si‑MALAT1 attenuates thymic cancer cell proliferation and promotes apoptosis via the miR‑145‑5p/HMGA2 pathway
Affiliations: Department of Cardiovascular Surgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, P.R. China, Department of Ophthalmology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, P.R. China
- Published online on: June 3, 2021 https://doi.org/10.3892/ol.2021.12846
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Metastasis‑associated‑lung‑adenocarcinoma-transcript‑1 (MALAT1) is a long non‑coding RNA that is considered a potential tumor marker. The present study aimed to investigate the effect and mechanism of MALAT1 on cell proliferation and apoptosis in thymic cancer cells. IU‑TAB‑1, A549, HCT‑116 and 293T cells were screened by reverse transcription‑quantitative PCR to assess high‑mobility group AT‑hook 2 (HMGA2) expression in various types of cancer cells and were transfected with small interfering (si)RNA targeting MALAT1 (si‑MALAT1). Cell proliferation was evaluated by Cell Counting Kit‑8 assay. Cell apoptosis and cell cycle were examined using flow cytometry. The protein expression of cyclin D1, cyclin E, Bax, Bcl‑2 and HMGA2 was determined by western blot analysis, while the associations between MALAT1 and microRNA (miR)‑145‑5p and between HMGA2 and miR‑145‑5p were determined by luciferase reporter assay. Among the four cell lines evaluated, IU‑TAB‑1 showed the highest expression of MALAT1; thus, IU‑TAB‑1 cells were selected for subsequent experiments. Compared with the findings in the control group, si‑MALAT1 significantly decreased the cell proliferation of IU‑TAB‑1 cells, whereas the apoptosis levels and number of cells in G2 phase were increased. The protein expression levels of cyclin D1, cyclin E, Bcl‑2 and HMGA2 were significantly decreased in the si‑MALAT1 group compared with those in the control group, while Bax levels were significantly increased. After treatment with si‑MALAT1 in combination with miR‑145‑5p mimics or inhibitors, cell proliferation and apoptosis were respectively enhanced and inhibited in IU‑TAB‑1 cells. miR‑145‑5p inhibited the luciferase activity of IU‑TAB‑1 cells transfected with the MALAT1 or HMGA2 3' untranslated region. In conclusion, si‑MALAT1 significantly attenuated cell proliferation and apoptosis via the miR‑145‑5p/HMGA2 pathway in thymic cancer cells.