MiR-1306-5p predicts favorable prognosis and inhibits proliferation, migration, and invasion of colorectal cancer cells via PI3K/AKT/mTOR pathway

Cell Cycle. 2022 Jul;21(14):1491-1501. doi: 10.1080/15384101.2022.2054245. Epub 2022 Apr 13.

Abstract

MicroRNAs (miRNAs) play a critical role in the occurrence and progression of colorectal cancer. Our study aims to explore the role of miR-1306-5p in cell malignant phenotypes of colorectal cancer cells. RT-qPCR was performed to assess the expression of miR-1306-5p in colorectal cancer samples and cell lines. The effects of miR-1306-5p on cell proliferation, migration, and invasion were evaluated through the CCK-8 assay, wound healing assay, and transwell invasion assay, respectively. Apoptosis was detected by flow cytometry. Luciferase reporter assay was used to predict the target gene of miR-1306-5p. Western blot was used to detect the expression levels of signal pathway molecules and target proteins. We found that miR-1306-5p was low-expressed in colorectal cancer tissues and cell lines, and its expression was also associated with colorectal cancer development and prognosis. MiR-1306-5p overexpression led to a decrease in colorectal cancer cell proliferation, migration, and invasion, while promoting apoptosis. Moreover, it was discovered that SLCO2A1 was a target of miR-1306-5p. By targeting SLCO2A1, overexpression of miR-1306-5p could inhibit the PI3K/AKT/mTOR signaling pathway. Overexpression of miR-1306-5p inhibited the colorectal cancer cell malignant phenotypes via regulating PI3K/AKT/mTOR signaling pathway regulation by targeting SLCO2A1. Therefore, miR-1306-5p can be a prospective therapeutic target for treating colorectal cancer.

Keywords: SLCO2A1; colorectal cancer; invasion; miR-1306-5p; migration.

MeSH terms

  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Colorectal Neoplasms* / pathology
  • Humans
  • MicroRNAs* / metabolism
  • Neoplasm Invasiveness
  • Organic Anion Transporters*
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • TOR Serine-Threonine Kinases / genetics
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • MicroRNAs
  • Organic Anion Transporters
  • SLCO2A1 protein, human
  • MTOR protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases

Grants and funding

The author(s) reported that there is no funding associated with the work featured in this article.