Research Papers:

Reactive stroma component COL6A1 is upregulated in castration-resistant prostate cancer and promotes tumor growth

Yi-Ping Zhu _, Fang-Ning Wan, Yi-Jun Shen, Hong-Kai Wang, Gui-Ming Zhang and Ding-Wei Ye

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Oncotarget. 2015; 6:14488-14496. https://doi.org/10.18632/oncotarget.3697

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Yi-Ping Zhu1,2,*, Fang-Ning Wan1,2,*, Yi-Jun Shen1,2, Hong-Kai Wang1,2, Gui-Ming Zhang1,2 and Ding-Wei Ye1,2

1 Department of Urology, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China

2 Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China

* These authors have contributed equally to this work

Correspondence to:

Ding-Wei Ye, email:

Keywords: castration-resistant prostate cancer, COL6A1, reactive stroma, tumorigenesis

Received: January 12, 2015 Accepted: March 01, 2015 Published: March 30, 2015


Castration-resistant prostate cancer (CRPC) remains the most critical challenge in the clinical management of prostate cancer (PCa). Reactive stromal changes in PCa are likely involved in the emergence of CRPC. In the present study, we identified a novel oncogene termed COL6A1 which was upregulated in the reactive stroma of CRPC. We established an androgen-independent LNCaP (LNCaP-AI) cell line in steroid-reduced (SR) medium within 2 months. We examined COL6A1 expression with western blot during the LNCaP-AI induction, and studied the function of COL6A1 in vitro and in vivo. Immunohistochemical staining of COL6A1 was performed in ten pairs of androgen-sensitive PCa and CRPC samples. We demonstrated that COL6A1 expression was markedly increased in LNCaP-AI cells and CRPC tissues compared with LNCaP cells and paired androgen-sensitive PCa specimens. In vitro, COL6A1 knockdown resulted in G1-S cell cycle arrest and descended vitality. Overexpression of COL6A1 was associated with accelerated S phase entry and elevated vitality in prostate cancer cells. COL6A1 also promoted tumorigenesis of LNCaP cells in vivo. Taken together, these data suggest an important role of COL6A1 in the molecular etiology of castration-resistant prostate cancer, and support the potential use of COL6A1 in CRPC therapy.

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