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FH535 inhibits proliferation and migration of colorectal cancer cells by regulating CyclinA2 and Claudin1 gene expression
- Tu, Xuezi, Hong, Dan, Jiang, Yiyan, Lou, Zhefeng, Wang, Keke, Jiang, Yiwen, Jin, Longjin
- Gene 2019 v.690 pp. 48-56
- antineoplastic agents, cell cycle, cell movement, colorectal neoplasms, gene expression, gene expression regulation, humans, messenger RNA, neoplasm cells, protein content, signal transduction, therapeutics
- Wnt signaling pathway plays a major role in the progression of colorectal cancer (CRC). Small molecules which can cut off this signal transduction can be promising anti-cancer drugs for CRC therapy. Therefore, we aimed to investigate the mechanisms of FH535, an inhibitor of the Wnt signaling pathway, on inhibiting proliferation and migration of colorectal cancer cells DLD-1 and SW620. We found that FH535 could significantly suppress the growth of DLD-1 and SW620 cells in a concentration-dependent and time-dependent manner. The results of cell cycle tests showed that FH535 could significantly induce G2/M arrest in colorectal cancer cells. Transwell and Wound-healing assays revealed that FH535 notably inhibited cell migration. Moreover, we found that FH535 down-regulated β-catenin and CyclinA2 expressions while up-regulating Claudin-1 expression at both mRNA and protein levels, which may contribute to the FH535-induced inhibitory effect on proliferation and migration in human colorectal cancer cells. Our study revealed that FH535 inhibited proliferation and migration of colorectal cancer cells by regulating CyclinA2 and Claudin1 gene expression, which enriches regulatory network of FH535 and may contribute to being promising anti-cancer drugs for CRC therapy.