AI Article Synopsis
- LncRNAs play a crucial role in various cellular processes and are emerging as potential targets for cancer therapy, specifically focusing on colon cancer in this study.
- CASC2 is found to be significantly reduced in colon cancer tissues, and its overexpression hinders the growth of HT-29 cancer cells by promoting apoptosis and autophagy through changes in specific protein levels.
- CASC2 regulates TRIM16 via the microRNA-214 pathway, and both CASC2 overexpression and TRIM16 silencing inhibit cancer cell growth, suggesting that targeting CASC2 could be a promising strategy for colon cancer treatment.
Article Abstract
Long non-coding RNAs (LncRNAs) have been shown to be involved in diverse cellular and physiological processes. Recent studies have proved their potential as the prospective therapeutic targets for cancer treatment. Herein, we examined the role of LncRNA CASC2 in human colon cancer. The gene expression analysis showed that LncRNA CASC2 is significantly suppressed in colon cancer tissues and cell lines. The immunohistochemistry also showed considerable increase of the Ki67 in colon cancer tissues suggestive of their aggressiveness. Overexpression of CASC2 inhibited the growth of HT-29 cells. The inhibition of HT-29 growth was due to the induction of apoptosis which was accompanied by upsurge of Bax, depletion of Bcl-2 and activation of caspase-3 cleavage. Electron microscopic analysis showed CASC2 overexpression also induced autophagy in the HT-29 cells which was associated with increase in LC3B II and Beclin 1 expression. Bioinformatic approaches and dual luciferase assay showed that CASC2 controls the TRIM16 via microRNA-214 axis. TRIM16 was found to be overexpressed in all the colon cancer tissues and cell lines. Overexpression of CASC2 caused significant inhibition of TRIM16. Additionally, silencing of TRIM16 resulted in the inhibition of HT-29 cell growth similar to that of CASC2 overexpression. Taken together, CASC2 may prove to be an important therapeutic target for colon cancer treatment.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7344075 | PMC |
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