A new novel gene ABCC5 promotes castration-resistant prostate cancer progression through ERK carcinogenic pathway

Date 24 November 2018
Event ESMO Asia 2018 Congress
Session Poster display - Cocktail
Topics Prostate Cancer
Cancer Biology
Translational Research
Presenter Guangjie Ji
Citation Annals of Oncology (2018) 29 (suppl_9): ix67-ix73. 10.1093/annonc/mdy434
Authors G. Ji
  • Department Of Urology, Peking University First Hospital, 100034 - Beijing/CN



To explore the mechanism of Castration-Resistant Prostate Cancer(CRPC) progression, providing the potential therapeutic target effectively for advanced prostate cancer treatment.


We compared the differentiation expressed genes of prostate cancer primary tumor and metastases from three GEO gene datasets (GDS2545, GDS3546). Then we analysis the effect of these differential expression genes on the Gleason grade group(GGG), free biochemical recurrence(BCR) and overall survival(OS) of prostate cancer in The Cancer Genome Atlas(TCGA). The relation of the expression level of ABCC5 and the time of CRPC progression of 50 patients in our hospital from 2011-2016 was detected by immunohistochemistry technology. Also, we knock down the ABCC5 by shRNA of CRPC cell line C4-2, and test the effects of ABCC5 on cell growth. Finally, we probe the possible mechanism of ABCC5 by gene set enrichment analysis(GSEA).


The expression of ABCC5 was higher in metastases of prostate cancer than in primary tumor (p < 0.0001). and in high ABCC5 patients with higher BCR (p < 0.0001, HR = 2.3) and lower OS(p < 0.0001, HR = 12) and higher GGG(p = 0.001) and shorter time of progression to CRPC, compared with low ABCC5 group. ABCC5 could accelerate the CRPC cell growth and inhibit CRPC cell apoptosis. ERK carcinogenic pathway was found enrichment greatly in high ABCC5 prostate cancer(p < 0.001).


ABCC5 could have the potential ability to enhance the aggressiveness of prostate cancer to involve into CRPC by ERK carcinogenic pathway, which would bring a new vision for CRPC precision therapy.

Editorial acknowledgement

Clinical trial identification

Legal entity responsible for the study

Guangjie Ji.


Has not received any funding.


The author has declared no conflicts of interest.