concentration is urgently needed to do [[13], [14], [15]].

Fortunately, another light-driven catalytic strategy-photoredox catalysis (PC)-operates through direct electron transfer between substrates and photoexcited catalysts, which subsequently engage in reactions with other biomolecules, thereby eliminating the dependence on oxygen [[16], [17], [18], [19]]. Currently, Ir(III)- and Ru(II)-based metal complexes offer distinct advantages over organic PSs, which are mainly reflected in their photostability, long excited-state lifetimes, and capacity not only to generate intracellular ROS but also to exhibit broad light-driven anticancer bioactivities via photoredox catalysis [[20], [21], [22]]. Notably, recent works have revealed that excited-state Ru(II) polypyridyl complexes can catalyze the oxidation of nicotinamide adenine dinucleotide (NADH) [23,24]. As an essential coenzyme, NADH is involved in over 400 intracellular redox reactions and serves as the primary source of electrons in the mitochondrial electron transport chain (ETC), which plays a critical effect in maintaining cellular redox homeostasis and counteracting ROS-induced damage [25,26]. Consequently, the photooxidation of intracellular NADH catalyzed by photoactive Ru(II) polypyridyl complexes can disrupt cellular redox homeostasis and metabolism, offering a promising new approach for developing catalytic anticancer drugs [27,28]. As recently reported by Tedeschi et al., the significant upregulation of NADH concentrations in cancer cells suggests that this photocatalytic anticancer therapy of intracellular NADH oxidation could provide selectivity against cancer cells over normal cells [29]. Remarkably, the depletion of NADH by photoactive Ru (Ⅱ) complexes in cancer cells may also offer an novel mechanism of drug action to counteract hypoxia-associated drug resistance in tumors [24,30].

However, the poor water solubility, low bioavailability, systemic toxicity, and lack of targeting ability of these complexes result in low therapeutic indices, hindering their clinical application. One promising approach to tackling these challenges is to utilize nanoparticles as delivery carriers for the complexes, leveraging their small size, water solubility, high specific surface area, tunable drug release profiles, and multifunctional properties [31,32]. Leveraging the enhanced permeability and retention (EPR) effect of solid tumors, these nanoparticles can passively accumulate in solid tumors while protecting healthy cells, significantly improving solubility, biodistribution, pharmacokinetics, ultimately reducing the adverse effects commonly associated with conventional therapeutics [33]. Currently, there are many studies on incorporating Ru(II) polypyridine complexes into nanoparticles for designing advanced nanomaterials with unique and attractive biomedical application properties [[34], [35], [36]]. The latest is that the direct coordination of drugs and metals to form nanomaterials has aroused great interest, and given us some inspiration, as they have higher drug loading capacity and responsiveness to the tumor microenvironment [37]. In this work, we pioneered the use of Ru(dcbpy)3Cl2 as an organic ligand coordinated with metal Mn to form metal-organic coordination polymers (Mn-Ru MOCPs). The resulting Mn-Ru MOCPs exhibit a sheet-like nanostructure with strong visible light absorption ability and photostability. Under light irradiation, the Mn-Ru MOCPs can generate intracellular singlet oxygen via type II pathway, and catalyze the oxidation of intracellular NADH with significantly high TOF (175 h−1) photocatalysis. At the same time, they can also catalyze the NADH-driven reduction of cytochrome c (cyt c). Hence, upon light irradiation, they initiate a cascade of cellular responses, including a burst of ROS, the depletion of NADH and ATP, and the collapse of the mitochondrial membrane potential, which collectively trigger apoptosis. Additionally, the dual functionality of Mn-Ru MOCPs extends to their use as an MRI contrast agent, facilitating precise MRI-guided photo-catalytic anticancer effect in tumor bearing mice (Scheme 1).

Scheme 1.

Scheme 1

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Schematic illustration of the Mn-Ru MOCPs' synthesis and its function as an MRI contrast agent, enabling guided photo-catalytic anticancer therapy.

