ArticlePLoS biology2025
The cell cycle regulator PLK1 promotes murine melanoma progression by regulating the transcription factor BACH1.
Article in PLoS biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- MicroRNAs and Cellular Senescence in Melanoma: An Underexplored Link to Tumor Progression-A Systematic Review with Bioinformatics Analyses.International journal of molecular sciences · 2026Pooled it
- A tailored in vivo CRISPR screen identifies BAP1 as a potent tumor suppressor of sarcoma.JCI insight · 2026Article
- Cell-cycle-dependent regulation of DNA end resection by PLK1 and PLK3 without CtIP level modulation.iScience · 2026Article
Corrections and comments
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Authors and funding
12 authors.
Funding
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 both BRAFV600E and PLK1, identifying a synergistic efficiency to this approach to suppress tumor growth. Overall, we have discovered a novel function of PLK1 that is independent of the cell cycle, which could pave new ways for melanoma therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.