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Medical Science Monitor Basic Research


eISSN: 1643-3750

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Suppression of Long Non-Coding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Potentiates Cell Apoptosis and Drug Sensitivity to Taxanes and Adriamycin in Breast Cancer

Jie Yu, Taobo Jin, Tianya Zhang

(Department of General Surgery I, Zhuji Central Hospital, Zhuji, Zhejiang, China (mainland))

Med Sci Monit 2020; 26:e922672

DOI: 10.12659/MSM.922672

BACKGROUND: The long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is expressed highly in various types of tumors. Moreover, the tumor-initiating role of MALAT1 has been probed in the context of breast cancer. This study was set to investigate the regulatory role of MALAT1 on the chemosensitivity of breast cancer cells to taxanes (Tax) and adriamycin (Adr).
MATERIAL AND METHODS: Following the measurement of MALAT1 expression in patients with breast cancer by means of qRT-PCR, the connection between the MALAT1 expression pattern and the prognosis of breast cancer patients as well as the molecular typing of breast cancer patients was analyzed using Kaplan-Meier survival analysis and receiver operating characteristic (ROC) curves. Next, the analysis between the expression of MALAT1 and the clinical symptoms of breast cancer patients was carried out. Subsequently, we generated taxane-resistant MCF-7 cells (MCF-7/Tax) and purchased Adr-resistant MCF-7 cells (MCF-7/Adr). Finally, the proliferation, apoptosis and drug resistance of resistant and parental cells were evaluated after transfection of silencing MALAT1 into these cells.
RESULTS: MALAT1 was highly expressed in the breast cancer tissues. Moreover, patients with relative overexpression of MALAT1 had worse prognosis. MALAT1 expression was remarkably promoted in MCF-7/Tax and MCF-7/Adr cells, whose sensitivity to Tax and Adr was enhanced following MALAT1 knockdown.
CONCLUSIONS: MALAT1 was elevated in breast cancer tissues and MCF-7-resistant cells, relative to corresponding controls and downregulation of MALAT1 inhibited the growth and chemoresistance of breast cancer cells to Tax and Adr.

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