2. Results

2.1. Preparation and characterization of Mn-Ru MOCPs

The Mn-Ru MOCPs were synthesized via a straightforward, one-step solvothermal reaction between Ru(dcbpy)3Cl2 ligand and manganese chloride (Fig. 1a), the tangerine color of the raw material Ru(dcbpy)3Cl2 turned into orange Mn-Ru MOCPs product (Fig. S1), the detailed synthesis steps can be found in the Supporting Information. Firstly, the morphology of the fabricated Mn-Ru MOCPs was characterized, and SEM image (Fig. S2) showed that it was a sheet-like structure with a width of ∼200 nm, which can be further confirmed by its TEM image (Fig. 1b). The element mapping images (Fig. 1c and Fig. S3) proved the existence of Ru, Mn, N, and O elements in Mn-Ru MOCPs, which were derived from manganese chloride and Ru(dcbpy)3Cl2, respectively. Fourier transform infrared spectroscopy (FTIR) were employed to monitor the changes in functional groups of the products prior to and subsequent to the coordination reaction. As shown in Fig. 1d, the hydroxyl stretching vibration peak of Ru(dcbpy)3Cl2 monomer on carboxylic acid at 3100 cm−1 was significantly reduced in Mn-Ru MOCPs, indicating that carboxylic acid has undergone coordination reaction. In addition, the shift of the C=O stretching vibration peak from 1710 cm−1 (Ru(dcbpy)3Cl2 monomer) to 1590 cm−1 (Mn-Ru MOCPs) further confirmed the success of the coordination reaction [38]. As evidenced by UV–Vis absorption and fluorescence emission spectra (Fig. 1e), the characteristic peaks of the Mn-Ru MOCPs showed a close yet shifted profile compared to Ru(dcbpy)3Cl2, a shift attributable to the coordination reaction, which is consistent with the reported literature [39]. X-ray photoelectron spectroscopy (XPS) survey analysis confirmed the presence of C, Ru, N, O, and Mn in Mn-Ru MOCPs (Fig. S4). The high-resolution spectrum of Ru 3d shown a main pair of peaks located at 284.9 eV (Ru 3d3/2) and 280.8 eV (Ru 3d5/2), which can be assigned to Ru2+ (Fig. 1f) [40]. The Mn 2p spectrum in Fig. 1g can be deconvoluted into a set of spin orbit double peaks and their satellite peaks. The doublet is located at 641.2 eV (Mn 2p3/2) and 653.1 eV (Mn 2p1/2), which is and can be assigned to Mn2+ [41]. Furthermore, as shown in Fig. S4, the N 1s spectrum of Mn-Ru MOCPs exhibited a single peak located at 399.8 eV, which corresponded to pyridinic N; the O 1s line can be fitted to two different signals that correspond to carboxylate oxygen (530.9 eV) and adsorbed oxygen (532.8 eV) [42]. Having established the successful synthesis of the Mn-Ru MOCPs, we proceeded to evaluate their potential for photo-catalytic anticancer activity. As a preliminary step, their aqueous dispersibility was confirmed by preparing a stable solution in PBS (500 μg mL−1). As shown in Fig. 1h, the Mn-Ru MOCPs formed a homogeneous yellow solution in PBS and maintained this dispersion without visible aggregation for 24 h, demonstrating excellent stability.

Fig. 1.

Fig. 1

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Preparation and Characterization of Mn-Ru MOCPs: (a) the synthesis procedures; (b) TEM; and (c) elemental mapping images of Mn-Ru MOCPs; (d) FTIR vibration spectra and (e) absorption (solid) and fluorescence (dashed) spectra for Ru(dcbpy)3Cl2 and Mn-Ru MOCPs; (f) high-resolution Ru 3d and (g) Mn 2p XPS spectra of Mn-Ru MOCPs; (h) photographs of Mn-Ru MOCPs dispersed in PBS at different times (concentration: 500 μg mL−1).

