Mortalin promotes the evolution of androgen-independent prostate cancer through Wnt/β-catenin signaling pathway

TL;DR

Mortalin helps prostate cancer become resistant to hormone therapy by activating a key signaling pathway, suggesting it could be a new target for treatment.

Contribution

This study identifies Mortalin as a novel driver of androgen-independent prostate cancer through the Wnt/β-catenin pathway.

Findings

Mortalin is upregulated in prostate cancer tissues and promotes tumor progression.

Mortalin regulates epithelial-mesenchymal transition via the Wnt/β-catenin pathway.

Mortalin may serve as a promising immunotherapeutic target for prostate cancer.

Abstract

Prostate cancer (PC) is a major global health concern affecting male individuals. Among its variants, androgen-independent prostate cancer exhibits slow progression and lacks effective treatment targets, rendering it insensitive to hormone therapy. Recent reports have highlighted the significance of Mortalin, an important oncogene, in tumor migration and invasion through various signaling pathways. Experimental evidence from in-vivo and in-vitro studies indicate upregulated expression of Mortalin in prostate cancer tissues. Moreover, it has been shown to regulate the epithelial-mesenchymal transition (EMT) process via the Wnt/β-catenin signaling pathway, thereby promoting prostate cancer proliferation and metastasis. These findings suggest that Mortalin may serve as a promising novel immunotherapeutic target for prostate cancer.

The online version contains supplementary material available at 10.1186/s12935-024-03345-x.

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