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CDO1 is a new biomarker to discriminate aggressive forms of prostate cancer

ABSTRACT: Worldwide, prostate cancer (PCa) ranks second in terms of incidence and eighth in terms of mortality. While most cancers remain silent after initial treatment, some tumors recur. At present, we are unable to predict which patients are at risk of recurrence. In order to determine this risk of recurrence as early as at the biopsy stage, and to enable better therapeutic management of patients, it is essential to identify new biomarkers. In this study, we have demonstrated that Cysteine Dioxygenase CDO1 could be a predictive marker in PCa progression. In PCa, CDO1 expression could be regulated by methylation and androgen signaling pathway. Furthermore, inhibition of CDO1 expression in VCaP prostate cancer cells led to increased cell migration and non-adherent growth. Finally, transcriptomic analysis of these cells with inhibited CDO1 expression demonstrates the complex role of CDO1 and its involvement in the mechanisms regulating endoplasmic reticulum stress and protein unfolding. Altogether, these results describe the loss of CDO1 as a marker of aggressiveness in PCa. Furthermore, the loss of CDO1 is thought to be responsible for tumor progression in vitro by acting on multiple signaling pathways.

ORGANISM(S): Homo sapiens

PROVIDER: GSE326541 | GEO | 2026/07/15

REPOSITORIES: GEO

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Project description:The androgen receptor (AR) plays a key role in progression to incurable androgen-ablation resistant prostate cancer (PCA). We have identified three novel AR splice variants lacking the ligand binding domain (designated as AR3, AR4 and AR5) in hormone insensitive PCA cells. AR3, one of the major splice variants expressed in human prostate tissues, is constitutively active and its transcriptional activity is not regulated by androgens or antiandrogens. Immunohistochemistry analysis on tissue microarrays containing 429 human prostate tissue samples shows that AR3 is significantly upregulated during PCA progression and AR3 expression level is correlated with the risk of tumor recurrence after radical prostatectomy. Overexpression of AR3 confers ablation-independent growth of PCA cells while specific knock-down of AR3 expression (without altering AR level) in hormone resistant PCA cells attenuates their growth under androgen-depleted conditions in both cell culture and xenograft models, suggesting an indispensable role of AR3 in ablation-independent growth of PCA cells. Furthermore, AR3 may play a distinct yet essential role in ablation-independent growth through regulating a unique set of genes including AKT1, which are not regulated by the prototype AR. Our data suggest that aberrant expression of AR splice variants may be a novel mechanism underlying ablation-independence during PCA progression and AR3 may serve as a prognostic marker to predict patient outcome in response to hormonal therapy. Given that these novel AR splice variants are not inhibited by currently available anti-androgen drugs, development of new drugs targeting these AR isoforms may potentially be effective for treatment of ablation-resistant PCA. Total RNA was extracted from CWR-R1 and 22Rv1 cells treated with shAR3-1, shARa and the scrambled shRNA control, respectively. Each of CWR-R1 and 22Rv1 cells treated with shAR3-1 was compared with the scrambled shRNA control. The same experiments were performed for the cells treated with shARa.

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CDO1 is a new biomarker to discriminate aggressive forms of prostate cancer

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