2.2. Phototherapy performance of Mn-Ru MOCPs

Photosensitizer performance of Mn-Ru MOCPs: To assess the potential of Mn-Ru MOCPs in PDT, we firstly measured the production of 1O2 by the oxidation of (1,3-diphenylisobenzofuran) (DPBF). The exposure of DPBF to 1O2 triggers a specific reaction that converts it into non-fluorescent, non-absorptive species. The characteristic absorbance at 410 nm of DPBF decreased gradually with the increment of photoirradiation duration, demonstrating the generation of 1O2 (Fig. 2a). However, the DPBF oxidation by Mn-Ru MOCPs in the absence of photoirradiation or with laser alone was minimal (Fig. S5). Furthermore, singlet oxygen sensor green (SOSG), which exhibits a distinct fluorescence peak at 525 nm upon reaction with 1O2, was used to detect 1O2 generation. As illustrated in Fig. 2b, the SOSG fluorescence intensity exhibited a progressive increase upon photoirradiation of the Mn-Ru MOCPs. To further substantiate the 1O2 generation, electron spin resonance (ESR) was employed with 2,2,6,6-tetramethylpiperidine (TEMP) as the 1O2 trapping agent. As observed in Fig. 2c, the characteristic triplet signal (1:1:1 intensity) of the TEMP-1O2 adduct was detected in the range of 3460–3550 GM for the Mn-Ru MOCPs mixture under photoirradiation. Comparatively, no significant 1O2 signals were detected in the ESR spectra of Mn-Ru MOCPs alone or water solvents under photoirradiation. Additionally, methylene blue (MB) was deployed as a trapping agent for hydroxyl radicals (•OH). The lack of a noticeable change in MB's absorption profile (Fig. S6) confirmed that Mn-Ru MOCPs with photoirradiation minimally produces •OH. Furthermore, the photostability of Mn-Ru MOCPs was evaluated following a 45-min exposure to photoirradiation by analyzing its absorption and emission spectra (Fig. 2d and e). The findings demonstrated that Mn-Ru MOCPs maintained high photostability under photoirradiation, indicating its potential as an effective photosensitizing agent.

Fig. 2.

Fig. 2

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Phototherapy performance of Mn-Ru MOCPs: (a) the DPBF absorption and (b) the SOSG fluorescence changes of Ru-Mn MOCPs at different periods of laser irradiation; (c) ESR spectra trapped by TEMP of Ru-Mn MOCPs solution under different conditions; (d) the absorption and (e) emission spectra of Ru-Mn MOCPs after different laser irradiation durations in PBS solution; (f) the absorption spectra of Ru-Mn MOCPs at different periods of laser irradiation in the presence of NADH; the inserted photo shows the results of the Quantofix peroxide test rod after photocatalysis; (g) the dependence of lnA/A0 at 339 nm in Figure (f) on irradiation time; (h) ESR spectra trapped by CYPMPO of Ru-Mn MOCPs solution with/without laser irradiation; (i) the absorption spectra after different irradiation times for Ru-Mn MOCPs (10 μg mL−1) mediated photocatalytic reduction of oxidized cyt c (10 μM) by NADH (50 μM), the arrows indicate the direction of the absorbance change over time.

Photocatalytic oxidation of NADH: NADH, a crucial coenzyme acting as an electron and proton donor, is involved in over 400 cellular redox reactions. Targeting NADH to disrupt the redox equilibrium can lead to the eradication of cancer cells. Consequently, we evaluated the photocatalytic oxidation efficacy of Mn-Ru MOCPs towards NADH by monitoring the UV–vis absorption spectral changes during photoirradiation, wherein the absorbance of the NADH peak at 339 nm diminished as it was oxidized to NAD+. As anticipated, the characteristic absorption peak of NADH at approximately 339 nm exhibited a time-dependent decrease upon photoirradiation in the presence of Mn-Ru MOCPs (Fig. 2f). Additionally, the generation of H2O2, a byproduct of NADH oxidation, was confirmed using H2O2 test strips (Inset of Fig. 2f). Notably, with only 10 μM Mn-Ru MOCPs, nearly 200 μM of NADH was depleted after 24 min of irradiation. The computed photooxidation turnover number (TON) for NADH oxidation by Mn-Ru MOCPs was approximately 19.1 under these conditions. The turnover frequency (TOF) was determined to be 175 h−1 based on the reduction in NADH concentration following photoirradiation (Fig. 2g). The Mn-Ru MOCPs also showed equivalent or better NADH oxidation TOF than other reported Ru-complexes (Table S1). Furthermore, a series of control experiments (Fig. S7) established that both Mn-Ru MOCPs and light are essential for the continuous production of NAD+ in the aforementioned photo-catalytic process.

