miR‑187‑3p increases gemcitabine sensitivity in breast cancer cells by targeting FGF9 expression
Autor: | Weiwei Liu, Yingqi Wu, Xinghui Yu, Haina Yu, Li Tao, Lan-fang Liu, Junwei Liang, Yashun Qiao |
---|---|
Rok vydání: | 2020 |
Předmět: |
Cancer Research
Oncogene business.industry fibroblast growth factor 9 Cell gemcitabine microRNA-187-3p Cancer Articles General Medicine Cell cycle medicine.disease Gemcitabine breast cancer medicine.anatomical_structure Breast cancer Immunology and Microbiology (miscellaneous) Apoptosis medicine Cancer research Viability assay business medicine.drug |
Zdroj: | Experimental and Therapeutic Medicine |
ISSN: | 1792-1015 1792-0981 |
DOI: | 10.3892/etm.2020.8770 |
Popis: | Breast cancer is the most common type of malignancy in women, which remains a significant health concern worldwide. Gemcitabine is a frequently applied anticancer pharmacological agent. However, the efficacy of gemcitabine is limited by chemoresistance. In the present study, a combination of reverse transcription quantitative-PCR, cell viability, flow cytometry, luciferase reporter assay and western blot analysis were performed to elucidate the potential effects of miR-187-3p on gemcitabine sensitivity in the breast cancer cell line, MDA-MB-231. The results revealed that miR-187-3p was significantly decreased in the breast cancer tumor tissues. Moreover, the overexpression of miR-187-3p significantly inhibited cell viability and promoted apoptosis in MDA-MB-231 cells. In addition, miR-187-3p overexpression enhanced the anti-proliferative and pro-apoptotic effects of gemcitabine, indicating that miR-187-3p regulated gemcitabine sensitivity in breast cancer cells. Mechanistically, miR-187-3p negatively regulated the expression of fibroblast growth factor 9 (FGF9) by binding to its 3'-untranslated region. Overexpression of FGF9 reversed the aforementioned effects of miR-187-3p overexpression on cell viability and apoptosis in the presence of gemcitabine. In conclusion, the present study indicated that miR-187-3p increased gemcitabine sensitivity in breast cancer cells by targeting FGF9 expression. |
Databáze: | OpenAIRE |
Externí odkaz: | |
Nepřihlášeným uživatelům se plný text nezobrazuje | K zobrazení výsledku je třeba se přihlásit. |