MicroRNA-301a-3p promotes triple-negative breast cancer progression through downregulating MEOX2

Breast cancer is one of the most frequently diagnosed malignancies among women. Triple-negative breast cancer (TNBC) represents a significant challenge for breast oncologists, as the availability of effective therapies for this aggressive disease is limited. The molecular mechanisms underlying TNBC development are not fully understood. Previous studies have demonstrated that microRNAs (miRNAs/miRs) play important roles in the development of various types of cancer, including breast cancer; however, the role of miRNAs in TNBC remains undetermined. The results of the present study revealed that miR-301a-3p may function as an oncogenic miRNA in TNBC. Based on The Cancer Genome Atlas data, miR-301a-3p expression levels were found to be upregulated in breast cancer tissues. Reverse transcription-quantitative PCR analysis demonstrated that the expression levels of miR-301a-3p were upregulated in TNBC tissues compared with non-TNBC tissues, and in MDA-MB-231 cells compared with normal MCF-10A breast cells. miR-301a-3p mimics and inhibitors were subsequently used to overexpress and knock down miR-301a-3p expression, respectively, in MDA-MB-231 cells. Biological functional experiments demonstrated that miR-301a-3p overexpression increased the viability, and the migratory and invasive abilities of MDA-MB-231 cells. By contrast, miR-301a-3p knockdown exerted the opposite effects on MDA-MB-231 cells. Cell apoptosis was negatively regulated by miR-301a-3p. Moreover, overexpression of miR-301a-3p was found to downregulate the expression levels of mesenchyme homeobox 2 (MEOX2). The expression levels of miR-301a-3p were negatively correlated with the expression levels of MEOX2 in clinical tissue specimens from patients with TNBC. Subsequently, the knockdown of MEOX2 expression promoted the viability of MDA-MB-231 cells. In conclusion, the results of the present study suggested that miR-301a-3p may serve as an oncogenic miRNA in TNBC by regulating MEOX2 expression.