To further validate the photo-induced oxidation of NADH, ESR spectroscopy was applied to identify radical species formed upon irradiation. The scavenger for carbon-centered radicals 5 - (2, 2 - dimethyl - 1, 3-propoxycyclo-phosphoryl) - 5 - methyl - 1 - pyrroline - N - oxide (CYPMPO) was utilized to specifically detect the NAD• radical. ESR spectra, as illustrated in Fig. 2h, confirmed the presence of the CYPMPO -NAD radical adduct in an aqueous solution of NADH and Mn-Ru MOCPs during photoirradiation. These findings suggest that NADH undergoes a one-electron oxidation to form the NADH+• radical, which then experiences deprotonation to form the NAD• radical. This NAD• radical intermediate subsequently undergoes intramolecular rearrangement to yield NAD+. The ESR data support a mechanism which an electron is transferred from NADH to the laser-excited Mn-Ru MOCPs, leading to the observed photo-oxidation of NADH.

Photoreduction of cyt c: The NAD+/NADH redox couple is a pivotal electron donor and transporter in cellular metabolism, intricately linked to the efficiency of the ETC and crucial for the preservation of cellular redox balance. Within the mitochondrial ETC, cytochrome c (cyt c) is localized in the intermembrane space and facilitates electron transfer between complex III and complex IV. However, under conditions of irreversible mitochondrial dysfunction, cyt c translocates to the cytosol, thereby triggering caspase-dependent apoptotic pathways. The redox state of cyt c can be reliably monitored by absorption spectroscopy. As depicted in Fig. 2i, the photocatalytic activity of Mn-Ru MOCPs under 488 nm irradiation markedly enhances the redox reaction between the hemoprotein cyt c (Fe3+) and NADH. In contrast, control experiments exhibited no significant alterations in the UV spectra, indicating that the presence of NADH, Mn-Ru MOCPs, and light irradiation are essential for the reduction of cyt c (Fe3+) to its (Fe2+) form (Fig. S8).

2.3. Synergistic phototherapy of Mn-Ru MOCPs in vitro

Cytotoxicity of Mn-Ru MOCPs: To assess in vitro phototherapy efficiency, the cytotoxicity of Mn-Ru MOCPs against 4T1 breast cancer cells was evaluated using the Cell Counting Kit-8 (CCK-8) assay. As depicted in Fig. 3a, the viability of 4T1 cells remained consistently above 90 % following a 24 h co-incubation period, and further remained above 85 % after a 48-h co-incubation. These findings indicate that Mn-Ru MOCPs exerts minimal toxicity to cells even at elevated concentrations in the absence of photoirradiation. For PDT assessment, 4T1 cells were treated with varying concentrations of Mn-Ru MOCPs for 12 h, subsequent to which the cells were subjected to 10 min of photoirradiation using a 488 nm laser (60 mW cm−2). Cell viability was then assessed after an additional 4 h of cultivation. Upon photoirradiation, the viability of 4T1 cells progressively decreased with escalating concentrations of Mn-Ru MOCPs (Fig. 3b). A similar trend was also found in a complementary cytotoxicity assay using the same Mn-Ru MOCPs concentration (80 μg mL−1) and a range of photoirradiation durations (Fig. S9).

Fig. 3.

Fig. 3

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Assessment of cellular uptake and distribution of Mn-Ru MOCPs and therapeutic efficacy of Mn-Ru MOCPs in vitro: (a) cell viabilities of 4T1cells after 24 h (green columns) and 48 h (orange columns) incubated with the Mn-Ru MOCPs at different concentrations (mean ± SD, n = 3); (b) dose-dependent viability of 4T1 cells treated with the Mn-Ru MOCPs at different concentrations under laser (orange columns) or dark (green columns) conditions; (c) time-dependent accumulation of Mn-Ru MOCPs (80 μg mL−1) in 4T1 cells, as visualized by CLSM. red fluorescence indicates the probes; blue: DAPI (nuclei), scale bar: 10 μm; (d) subcellular localization of Mn-Ru MOCPs in 4T1 cells, scale bar: 10 μm; (e) semi-quantitative analysis via line-scanning intensity profiles, scale bar: 10 μm; (f) cellular Ru uptake quantified by ICP-MS (mean ± SD, n = 3).

