LncRNA ZNF667-AS1 Targets miR-523-3p/KIF5C Axis to Hinder Colon Cancer Progression

LncRNA ZNF667-AS1 plays an important role in the carcinogenesis and progression of various cancers. However, their role in colon cancer (CC) remains unclear. The expression of ZNF667-AS1, KIF5C, and miR-523-3p in CC cells and tissues was analyzed using RT-qPCR and western blotting. CCK-8 scratch-wound assay, western blotting, and flow cytometry were conducted to investigate the malignant activity of CC in vitro. Luciferase reporter, RNA pull-down, and Ago2 immunoprecipitation (RIP) experiments were conducted to ascertain the association of miR-523-3p with ZNF667-AS1 and KIF5C 3MODIFIER LETTER PRIMEUTR. Xenograft tumor experiments were also performed. CC cells and tissues showed low expression of NF667-AS1 and KIF5C and elevated expression of miR-523-3p. ZNF667-AS1 overexpression attenuates proliferation and migration of CC cells, restores inactivated apoptosis in vitro, and inhibits tumor growth in vivo. MiR-523-3p targets both ZNF667-AS1 and the KIF5C 3MODIFIER LETTER PRIMEUTR. ZNF667-AS1 overexpression in SW480 and SW620 cells attenuated the oncogenic effect of miR-523-3p in CC. However, this attenuating effect was counteracted by KIF5C overexpression. ZNF667-AS1 sequestered miR-523-3, reducing miR-523-3p-mediated inhibition of KIF5C expression, thereby repressing colon carcinogenesis in vitro. Our findings shed light on a novel anticancer strategy that could potentially combat CC.

Automated summary

The study found that long non-coding RNA ZNF667-AS1 plays an important role in the carcinogenesis and progression of colon cancer. The overexpression of ZNF667-AS1 can attenuate the proliferation and migration of colon cancer cells, restore inactivated apoptosis, and inhibit tumor growth. This finding suggests a potential novel anticancer strategy for combating colon cancer.