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. 2024 Sep 20;6(21):5220–5257. doi: 10.1039/d4na00488d

Fig. 4. Schematic representation of the mechanism of action of PGA polyplexes loaded miR34a mimics and PLK1-siRNA. (a) A miR-34a binding site located in the MYC 3′-UTR. (b) Analysis of PLK1 and MYC protein levels in MiaPaCa2 cells treated with miRNA and siRNA monotherapies, as well as their combination. (c) Immunostaining of MYC in tumors from various in vivo treatment conditions. (d) MYC immunostaining of short-term and long-term formalin-fixed, paraffin-embedded (FFPE) pancreatic ductal adenocarcinoma (PDAC) specimens. (e) Quantification of MYC immunostaining using histology scores, with a scale of 0 to 3 (0 – none, 1 – weak, 2 – moderate, 3 – high). (f) Cell viability assessment of cMYC-overexpressing MiaPaCa2 cells versus naive cells after 48 hours of combined treatment, with corresponding MYC immunoblotting shown below the graph. (g) Proposed model of synergistic interaction through MYC as a shared target for miR-34a and PLK1. STS indicates short-term survivors, LTS indicates long-term survivors, and cMYC OE denotes cMYC overexpression. Data are expressed as mean ± SD. This figure is reproduced from ref. 93 with permission from Nature, copyright (2018).

Fig. 4