Cellular uptake of Mn-Ru MOCPs: The efficacious uptake of therapeutic agents by 4T1 cells is a prerequisite for attaining optimal therapeutic outcomes. In this investigation, the internalization dynamics of Mn-Ru MOCPs by 4T1 cells were examined utilizing confocal laser scanning microscopy (CLSM) and flow cytometry. As shown in Fig. 3c, the intracellular fluorescence intensity escalated with the extension of co-incubation duration from 0 to 8 h, signifying a time-dependent manner of Mn-Ru MOCPs uptake. Furthermore, distinct cellular boundaries were observable at the 12 h (Fig. S10). Consequently, for subsequent cellular assays, a 12 h incubation period with Mn-Ru MOCPs was selected, given the optimal cellular internalization at this juncture. To quantitatively ascertain the internalization of Mn-Ru MOCPs by 4T1 cells, flow cytometric analysis was conducted to measure the intracellular fluorescence. The geometric mean fluorescence intensity of cells exposed to Mn-Ru MOCPs for 12 h was observed to be 10.5-fold higher compared to that of the non-treated control group (Fig. S11).

Cellular distribution of Mn-Ru MOCPs: Subsequently, the subcellular distribution of Mn-Ru MOCPs was investigated. Notably, as depicted in Fig. 3d, the red fluorescence emitted by Mn-Ru MOCPs overlapped very well with that of the Mito-Tracker, indicating a significant degree of co-localization. Further quantitative analysis of the co-localization imaging using ImageJ software revealed a Pearson's Correlation coefficient of 0.75, suggesting a substantial overlap between the distributions of Mn-Ru MOCPs and mitochondrial (Fig. 3e). This finding was corroborated by Inductively coupled plasma-mass spectrometry (ICP-MS) measurements (Fig. 3f), which demonstrated that 80.4 % of internalized Ru was associated with the mitochondrial fraction. Collectively, these observations indicate a predominant mitochondrial localization of Mn-Ru MOCPs. Such targeting of mitochondria is crucial for the exertion of significant anticancer effects, given the organelle's central role in cellular processes like energy production, intracellular redox homeostasis, and metabolic regulation. Consequently, any disruption to mitochondrial function by Mn-Ru MOCPs is anticipated to lead to cellular demise.

Mitochondrial membrane potential: Given that approximately 80 % of Mn-Ru MOCPs is localized within the mitochondria, the potential mitochondrial damage was examined. The mitochondrial membrane potential (Δψmt), which is vulnerable to impairments in the electron transport chain (ETC), plays a critical function in mitochondrial regulation and the release of cytochrome c. As illustrated in Fig. 4a, the Δψmt was monitored with the JC-1 probe. A loss of Δψm causes JC-1 to shift from red fluorescent aggregates to green monomers, thereby converting the fluorescence signal in confocal images. Neither photoirradiation alone nor Mn-Ru MOCPs alone induced significant Δψmt loss. However, a shift in JC-1 fluorescence from red to green was observed in the group treated with Mn-Ru MOCPs and subsequent photoirradiation, indicating a disruption in the mitochondrial ETC. This indicates that the photocatalytic activity of Mn-Ru MOCPs may lead to the impairment of mitochondrial function, which is crucial for its anticancer activity, as mitochondria are central to cellular processes such as energy production, maintenance of intracellular redox balance, and metabolism. Damage to the mitochondria by Mn-Ru MOCPs is expected to trigger cell death pathways.

Fig. 4.

Fig. 4

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Assessment of Mitochondrial membrane potential, intracellullar NADH and ATP, and ROS generation of Mn-Ru MOCPs (80 μg mL−1) in vitro: (a) assessment of mitochondrial membrane potential in 4T1 cells via JC-1 staining following various treatments, scale bar: 200 μm; (b) the intracellular NADH and (c) ATP level in 4T1 cells following a 12 h incubation with the Mn-Ru MOCPs with (orange columns) or without (green columns) the laser illumination; (d) the measurement of intracellular ROS of 4T1 cells by DCFH-DA staining under various treatments, scale bar: 50 μm; (e) the intracellular H2O2 level of 4T1 cells after 12 h incubated with the Mn-Ru MOCPs with (orange columns) or without (green columns) the laser illumination.

Intracellullar NADH and ATP: Given the pivotal functions of NADH and ATP in cellular biosynthesis, metabolism, and energy production, we conducted a thorough investigation into the effects of Mn-Ru MOCPs on the levels of these biomolecules within 4T1 cells. In the absence of light, Mn-Ru MOCPs did not exert any significant impact on cellular NADH or ATP levels. However, upon exposure to photoirradiation in the presence of Mn-Ru MOCPs, a marked decrease in intracellular NADH and ATP levels was observed, which was concentration-dependent (Fig. 4b and c). This decrease in NADH and ATP is likely due to the photoredox catalytic activity of Mn-Ru MOCPs, which may disrupt the cellular redox balance and energy metabolism, thereby enhancing the therapeutic efficacy of Mn-Ru MOCPs through a synergistic effect on cancer cells. Therefore, the ability of Mn-Ru MOCPs to modulate these essential molecules highlights their promise as a therapeutic agent for cancer treatment.

