LMNB2 promotes prostate cancer progression and epithelial-mesenchymal transition via the Wnt/β-catenin pathway

Prostate cancer (PCa) is a leading cause of cancer mortality in men. Lamin B2 (LMNB2) has been implicated in various cancers, but its functional role and molecular mechanisms in PCa progression remain poorly characterized.

We analyzed LMNB2 expression and clinical associations using transcriptomic data from TCGA, GEO and PCaDB. Functional enrichment analysis identified related pathways. LMNB2 was knocked down in PCa cell lines (LNCaP and PC-3) and its effects on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) were assessed. The Wnt/β-catenin pathway was investigated using agonist SKL2001. Subcutaneous xenograft models in nude mice were established for in vivo validation.

The experimental findings demonstrate that reduced expression of LMNB2 substantially impairs cellular proliferation, tumor formation ability, and the epithelial-to-mesenchymal transition phenotype in prostate carcinoma cells by interfering with Wnt/β-catenin pathway activation. Furthermore, LMNB2 knockdown effectively suppressed tumor growth in mouse xenograft models. Notably, immunohistochemical evaluation of tumor tissues from xenografts revealed significantly higher LMNB2 protein levels that were associated with poor patient prognosis. These comprehensive results establish LMNB2 as a critical oncogenic driver that promotes both primary tumor development and metastatic spread in prostate adenocarcinoma.

LMNB2 promotes prostate cancer progression by activating the Wnt/β-catenin signaling pathway and inducing EMT, highlighting its potential as a prognostic biomarker and therapeutic target.