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Introduction: 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 up-regulated in the reactive stroma of CRPC.Materials and Methods:We established an androgen independentLNCaP (LNCaP-AI)cell in steroid-reduced (SR) medium in 2 months.COL6A1 expression was examined by western blot during the LNCaP-AI induction.The function of COL6A1 was studied both in vitro and in vivo.Immunohistochemical staining of COL6A1 was performed in ten pairs of androgen sensitive PCa and CRPC samples.Results: We first 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.Over-expression of COL6A1was associated with accelerated S phase entry and elevated vitality in prostate cancer cells.COL6A1 could also promote tumorigenesis of LNCaP cell in vivo.Conclusions:Taken together, these data suggestan important role of COL6A1 in the molecular etiology of castration resistance prostate cancer and implicate the potential application of COL6A1 in CRPC therapy