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 dualluciferase 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.C