MiR-21-5p regulates colon adenocarcinom a cell progression and epithelial-mesenchymal transition by negatively regulating Tensin 1

Colon adenocarcinoma (COAD) is one of the most prevalent forms of cancer in the world. Still, the molecular mechanism of COAD development remains unknown, making it especially important to investigate the molecular mechanism of COAD development and identify new therapeutic targets.

A real-time fluorescence quantification polymerase chain reaction (RT-qPCR) was used to determine the level of miR-21-5p expression in COAD tissues and cell lines. Both miR-21-5p silencing and overexpression were performed in LOVO and T84 cell lines. Cell viability, apoptosis rate, migration, and invasion ability were determined using MTT, flow cytometry, and the Transwell assay, respectively. Western blot was applied to detect the levels of protein expression associated with the epithelial-mesenchymal transition (EMT).

Using a dual luciferase reporter gene, the targeting connection among miR-21-5p and Tensin 1 was validated. Tensin 1 expression was silenced to investigate its effect on miR-21-5p inhibitor activity in COAD cells. Subcutaneous tumor-forming animal experiments in nude mice were used to investigate the effect of miR-21-5p on COAD tumor growth in vivo. Ki-67 expression was identified through immunohistochemistry. MiR-21-5p was found in high concentrations in COAD tissues and cells. Overexpression of miR-21-5p increased COAD cell line viability and EMT, facilitated cell migration and invasion, and inhibited apoptosis. Tensin 1 was regulated negatively by miR-21-5p. Tensin 1 silencing reversed the effect of miR-21-5p silencing on COAD cells. Subcutaneous tumor formation experiments in nude mice revealed that inhibiting miR-21-5p expression slowed the growth rate of tumor volume.

According to immunohistochemical results, the percentage of Ki-67-positive cells was significantly lower in the anti-miR-21-5p group. MiR-21-5p levels were upregulated in COAD cells, and reducing miR-21-5p expression inhibited COAD cell viability, migration, invasion, and EMT in vitro. Tensin 1 negatively regulated miR-21-5p, which regulated COAD cell and EMT progression.