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