MiR-34a-5p suppresses colorectal cancer cell proliferation through silencing Microtubule Actin Crosslinking Factor 1 (MACF1) gene

Abstract

BackgroundColorectal cancer (CRC) is the third most frequent cancer in both males and females. CRC results from multiple causes including genetic, epigenetic, and environmental insults. One of the newly identified oncogenes is the Microtubule Actin Crosslinking Factor 1 (MACF1) gene. MACF1 plays a critical role in colon cancer cell proliferation and progression through Wnt /β catenin pathway. Accordingly, we hypothesized that targeting MACF1 would affect CRC progression. Methodsbioinformatics analysis revealed that MACF1 is a target of miR-34a-5p. miR-34a-5p and MACF1 relative expression were measured in 40 colorectal cancers, 40 nonmalignant colon tissue samples using RT- qPCR. "CaCo2" cells line was transfected with miR-34a-5p mimic to assess the effect of MACF1 gene silencing on colorectal cell growth in vitro. ResultsmiR-34a-5p relative expression was significantly lowered in the colorectal cancer group than its expression in nonmalignant groups (P < 0.01). While MACF1 expression was significantly overexpressed in the colorectal cancer group as compared to the nonmalignant groups (P < 0.01). CaCo2 cells' proliferation significantly inhibited after transfection with miR-34a-5p mimic. This inhibited growth was associated with a significant decrease in MACF1 expression. ConclusionThese findings suggest that miR-34a-5p may inhibit colorectal cancer cell proliferation through downregulation of MACF1a member of Wnt/β catenin signaling. This study highlights the novel role of MACF1 as an indicative biomarker and therapeutic goal in colorectal cancer.