NEXN targeting MYOCD by facilitating EMT-related β-catenin nuclear translocation modulates the metastasis of...

Area of Science:

• Oncology
• Molecular Biology
• Cell Biology

Background:

• Nexilin F-actin binding protein (NEXN) is vital for heart structure.
• The role of NEXN in hepatocellular carcinoma (HCC) progression remains largely unknown.

Purpose of the Study:

• To investigate the function and prognostic significance of NEXN in HCC.
• To elucidate the molecular mechanisms underlying NEXN's role in HCC.

Main Methods:

• Analysis of NEXN expression in HCC tissues and correlation with patient survival.
• In vitro and in vivo experiments to assess the effects of NEXN overexpression on HCC cell behavior and tumor growth.
• Investigation of the molecular pathways affected by NEXN, including epithelial-mesenchymal transition (EMT) and WNT/β-catenin signaling.

Main Results:

• NEXN expression was significantly reduced in HCC tissues, with lower levels correlating with poorer overall, disease-free, and progression-free survival.
• Overexpression of NEXN suppressed HCC cell proliferation, colony formation, migration, and invasion in vitro, and inhibited tumor formation in vivo.
• NEXN overexpression led to decreased expression of mesenchymal markers, partial upregulation of E-cadherin, reduced nuclear β-catenin accumulation, and modulated EMT via the NEXN-MYOCD-β-catenin axis.

Conclusions:

• Diminished NEXN expression promotes HCC progression and metastasis by facilitating EMT through the NEXN-MYOCD-β-catenin signaling pathway.
• NEXN acts as a tumor suppressor in HCC.
• Targeting the NEXN-MYOCD-β-catenin axis offers a potential therapeutic strategy for HCC metastasis.