title: MYO6 knockdown inhibits the growth and induces the apoptosis of prostate cancer cells by decreasing the phosphorylation of ERK1/2 and PRAS40.
abstract: Prostate cancer is the second most frequently diagnosed cancer among males around the world. Myosin VI (MYO6), as a motor protein, has been reported to be implicated in cancer-related cell migration and cellular functions. To investigate the role of MYO6 in prostate cancer, immunohistochemical analysis was firstly applied to prostate cancer tissues and revealed that MYO6 was closely related with the Gleason score in prostate cancer. Then we used specific short hairpin RNA (shRNA) to downregulate MYO6 expression in DU145 and PC-3 cells and found that decreased MYO6 expression significantly suppressed cell proliferation, as determined by MTT and colony formation assays. Flow cytometry confirmed that the suppression of MYO6 promoted cell cycle arrest at the G2/M and sub-G1 phase in the DU145 cells. Furthermore, PathScan intracellular signaling array analysis demonstrated that the phosphorylation of ERK1/2 and PRAS40 was downregulated in the DU145 cells following MYO6 knockdown. Knockdown of MYO6 downregulated the expression of AKT3 and upregulated the expression of PARP, as confirmed by western blot analysis. These results suggest that MYO6 plays an essential role in the progression of prostate cancer and silencing of MYO6 may be a promising therapeutic approach for prostate cancer.
authors.affiliation: Department of Urology, Fuzhou Dongfang Hospital, Xiamen University, Xiamen 361005, P.R. China.
authors.forename: Dong
authors.initials: D
authors.lastname: Wang
authors.affiliation: Department of Urology, Lushan Sanatorium of the PLA, Lushan 332000, P.R. China.
authors.forename: Libing
authors.initials: L
authors.lastname: Zhu
authors.affiliation: Department of Urology, Fuzhou General Hospital, Fujian Medical University, Fuzhou, Fujian 350025, P.R. China.
authors.forename: Min
authors.initials: M
authors.lastname: Liao
authors.affiliation: Department of Urology, Fuzhou General Hospital, Fujian Medical University, Fuzhou, Fujian 350025, P.R. China.
authors.forename: Tengyue
authors.initials: T
authors.lastname: Zeng
authors.affiliation: Department of Urology, Fuzhou General Hospital, Fujian Medical University, Fuzhou, Fujian 350025, P.R. China.
authors.forename: Wenli
authors.initials: W
authors.lastname: Zhuo
authors.affiliation: Department of Urology, Fuzhou General Hospital, Fujian Medical University, Fuzhou, Fujian 350025, P.R. China.
authors.forename: Shunliang
authors.initials: S
authors.lastname: Yang
authors.affiliation: Department of Urology, Fuzhou Dongfang Hospital, Xiamen University, Xiamen 361005, P.R. China.
authors.forename: Weizhen
authors.initials: W
authors.lastname: Wu
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics*; D017209:Apoptosis / Q000235:genetics*; D059447:Cell Cycle Checkpoints / Q000235:genetics; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics*; D015536:Down-Regulation / Q000235:genetics; D055785:Gene Knockdown Techniques / Q000379:methods; D006801:Humans; D020935:MAP Kinase Signaling System / Q000235:genetics*; D008297:Male; D018995:Myosin Heavy Chains / Q000235:genetics*; D010766:Phosphorylation / Q000235:genetics*; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000473:pathology; D034622:RNA Interference / Q000502:physiology; D034741:RNA, Small Interfering / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics
chemical_list: C484523:AKT1S1 protein, human; D048868:Adaptor Proteins, Signal Transducing; D034741:RNA, Small Interfering; C089785:myosin VI; D011065:Poly(ADP-ribose) Polymerases; D018995:Myosin Heavy Chains