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Role of androgen receptor in prostate cancer cell proliferation by use of RNAi / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12)1986.
Article in Chinese | WPRIM | ID: wpr-522451
ABSTRACT

AIM:

To study the role of androgen receptor (AR) in hormone-dependent and hormone-independent prostate cancer cell proliferation by knocking down AR expression with adenovirus-delivered siRNA.

METHODS:

Four well-designed siRNAs were synthesized and inserted into the adenovirus plasmid pShuttle-H1-Ri. The recombinant pShuttle-H1-Ri-AR plasmid was then co-transfected with pcDNA-AR to HEK293 cell line and Western blot was used to detect the inhibitory efficiency of different siRNAs on AR expression. Recombinant adenovirus containing more efficient siRNAs were prepared and used to infect three different humane prostate cancer cell lines including LNCapC4-2B and CWR22Rv1. The efficiency of knocking down AR expression was detected by Western blot. The effect of AR-knocking down on cell proliferation was detected by MTT colorimetric assay.

RESULTS:

All of the four designed siRNAs could knock down AR expression in transient co-transfection. Infecting with recombinant adenovirus containing more efficient siRNAs in hormone-dependent and hormone-independent prostate cancer cell lines specifically knocked down AR expression with high efficiency. Knocking down AR expression significantly decreased the proliferation rate in all these prostate cancer cells.

CONCLUSION:

The suppressed expression of AR in prostate cell lines mediated by siRNA could efficiently inhibit the cell proliferation, and these results show that AR plays an important role in the proliferation of hormone-dependent and hormone-independent prostate cancer cells. AR is an important therapeutic target for the treatment of prostate cancer.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 1986 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 1986 Type: Article