lncRNA MALAT1 participates in metformin inhibiting the proliferation of breast cancer cell
| Autor: | Shanyu Zheng, Kexun Yuan, Bing Wang, Tianye Li, Zihan Wu, Jin Zhang, Zhenzhen Hao, Yiquan Song, Ziyan Zhou, Qi Zhao, Yongye Huang, Yunhao He |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Cyclin-Dependent Kinase Inhibitor p21
0301 basic medicine autophagy Cell cycle checkpoint endocrine system diseases Apoptosis Breast Neoplasms CHOP 03 medical and health sciences 0302 clinical medicine Breast cancer Humans Hypoglycemic Agents Medicine MALAT1 Cyclin B1 Endoplasmic Reticulum Chaperone BiP Cell Proliferation business.industry Cell growth Voltage-Dependent Anion Channel 1 digestive oral and skin physiology nutritional and metabolic diseases HOTAIR Original Articles Cell Biology medicine.disease Metformin 030104 developmental biology 030220 oncology & carcinogenesis MCF-7 Cells Cancer research Molecular Medicine Original Article Beclin-1 Female RNA Long Noncoding ER stress business Microtubule-Associated Proteins Transcription Factor CHOP medicine.drug |
| Zdroj: | Journal of Cellular and Molecular Medicine |
| ISSN: | 1582-4934 1582-1838 |
| DOI: | 10.1111/jcmm.16742 |
| Popis: | In recent years, the repurposing of conventional and chemotherapeutic drugs is recognized as an alternative strategy for health care. The main purpose of this study is to strengthen the application of non‐oncological drug metformin on breast cancer treatment in the perspective of epigenetics. In the present study, metformin was found to inhibit cell proliferation, promote apoptosis and induce cell cycle arrest in breast cancer cells at a dose‐dependent manner. In addition, metformin treatment elevated acH3K9 abundance and decreased acH3K18 level. The expression of lncRNA MALAT1, HOTAIR, DICER1‐AS1, LINC01121 and TUG1 was up‐regulated by metformin treatment. In metformin‐treated cells, MALAT1 knock‐down increased the Bax/Bcl2 ratio and enhanced p21 but decreased cyclin B1 expression. The expression of Beclin1, VDAC1, LC3‐II, CHOP and Bip was promoted in the cells received combinatorial treatment of metformin and MALAT1 knock‐down. The reduced phosphorylation of c‐Myc was further decreased in the metformin‐treated cells in combination with MALAT1 knock‐down than metformin treatment alone. Taken together, these results provide a promising repurposed strategy for metformin on cancer treatment by modulating epigenetic modifiers. |
| Databáze: | OpenAIRE |
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