A functional variant rs1464938 in the promoter of fibroblast growth factor 12 is associated with an increased risk of bladder transitional cell carcinoma

Wu, Jun; Huang, Huawu; Huang, Qun; Qiu, Rong; Huang, Min-Yu; Meng, Dongdong

doi:10.1016/j.cyto.2020.155294

Cited by 1 publication

(1 citation statement)

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“…Therefore, it is very important to discover biomarkers related to CRC progression. FGF12 , a kind of inflammatory cytokine, has been demonstrated to be a bladder cancer risk locus by genome-wide association study (GWAS) [ 21 ]. However, the mechanism of FGF12 in the occurrence and metastasis of CRC is unclear.…”

Section: Discussionmentioning

confidence: 99%

Depletion of Fibroblast Growth Factor 12 Restrains the Viability, Stemness, and Motility of Colorectal Cancer

Gao

Liao

et al. 2022

BioMed Research International

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Background. Colorectal cancer (CRC) is a leading cause of cancer-related death. CRC patients have a poor prognosis due to tumor metastasis and recurrence. Fibroblast growth factor 12 (FGF12), a member of the FGF family, is highly expressed in several cancers. However, little is known about the roles of FGF12 in CRC progression. Methods. The overall survival (OS) of CRC patients was detected via Kaplan–Meier analysis. The FGF12 expression in both CRC tissues and cells was analyzed by qRT-PCR, immunohistochemistry (IHC), and western blotting (WB). LoVo and SW480 cells were transfected with shFGF12 lentivirus to silence FGF12. In vivo and in vitro experiments were performed to explore the FGF12 functions in CRC, including CCK-8, Edu, flow cytometry, Transwell, EMT, cancer stemness, and tumor xenograft experiments. Results. FGF12 was upregulated in both CRC cells and tissues. High expression of FGF12 indicated a shorter OS in CRC patients. FGF12 knockdown inhibited the proliferation, invasion, stemness, and EMT of CRC cells. FGF12 knockdown promoted CRC cell apoptosis in vitro. 740 Y-P (a PI3K/AKT pathway activator) restored the proliferation, stemness, invasion, and EMT in FGF12-deficient cells and reversed LoVo cell apoptosis induced by FGF12 depletion. Depletion of FGF12 inhibited tumor growth, EMT, cancer stemness, and PI3K/AKT pathway in a xenograft mouse model. Conclusions. FGF12 predicts bad clinical outcome and modulates the viability, stemness, and motility of CRC cells. Our study may provide a new insight for the diagnosis and treatment of CRC.

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Section: Discussionmentioning

confidence: 99%