Although primary cilia abnormalities have been frequently observed in multiple cancers, including prostate cancer (PCa), the molecular mechanisms underlying primary ciliogenesis repression in PCa cells remain unclear. Transforming acidic coiled-coil protein-3 (TACC3), whose deregulation has been implicated in the pathogenesis of several types of cancer, is a key centrosomal protein that plays a crucial role in centrosome/microtubule dynamics, potentially impacting primary cilium generation. Here, we showed that TACC3 was markedly upregulated in PCa and that knockdown of TACC3 restrained tumorigenesis and tumor growth in vitro and in vivo. Additionally, we found that TACC3 interacts with filamin A, and elevated levels of TACC3 disrupted the interaction between filamin A and meckelin, thereby restraining primary cilium formation in PCa cells.

中文翻译：

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TACC3促进前列腺癌细胞增殖并抑制初级纤毛形成。

尽管在包括前列腺癌（PCa）在内的多种癌症中经常观察到原发性纤毛异常，但仍不清楚PCa细胞中原发性纤毛发生抑制的分子机制。转化酸性卷曲螺旋蛋白3（TACC3），其失调与多种类型的癌症的发病机制有关，是一种关键的中心体蛋白，在中心体/微管动力学中起着至关重要的作用，可能会影响初级纤毛的产生。在这里，我们显示了PCa中TACC3明显上调，而敲除TACC3抑制了体内外的肿瘤发生和肿瘤生长。此外，我们发现TACC3与纤维蛋白A相互作用，并且升高的水平的TACC3破坏了纤维蛋白A和meckelin之间的相互作用，从而抑制了PCa细胞中初级纤毛的形成。