ROS generation in cells: To explore cellular oxidative stress induced by Mn-Ru MOCPs, the levels of intracellular ROS were quantified using 2,7-dichlorofluorescein diacetate (DCFH-DA). From Fig. 4d, it can be seen that the groups treated with either Mn-Ru MOCPs alone or photoirradiation alone, as well as the untreated control group, showed low levels of DCFH-DA signal. Conversely, strong green fluorescence from DCFH-DA was detected in the group treated with both Mn-Ru MOCPs and photoirradiation. Indeed, in accordance with the experimental outcomes, Mn-Ru MOCPs-initiated photosensitization triggered a dose-dependent increase in intracellular H2O2 levels compared to the control group (Fig. 4e). These findings suggest that Mn-Ru MOCPs-mediated phototherapy disrupts cellular redox balance and lead to enhanced oxidative stress.

Mechanism of cell death: Furthermore, to provide direct insight into the photo-cytotoxic effects of Mn-Ru MOCPs on 4T1 cells, a cell double staining experiment was conducted to observe the treated cells (calcein AM (AM) and propidium iodide (PI)). As anticipated, treatments with either Mn-Ru MOCPs alone or photoirradiation alone resulted in robust AM fluorescence and minimal PI fluorescence, indicative of minimal cytotoxicity to the 4T1 tumor cells. In contrast, the group subjected to both Mn-Ru MOCPs and photoirradiation exhibited diminished green fluorescence from AM and enhanced red fluorescence from PI, signifying significant cellular damage and the induction of cell death (Fig. 5a). Owing to the perturbation of the mitochondrial membrane potential (MMP) is associated with the initiation of apoptosis. To elucidate the mechanism underlying cell death, annexin V-FITC/propidium iodide (PI) co-staining was performed. Control cells maintained in the dark or exposed to light alone, as well as those treated with Mn-Ru MOCPs in the absence of light, remained negative for annexin V-FITC and PI staining, suggesting cellular viability. A substantial portion of the cells treated with Mn-Ru MOCPs and subsequently irradiated were co-stained with both annexin V-FITC and PI, suggesting late-stage apoptosis and/or necrosis (Fig. 5b) which can be more intuitively demonstrated by the statistical results in Fig. 5c. Quantitative flow cytometric analysis corroborated the findings from CLSM. As depicted in Fig. 5d, the majority of 4T1 cells treated with Mn-Ru MOCPs (10 mM) in the dark were viable, located in the bottom left quadrant (94.1 %). Upon exposure to 488 nm light for 10 min, the apoptotic cell population in the right quadrant increased significantly to 61.47 %, a marked difference compared to cells exposed to light alone (Fig. S12). Overall, these findings suggest that our synthesized Mn-Ru MOCPs could be a promising candidate for facilitating equivalent or better efficient synergistic phototherapy (PC/PDT) to eliminate cancer cells when compared to the performance of other reported Ru-complexes in synergistic phototherapy (Table S1).

Fig. 5.

Fig. 5

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Assessment of in vitro therapy of Mn-Ru MOCPs: (a) live/dead double staining of 4T1 cells using Calcein AM/PI, scale bar: 200 μm) and (b) Annexin V-FITC/PI (scale bar: 100 μm) after different treatments; (c) the fluorescence semi-quantitative analysis of different groups in Figure b; (d) flow cytometry analysis results of apoptosis in 4T1 cells (Annexin V-FITC and PI staining), the upper is blank control, the under cells were treated with Mn-Ru MOCPs with laser irradiation.

