Table 1.
In vitro or in vivo models studying the role of CAFs in BCa.
| Year | Author | Fibroblasts used/source | Animal model | Finding/comments | Ref. |
|---|---|---|---|---|---|
| 2022 | Lu et al. | Tissues from BCa patients | Xenograft mouse model | Exosomal miR-93-5p derived from CAFs confers oncogenicity on BCa cells via sponging PAFAH1B1. | 47 |
| 2022 | Shan et al. | Tissues from BCa patients | Subcutaneous tumor model | CAF-exos and exosomal miR-148b-3p can reduce apoptosis and promote EMT, metastasis and drug resistance in BCa cells and that these effects can be reversed by PTEN overexpression via downregulation of the Wnt/β-catenin pathway. | 70 |
| 2021 | Camargo et al. | Tissues from BCa patients | – | 3D model based on acellular scaffolds provide a novel platform for elucidating the paracrine signaling of BCa and how this molecular signaling can alter the phenotypes of fibroblasts. | 76 |
| 2021 | Yang et al. | Tissues from BCa patients | – | CAFs promote cell proliferation and invasion of human BC cells through Wnt/IL1β signaling feedback. | 37 |
| 2021 | Dong et al. | human Foreskin Fibroblast cells were induced into CAFs by T24 cells | – | CAFs affected T24 cell growth, invasion, and metabolic phenotype through autophagy. | 39 |
| 2021 | Caston et al. | CAF19 | – | Tumors grown in the presence of CAFs were sensitized to the combination of STAT3 and Ref-1 inhibition. | 80 |
| 2020 | Luo et al. | Tissues from BCa patients | – | 1. The exosomes released from CAFs promote BCa cell proliferation and invasion. 2. Regulation of LINC00355 expression in exosomes released from CAFs might be a putative therapeutic strategy against the pathogenesis of BCa. |
69 |
| 2020 | Zhou et al. | Tissues from BCa patients | Xenograft mouse model | 1. CAFs-derived MFAP5 promotes the bladder cancer proliferation and metastasis. 2. MFAP5-mediated PI3K-AKT signaling activated the DLL4/NOTCH2 pathway axis in bladder cancer. |
44 |
| 2019 | Long et al. | Tissues from BCa patients | Xenograft mouse model | CAFs could increase BCa cell resistance to cisplatin by increasing ERβ/Bcl-2 signalling. | 10 |
| 2019 | Mullenders et al. | Tissues from BCa patients | – | Human BCa organoids are successfully derived from resected tumors and biopsies and biopsies and cultured and passaged for prolonged periods. | 77 |
| 2019 | Goulet et al. | Healthy primary bladder fibroblasts (HFs) were induced into CAFs (iCAFs) by bladder cancer-derived exosomes. | – | 1. The IL-6 cytokine was highly expressed by CAFs, and its receptor IL-6R was found on RT4 BCa cells. 2. Inhibition of CAFs-secreted IL-6 by neutralizing antibody significantly reversed the IL-6-induced EMT phenotype. |
50 |
| 2015 | Miao et al. | NIH3T3 fibroblasts | Stroma-rich bladder cancer model (SRBC) | 1. Off targeted nanoparticles (NP) damaged CAF initially inhibited tumor growth, chronic exposure of CAF to cisplatin NP led to elevated secretion of Wnt16 in a paracrine manner that supported tumor cell resistance and stroma reconstruction. 2. Knockdown of Wnt16 in the damaged CAF could be a promising combinatory strategy to improve efficacy of NP delivered cisplatin in a SRBC. |
73 |
| 2015 | Zhuang et al. | Tissues from BCa patients | – | CAFs induces EMT and invasion of human UBC cells through the TGFβ1-ZEB2NAT-ZEB2 axis. | 35 |
| 2015 | Grimm et al. | Tissues from BCa patients | – | Fibroblasts enhance migration and invasion of bladder cancer cells with the involvement of MCP-1 and HGF as stimulatory factors | 45 |
| 2015 | Shi et al. | human Foreskin Fibroblast cells were induced into CAFs by T24 cells | – | Overexpression of monocarboxylate anion transporter 1 and 4 in T24-induced CAFs regulates the progression of bladder cancer cells in a 3D microfluidic device | 7 |
| 2014 | Zhang et al. | NIH 3T3 | SRBC | Antineoplastic effect of Combo NP works by first targeting CAFs and is more effective as an anti-tumor therapy than Combo Free, GMP NP or Cisplatin NP alone. | 81 |