AI Article Synopsis

  • The study investigates how microRNA miR-642a-5p affects the movement and invasion of colon cancer cells by regulating COLL1A1.
  • It was found that miR-642a-5p levels are higher and COL1A1 levels are lower in colon cancer tissues, and their expression is linked to patient prognosis.
  • Overexpressing miR-642a-5p reduces cancer cell movement and invasion, while increasing COL1A1 has the opposite effect, suggesting miR-642a-5p acts as a suppressor in colon cancer progression.

Article Abstract

The aim of the present study was to explore the mechanism by which microRNA (miR)‑642a‑5p regulates the migration and invasion of colon cancer cells via collagen type I α1 (COL1A1). The characteristics of miR‑642a‑5p and COL1A1 were analysed through bioinformatics. Cancer and normal tissues were collected from patients with colon cancer. miR‑642a‑5p‑ and COL1A1‑overexpressing cell lines were constructed by transfection. A dual‑luciferase reporter assay was used to verify the targeting of COL1A1 by miR‑642a‑5p. Cell Counting Kit‑8, wound healing and Transwell assays were used to detect cell viability, migration and invasion, respectively. Protein and mRNA expression levels were examined by western blotting and reverse transcription‑quantitative PCR, respectively. The results revealed that miR‑642a‑5p expression was significantly upregulated and COL1A1 expression was downregulated in patients with colon cancer. Low levels of miR‑642a‑5p and high levels of COL1A1 were associated with a poor prognosis in patients with colon cancer. miR‑642a‑5p directly targeted the 3'‑untranslated region of COL1A1 and inhibited COL1A1 expression. Overexpression of miR‑642a‑5p inhibited cell viability, migration, invasion and epithelial mesenchymal transition. Overexpression of COL1A1 promoted cell viability, migration, invasion and EMT, and partially reversed the inhibitory effects of miR‑642a‑5p on colon cancer cells. In conclusion, miR‑642a‑5p inhibited colon cancer cell migration, invasion and EMT by regulating COL1A1.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7859924PMC
http://dx.doi.org/10.3892/or.2020.7905DOI Listing

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