银屑病是常见的慢性、复发性、炎症性皮肤病,角质形成细胞(keratinocyte,KC)增殖分化失调作为其发病原因之一,具体机制尚未明确。细胞外信号调节激酶(extracellular signal regulated kinase,ERK)信号通路在其中发挥着重要作用,微小RNA(...银屑病是常见的慢性、复发性、炎症性皮肤病,角质形成细胞(keratinocyte,KC)增殖分化失调作为其发病原因之一,具体机制尚未明确。细胞外信号调节激酶(extracellular signal regulated kinase,ERK)信号通路在其中发挥着重要作用,微小RNA(microRNA,miRNA)、长链非编码RNA(lncRNA)、细胞因子等作为ERK信号通路的上游分子参与调控银屑病表皮角质形成细胞的增殖与分化过程。文章旨在对这一通路在银屑病角质形成细胞过度增殖中的作用机制做一综述。展开更多
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 dihydrot...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.展开更多
文摘银屑病是常见的慢性、复发性、炎症性皮肤病,角质形成细胞(keratinocyte,KC)增殖分化失调作为其发病原因之一,具体机制尚未明确。细胞外信号调节激酶(extracellular signal regulated kinase,ERK)信号通路在其中发挥着重要作用,微小RNA(microRNA,miRNA)、长链非编码RNA(lncRNA)、细胞因子等作为ERK信号通路的上游分子参与调控银屑病表皮角质形成细胞的增殖与分化过程。文章旨在对这一通路在银屑病角质形成细胞过度增殖中的作用机制做一综述。
文摘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.