2.4. Synergistic phototherapy of Mn-Ru MOCPs in vivo

The temporal distribution of nanoparticles at tumor sites is fundamental to informing the optimal window for treatment. To evaluate the in vivo distribution and tumor-targeting efficacy of Mn-Ru MOCPs, magnetic resonance imaging (MRI) was conducted in nude mice bearing tumors due to the abundance of Mn in Mn-Ru MOCPs. Firstly, the MRI capability of Mn-Ru MOCPs was validated in vitro. As the concentration of Mn increased from 7.5 to 120 μM, the T1 image gradually became brighter (Fig. 6a). Furthermore, based on the T1 relaxation time of Mn at different concentrations, the unit concentration relaxation rate r1 of Mn-Ru MOCPs could be calculated as 6.73 mM−1s−1 (Fig. 6b), which proved that it can be used as the MRI contrast agent. Fig. 6c shows the in vivo MRI experimental procedure, the tumor models were constructed by subcutaneous injection of 4T1 cells into the mice. When the tumor volume of the mice reached ∼60 mm3, Mn-Ru MOCPs were injected and T1 MRI was observed at time nodes of 0, 1, 2, 8, and 24 h. The results are shown in Fig. 6d, prior to injection (0 h), the initial T1-MR signal at the tumor region was the weakest, after injection of Mn-Ru MOCPs, within 0–8 h, as nanoparticles gradually accumulated at the tumor site, the T1-MR signal was gradually increased, after 24 h, the T1-MR signal at the tumor site weakened, indicating that Mn-Ru MOCPs began to metabolize out of the tumor within 8–24 h. The quantitative analysis of Fig. 6d further confirmed that the T1-MR signal intensity reached the maximum value of 1500 at 8 h (Fig. 6e), demonstrating that Mn-Ru MOCPs mediated T1 MRI can clinically indicate the tumor site and monitor drug accumulation in the tumor site in real-time. Consequently, the photoirradiation time point was selected to be 8 h after injection, aligning with the period of maximum accumulation of Mn-Ru MOCPs in the tumor tissue. In addition, the T1 MRI results (Fig. 6d) indicated that the Mn-Ru MOCPs is mainly captured by the reticuloendothelial system of the liver and spleen during the initial administration, which is consistent with the behavior of most nanoscale materials.

Fig. 6.

Fig. 6

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In vivo distribution of Mn-Ru MOCPs: (a) T1-weighted MRI and (b) relaxation rate r1 of Mn-Ru MOCPs with different concentrations of Mn; (c) schedule of T1 MRI in mice using Mn-Ru MOCPs; (d) serial in vivo MRI of the tumor-bearing mice after Mn-Ru MOCPs administration; (e) time-dependent quantitative analysis of signal intensity in tumor regions (circled).

In light of the exceptional in vitro photo-activated anti-neoplastic properties of Mn-Ru MOCPs, an in-depth investigation was conducted to evaluate its in vivo phototherapeutic efficacy in a mouse model bearing 4T1 (breast carcinoma) tumors via intravenous administration (Fig. 7a). The experimental mice were stratified into four cohorts: (1) Control; (2) Mn-Ru MOCPs alone; (3) photoirradiation alone; (4) Mn-Ru MOCPs + photoirradiation. 2 h subsequent to the i.t. administration of Mn-Ru MOCPs, the tumors were subjected to photoirradiation. As depicted in Fig. 7b, a significant suppression of tumor growth was achieved in the cohort treated with Mn-Ru MOCPs in conjunction with photoirradiation, whereas the tumors in the control group, the Mn-Ru MOCPs alone group, and the photoirradiation alone group exhibited substantial growth. Upon the end of the study, the mice from each group were euthanized to facilitate the collection of tumors for photographic documentation and weight measurement (Fig. S13). Among the aforementioned groups, the cohort treated with Mn-Ru MOCPs and photoirradiation exhibited the lowest average tumor weight (Fig. 7c), which can be further verified by the photos of ex vivo tumors (Fig. S14), indicating that the Mn-Ru MOCPs + photoirradiation group has a significant tumor growth inhibitory effect. No significant difference in weight changes among the treatment groups, indicating that the therapeutic protocols were well-tolerated and devoid of significant adverse effects in the animal models (Fig. 7d).

Fig. 7.

Fig. 7

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Therapeutic efficacy of Mn-Ru MOCPs in vivo: (a) schedule of the tumor-bearing mouse therapeutic profile; (b) final tumor weight, (c) tumor volume, and (d) body weight of tumor-bearing mice receiving various treatments, (mean ± SD, n = 4); (e) representative hematoxylin-eosin and (f) TUNEL staining of tumor sections of various treatment group, scale bar: 100 μm; hematoxylin-eosin staining of (g) heart, (h) liver, (i) spleen, (j) lung, and (k) kidney organs after different treatment, scale bar: 100 μm.

