Journal of Medical Molecular Biology ›› 2023, Vol. 20 ›› Issue (4): 316-323.doi: 10.3870/j.issn.1672-8009.2023.04.007
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Abstract: Objective To investigate the potential molecular mechanism of LncRNA HOTAIR in regulating paclitaxel resistance in breast cancer cells. Methods The breast cancer paclitaxel-resistant cell lines (MCF7 / TR cells) were screened. The expression levels of HOTAIR and paclitaxel resistance indicators (cell proliferation rate, cell apoptosis rate, cell cycle, intracellular paclitaxel concentration) were then examined in the MCF7 / TR cells and the parental cells. Results After knockdown of HOTAIR, paclitaxel significantly inhibited the proliferation of MCF7 / TR cells, induced the cell apoptosis, and arrested the MCF7 / TR cells in the G1 phase. The intracellular concentration of paclitaxel in MCF7 / TR cells was increased after knockdown of HOTAIR. miR-130a-3p was found to be interacted with HOTAIR, and the expression level of miR-130a-3p was elevated after knockdown of HOTAIR. The intracellular paclitaxel concentration was significantly increased in the MCF7 / TR cells upon overexpression of miR-130a-3p. miR-130a-3p targeted the untranslated region at the 3′ end of ABCC5 mRNA, and the intracellular paclitaxel concentration was significantly increased when ABCC5 were overexpressed in MCF7 / TR cells. Conclusion LncRNA HOTAIR reduces the intracellular level of paclitaxel in paclitaxel-resistant cells through the miR-130a-3p / ABCC5 axis, and promotes the resistance of breast cancer cells to paclitaxel.
Key words: HOTAIR, miR-130a-3p, ABCC5, breast cancer, paclitaxel 
CLC Number:
R737. 9
HE Yu, YUAN Zhipeng, LU Zhibin, LIAO Jingsheng, JIA Jun. LncRNA HOTAIR Regulates Paclitaxel Resistance in Breast Cancer Cells through miR-130a-3p / ABCC5 [J]. Journal of Medical Molecular Biology, 2023, 20(4): 316-323.
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URL: http://tjqk.magtech.com.cn/yxfzswx/EN/10.3870/j.issn.1672-8009.2023.04.007
http://tjqk.magtech.com.cn/yxfzswx/EN/Y2023/V20/I4/316