
Identification of novel molecular target(s) is essential for designing newer mechanistically driven approaches for treating prostate cancer (PCa), one of the leading causes of morbidity and mortality in men. This study determined the role of polo‐like kinase 4 (PLK4), which regulates centriole duplication and centrosome amplification (CA) in PCa. CA is prevalent in PCa and arises predominantly by centriole overduplication instead of cell doubling events. Loss of centrioles is cellular stress that can promote senescence and suggests that PLK4 inhibition may be a viable therapeutic strategy in PCa.
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