LncRNA MALAT1 promotes breast cancer progression by sponging miR101-3p to mediate mTOR/PKM2 signal transmission.

Breast cancer (BC) is a common malignant tumor in women and exhibits a poor prognosis. This study examined the role and underlying mechanisms of long non-coding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in BC pathogenesis. The MALAT1 expression levels in BC cells and tissues were measured using quantitative reverse transcription-polymerase chain reactions. CCK-8 kits and wound healing and transwell assays were used to evaluate the cell growth, invasion, and migration of BC. Bioinformatics and dual-luciferase reporter analyses were conducted to identify MALAT1's potential targets. The protein levels in the mTOR/PKM2 pathway were assessed using Western blot analyses. The MALAT1 overexpressions in the BC tissues and cells were considered to be a predictor of poor prognosis. Therefore, MALAT1 downregulation significantly inhibited BC progression, including cell growth, invasion, and migration. MALAT1 was anticipated to be an miR-101-3p target according to the dual-luciferase reporter gene assay results. The miR-101-3p levels were indirectly proportional to the MALAT1 expressions and the suppressed BC cells. Additionally, the mTOR/PKM2 pathway was directly targeted by miR-101-3p. MALAT1 overexpression significantly decreased the miR-101-3p gene levels and increased the mTOR/PKM2 pathway protein expressions. This miR-101-3p inhibition blocked MALAT1. These findings suggest that lncRNA MALAT1 is related to BC pathogenesis using the miR101-3p/mTOR/PKM2 pathway and is a potential therapeutic target.