The cell cycle regulator PLK1 promotes murine melanoma progression by regulating the transcription factor BACH1.

ABSTRACT: Polo-like kinase 1 (PLK1), a critical cell cycle regulator, is associated with cancer progression and negatively correlates with patient survival in cutaneous melanoma based on clinical database analysis. In a melanoma mouse model induced by BRafCA mutation and Pten-deficiency, we observed that PLK1 overexpression mediated metabolic reprogramming to markedly accelerate tumor growth, promote metastasis, and shortened mice survival. Mechanistically, PLK1 stabilizes BTB domain and CNC homolog 1 (BACH1), which serves as a crucial transcription factor for genes involved in cancer metabolism and metastasis. Moreover, the PLK1/BACH1 axis confers resistance to Vemurafenib, a BRAFV600E inhibitor, in melanoma. In light of this finding, we attempted an innovative pharmacological combination targeting

SUBMITTER: Mao F 

PROVIDER: S-EPMC12643297 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature