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01.12.2012 | Research | Ausgabe 1/2012 Open Access

World Journal of Surgical Oncology 1/2012

3p21.3 tumor suppressor gene RBM5 inhibits growth of human prostate cancer PC-3 cells through apoptosis

World Journal of Surgical Oncology > Ausgabe 1/2012
Lijing Zhao, Ranwei Li, Chen Shao, Ping Li, Jian Liu, Ke Wang
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1477-7819-10-247) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

LZ performed all the experiments and drafted the manuscript. RL collected and provided the tissues. CS, PL, and JL have contributed part of the experiment, research design, and the data collection. KW oversaw the design of the study, was involved in the critically revised the manuscript. All authors have read and approved the final version of the manuscript.



Recent studies have indicated that the nuclear RNA-binding protein RBM5 has the ability to modulate apoptosis and suppress tumor growth. The aim of this study is to investigate the expression of RBM5 in human prostate cancer and its mechanism of tumor suppression.


The expression of RBM5 protein in cancerous prostatic tissues and normal tissues was examined by IHC. PC-3 cell line was used to determine the apoptotic function of RBM5 in vitro. PC-3 cells were transiently transfected with pcDNA3.1-RBM5. Cell viability was determined by MTT assay. Rhodamine 123 staining and Annexin V analysis were performed to observe the apoptotic activity of PC-3 cells overexpressing RBM5. Expression of apoptosis-related genes was assessed by western blot.


The expression of RBM5 protein was significantly decreased in cancerous prostatic tissues compared to the normal tissues. PC-3 cells overexpressing RBM5 showed not only significant growth inhibition compared with the vector controls, but also dysfunction of mitochondrial membrane potential and increased apoptotic activity. To further define RBM5 function in apoptotic pathways, we investigated differential expression profiles of various BH3-only proteins including Bid, Bad, and Bim, and apoptosis regulatory proteins include P53, cleaved caspase9, and cleaved caspase3. We found that the expression of both BH3-only proteins and apoptosis regulatory proteins was increased in RBM5 transfected cells.


The expression of RBM5 protein was significantly decreased in cancerous prostatic tissues, which suggests that RBM5 plays an important role in the pathogenesis of prostate cancer. RBM5 may induce the apoptosis of prostate cancer PC-3 cells by modulating the mitochondrial apoptotic pathway, and thus RBM5 might be a promising target for gene therapy on prostate cancer.
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