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Effect of androgen withdrawal on activation of ERKs and expression of cell cycle regulation molecules in human prostate carcinoma cells

Effect of androgen withdrawal on activation of ERKs and expression of cell cycle regulation molecules in human prostate carcinoma cells
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摘要 Objective: To explore the possible mechanisms of growth regression of human androgen dependent prostate carcinoma cells caused by androgen withdrawal. Methods: After 24 h of treatment with 1 × 10-9 mol/L dihydrotestosterone (DHT), the expression of phosphorylated ERK proteins and cell cycle regulation molecules including CDK2, CDK4, CDK6 and P27kip1 in human androgen dependent prostate carcinoma cell line LNCaP was measured by Western blot analysis 0 h, 8 h and 24 h of after androgen withdrawal. Human androgen independent prostate carcinoma cell line PC-3 was also examined as control. Results: Down-regulation of phosphorylated ERK, CDK2, CDK4 and CDK6 and up-regulation of P27kip1 were found initially in LNCaP cell line 8 h after androgen withdrawal. The levels of phosphorylated ERK and CDKs decreased continuously and reached the lowest after 24 h, while continuous elevation of P27kip1 was detected thereafter to 24 h. No expression change of phosphorylated ERK, CDKs and P27kip1 were detected in PC-3 cell line. Conclusion: The androgen withdrawal can cause ERKs activation decrease and cell cycle regulation molecules changes, which may be one of the mechanisms for inhibited growth of androgen dependent prostate carcinoma after androgen ablation by either operative or medicine methods. Abstact Objective:To explore the possible mechanisms of growth regression of human androgen dependent prostate carcinoma cells caused by androgen withdrawal.Methods:After 24 h of treatment with 1×10^-9 mol/L dihydrotestosterone(DHT),the expression of phosphorylated ERK proteins and cell cycle regulation molecules including CDK2,CDK4,CDK6 and P27^kip1 in human androgen dependent prostate carcinoma cell line LNCaP was measured by Wester blot analysis 0h,8h and 24h of after androgen withdrawal.Human androgen independent prostate carcinoma cell line PC-3was also examined as control.Results:Down-regula-tion of phosphorylated ERK,CDK2,CDK4 and CDK6 and up-regulation of P27^kip1 were found initially in LNCaP cell line 8h after androgen withdrawal.The levels of phosphorylated ERK and CDKs decreased con-tinuously and reached the lowest after 24h,while continuous elevation of P27^kip1 was detected thereafter to 24h.No expression change of phosphorylated ERK,CDKs and P27^kip1 were detected in PC-3 cell line.Conclu-sion:The androgen withdrawal can cause ERKs activation decrease and cell cycle regulation molecules changes, which may be one of the mechanisms for inhibited growth of androgen dependent prostate carcinoma after androgen ablation by either operative or medicine methods.
出处 《Journal of Medical Colleges of PLA(China)》 CAS 2002年第3期178-180,共3页 中国人民解放军军医大学学报(英文版)
关键词 prostate neoplasm CARCINOMA ANDROGEN PROLIFERATION cell cycle 人前列腺癌细胞 ERKs活化 表达 细胞周期调节分子 雄激素去除
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  • 1[1]Ito Y, Sasaki Y, Horimoto M et al. Activation of mitogen-activated protein kinases/extracellular signal-regulated kinases in human hepatocellular carcinoma [J]. Hepatology, 1998; 27 (4):951
  • 2[2]Weinberg RA. The retinoblastoma protein and cell cycle control [J]. Cell,1995;81(3):323
  • 3[3]Ye D, Mendelsohn J, Fan Z et al. Augmentation of a humanized anti-HER2mAb 4D5 induced growth inhibition by a human-mouse chimeric anti-EGF receptor mAb C225 [J]. Oncogene, 1999;18(3):731
  • 4[4]Seger R, Krebs EG. The MAPK signaling cascade [J]. FASEB, 1995;9(9):726
  • 5[5]Weinberg RA. The retinoblastoma protein and cell cycle control [J]. Cell,1995;81(2):323
  • 6[6]Gioeli D, Mandell JW, Petroni GR et al. Activation of mitogen-activated protein kinase associated with prostate cancer progression [J]. Cancer Res,1999;59(2) :279
  • 7[7]Grana X, Reddy EP. Cell cycle control in mammalian cells: Role of cyclins,cyclin-dependent kinase (CDKs), growth suppressor gene, and cyclin-dependent kinase inhibitors (CKIs) [J]. Oncogene, 1995;11(2):211
  • 8[8]Guan KL, Jenkin CW, Li Y et al. Growth suppression by p18, a p16INK4/MTSI- and p14INK4B/MTS2-related CDK6 inhibitor, correlates with wildtype pRb function [J]. Genes Dev, 1994;8(24):2939
  • 9[9]Ye D, Mendelsohn J, Fan Z et al. Androgen and epidermal growth factor down-regulate cyclin-dependent kinase inhibitor p27kipl and co-stimulate proliferation of MDA PCa 2a and MDA PCa 2b prostate cancer cells [J].Clin Can Res, 1999;5(8):2171
  • 10[10].Cordon-Cardo C, Koff A, Drobnjak M et al. Distinct altered patterns of p27kipl gene expression in benign prostatic hyperplasis and prostatic carcinoma [J]. J Natl Cancer Inst, 1998;90(17):1284

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