Furthermore, histological examination of tumor tissues via hematoxylin and eosin (H&E) staining revealed the most extensive regions of apoptosis and necrosis in the group treated with the combination of Mn-Ru MOCPs and photoirradiation (Fig. 7e), suggesting significant cellular damage within the tumor exclusively upon exposure to photoirradiation. In alignment with the H&E staining findings, a markedly elevated level of apoptosis was observed in the group treated with Mn-Ru MOCPs and photoirradiation, as depicted in Fig. 7f, conversely, the Control group, as well as the groups treated with either Mn-Ru MOCPs alone or photoirradiation alone, exhibited no significant tissue damage, as confirmed by both H&E and TUNEL staining. The biocompatibility of Mn-Ru MOCPs was assessed by examining H&E stained sections of the principal organs. As illustrated in Fig. 7g-k, compared to the PBS group, no obvious organ damage and abnormal pathological changes such as inflammation or hyperplasia were detected in these experimental groups. thereby indicating that Mn-Ru MOCPs did not elicit significant toxic side effects in vivo. Overall, Mn-Ru MOCPs have good biocompatibility during the efficacy observation period. On the one hand, the results of CCK-8 cell acute toxicity experiments showed that even at concentrations as high as 320 μg/mL, the cell viability remained above 85 % after a 48-h co-incubation (Fig. 3a), and the 14 day acute toxicity observation of mice injected with Mn-Ru MOCPs showed no significant weight loss or abnormal behavior (Fig. 7d); On the other hand, H&E stained sections of major organs (heart, liver, spleen, lungs, and kidneys) showed no significant histological damage observed 14 days after administration (Fig. 7g-k).

3. Conclusion

In conclusion, we have successfully developed a photo-responsive metal-organic coordination polymer, Mn-Ru MOCPs, that integrates photosensitizing and photoredox catalytic properties. This material operates through a dual mechanism-type II photodynamic action and photoredox catalysis-effect disrupting redox homeostasis and energy metabolism in cancer cells. Its remarkable ability to photocatalytically oxidize NADH, combined with mitochondrial targeting, leads to efficient apoptosis induction. In vivo studies confirmed pronounced antitumor efficacy, favorable biosafety and excellent MRI capabilities, highlighting the potential of Mn-Ru MOCPs as a promising platform for phototherapeutic applications. This work offers an innovative strategy for designing catalytic anticancer agents with clinical translation potential.

CRediT authorship contribution statement

Shengsheng Cui: Writing – original draft, Validation, Data curation. Yingbin Wang: Writing – review & editing, Software. Xinni Pan: Writing – original draft, Formal analysis. Yingao Jiao: Methodology. Cheng Cao: Visualization, Investigation. Xinyuan Cui: Software, Data curation. Yanfei Fu: Validation. Shujin Lin: Supervision, Resources. He Li: Visualization, Supervision. Yanlei Liu: Writing – review & editing, Funding acquisition, Conceptualization. You Wang: Writing – review & editing, Supervision, Funding acquisition.

Conflicts of interest

There are no conflicts to declare.

Declaration of competing interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Acknowledgements

This work was financially supported by the National Natural Science Foundation of China (No. 82073380; 82374163; 82172918), the Interdisciplinary Program of Shanghai Jiao Tong University (No. YG2024QNA53 and YG2025ZD19), the Shanghai Key Laboratory of Gynecologic Oncology (Grant No. FKZL-2023-01), Noncommunicable Chronic Diseases-National Science and Technology Major Project (NO. 2024ZD0530600; 2024ZD0530601).

Footnotes

This article is part of a special issue entitled: Multiscale Composites published in Materials Today Bio.

Appendix A

Supplementary data to this article can be found online at https://doi.org/10.1016/j.mtbio.2025.102642.

Contributor Information

He Li, Email: lihe1972@hotmail.com.

Yanlei Liu, Email: liuyanlei@sjtu.edu.cn.

You Wang, Email: wanghh0163@163.com.

Appendix A. Supplementary data

The following is/are the supplementary data to this article.

Multimedia component 1
mmc1.docx (13.7MB, docx)

Data availability

Data will be made available on request.

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Supplementary Materials

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Data Availability Statement

Data will be made available on request.

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