Long non-coding RNA MINCR promotes gallbladder cancer progression through stimulating EZH2 expression

Area of Science:

• Oncology
• Molecular Biology
• Genetics

Background:

• MYC-regulated long non-coding RNAs (lncRNAs) are implicated in cancer development.
• The specific role of MYC-induced long non-coding RNA (MINCR) in gallbladder cancer (GBC) tumorigenesis remains largely uncharacterized.

Purpose of the Study:

• To investigate the role of MINCR in gallbladder cancer (GBC) tumorigenesis.
• To explore the potential of MINCR as a prognostic marker and therapeutic target in GBC.

Main Methods:

• Quantitative real-time PCR to assess MINCR expression in GBC tissues and adjacent normal tissues.
• Correlation analysis to associate MINCR expression with clinical parameters (tumor volume, lymph node metastasis, overall survival).
• In vitro and in vivo experiments involving MINCR knockdown to evaluate its effects on GBC cell proliferation, invasion, apoptosis, and epithelial-mesenchymal transition (EMT).
• Analysis of the regulatory axis involving MINCR, miR-26a-5p, and enhancer of zeste homolog 2 (EZH2).

Main Results:

• MINCR was significantly upregulated in GBC tissues compared to normal tissues.
• High MINCR expression correlated positively with tumor volume and lymph node metastasis, and negatively with overall survival (OS).
• MINCR, miR-26a-5p, and EZH2 formed a regulatory axis influencing GBC cell proliferation, invasion, and apoptosis.
• MINCR knockdown suppressed GBC cell proliferation, reduced S-phase cells, increased apoptosis, and inhibited invasion by suppressing EMT.
• In vivo, MINCR silencing significantly reduced tumor volumes in GBC xenografts.

Conclusions:

• MINCR is upregulated in GBC and promotes tumorigenesis by regulating the miR-26a-5p/EZH2 axis.
• MINCR serves as a potential prognostic biomarker for GBC.
• Targeting MINCR may offer a novel therapeutic strategy for GBC.