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.

Colorectal cancer (CRC) is a major threat affecting human health. Studies have shown that miR-556-3p can regulate dab2ip and promote tumor deterioration, and up-regulation of BIM inhibits CRC cell progression. However, the interaction between miR-556-3p/dab2ip and BIM in CRC is unknown. We examined miR-556-3p expression in CRC tissues and cells by RT-qPCR. The impact of miR-556-3p/dab2ip and BIM on CRC cell behaviors were assessed by western blot, transwell and MTT assay. miR-556-3p was highly expressed in CRC and its overexpression increased CRC cell proliferation and migration as well as up-regulated dab2ip and Ki-67 expression. Besides, miR-556-3p could target the BIM and overexpressed miR-556-3p decreased BIM expression. However, silencing of BIM abrogated the impact of overexpressed miR-556-3p on CRC cell proliferation and migration. In conclusion, miR-556-3p/dab2ip promotes cell growth by down-regulating the expression of BIM, thereby promoting the progression of CRC.