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Updated: Dec 26, 2025

Isolation, Culture, and Characterization of Prostate Cancer-Associated Fibroblasts
Published on: August 1, 2025
TACC3 promotes prostate cancer cell proliferation and restrains primary cilium formation
Yunkai Qie1, Lin Wang1, E Du1
1Department of Urology, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Pingjiang Road 23, Hexi District, Tianjin, 300211, China.
Abstract:
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.
Insights
Transforming acidic coiled-coil protein-3 (TACC3) is upregulated in prostate cancer (PCa), inhibiting primary cilia formation. TACC3 knockdown restrains PCa tumor growth by restoring cilia function.
Area of Science:
- Oncology
- Cell Biology
- Molecular Mechanisms
Background:
- Primary cilia abnormalities are common in cancers like prostate cancer (PCa).
- The molecular basis for repressed primary ciliogenesis in PCa remains largely unknown.
- Transforming acidic coiled-coil protein-3 (TACC3) is a centrosomal protein involved in cell division and cancer pathogenesis.
Purpose of the Study:
- To investigate the role of TACC3 in primary ciliogenesis during prostate cancer progression.
- To elucidate the molecular mechanisms by which TACC3 affects primary cilia formation in PCa cells.
Main Methods:
- Quantitative analysis of TACC3 expression in PCa tissues.
- In vitro and in vivo experiments involving TACC3 knockdown in PCa cells.
- Co-immunoprecipitation assays to study protein interactions.
Main Results:
- TACC3 expression is significantly upregulated in PCa.
- Knockdown of TACC3 inhibits PCa cell proliferation and tumor growth.
- TACC3 interacts with filamin A and disrupts its association with meckelin, leading to impaired primary cilia formation.
Conclusions:
- TACC3 plays a critical role in suppressing primary ciliogenesis in prostate cancer.
- Targeting TACC3 may represent a novel therapeutic strategy for PCa by restoring cilia function and inhibiting tumor growth.
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