miR‑27a‑3p regulates proliferation and apoptosis of colon cancer cells by potentially targeting BTG1

Abstract

microRNA (miR/miRNA)-27a-3p has been reported to be abnormally expressed in various types of cancer, including colorectal cancer (CRC). B-cell translocation gene 1 (BTG1) has also been implicated with CRC. However, the association between miR-27a-3p and BTG1 in CRC, to the best of our knowledge, has not been investigated. In order to assess whether miR-27a-3p is associated with CRC, reverse transcription-quantitative PCR was performed on 20 paired CRC and paracancerous tissues for miRNA analysis. For the screening and validation of miR-27a-3p expression in colon cancer, several colon cancer cell lines (HCT-116, HCT8, SW480, HT29, LOVO and Caco2) and the normal colorectal epithelial cell line NCM460 were examined. The highest expression levels of miR-27a-3p were detected in the HCT-116, which was selected for further experimentation. The HCT-116 cells were divided into control, miR-27a-3p mimic and inhibitor groups, and cell proliferation was tested using an MTT assay. Additionally, miR-27a-3p inhibitor/mimic or BTG1 plasmid were transfected into the HCT-116 cells, and flow cytometry was performed to analyze cell cycle distributions. TUNEL analysis was performed to detect apoptosis. Protein levels of factors in the downstream signaling pathway mediated by miR-27a-3p [ERK/mitogen-activated extracellular signal-regulated kinase (MEK)] were detected. miR-27a-3p was revealed to be overexpressed in human CRC tissues and colon cancer cell lines. Knockdown of miR-27a-3p suppressed proliferation of HCT-116 cells and apoptosis was increased. It further markedly upregulated expression levels of BTG1 and inhibited activation of proteins of the ERK/MEK signaling pathway. In addition, overexpression of BTG1 in HCT-116 cells triggered G 1 /S phase cell cycle arrest and increased apoptosis via the ERK/MEK signaling pathway. In conclusion, the present study demonstrated that the effects of miR-27a-3p on colon cancer cell proliferation and apoptosis were similar to those of the tumor suppressor gene BTG1. The miR-27a-3p/BTG1 axis may have potential implications for diagnostic and therapeutic approaches in CRC.

BTG1 inhibits malignancy as a novel prognosis signature in endometrial carcinoma

“…The low expression of BTG1 may be involved in the occurrence and development of pancreatic ductal adenocarcinoma [48]. miR-27a-3p regulates the proliferation and apoptosis of colon cancer cells by potentially targeting BTG1 [49]. lncRNA DGCR5 can be used as a ceRNA for BTG1 to inhibit the progression of gastric cancer [50].…”

BTG1 inhibits malignancy as a novel prognosis signature in endometrial carcinoma

“…The low expression of BTG1 may be involved in the occurrence and development of pancreatic ductal adenocarcinoma [45] . miR-27a-3p regulates the proliferation and apoptosis of colon cancer cells by potentially targeting BTG1 [46] . lncRNA DGCR5 can be used as a ceRNA for BTG1 to inhibit the progress of gastric cancer [47] .…”

Inverse Correlation of miR-27a-3p and CDH5 Expression Serves as a Diagnostic Biomarker of Proliferation and Metastasis of Clear Cell Renal Carcinoma

“…[25,[32][33][34] Mir-27a-3p has been identi ed to promote tumor invasion and metastasis in gastric, colon, pancreatic, and nasopharyngeal cancers. [35][36][37][38] On the other hand, a tumor suppressor role has also been shown for miR-27a-3p in some cancers. For instance, it inhibits the proliferation of non-small cell lung cancer cells by targeting HOXB8.…”