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Role and mechanism of PTEN in Burkitt's lymphoma.

PTEN 在伯基特淋巴瘤中的作用及机制

  • 影响因子:3.07
  • DOI:10.3892/or.2020.7457
  • 作者列表:"Li C","Xu Y","Xin P","Zheng Y","Zhu X
  • 发表时间:2020-02-01
Abstract

The aim of the present study was to explore the possible mechanisms of phosphatase and tensin homolog (PTEN) in the pathogenesis of Burkitt's lymphoma, and provide novel information that can be used in the targeted treatment of this disease. PTEN lentiviral overexpression vector and short‑hairpin PTEN silencing vectors were constructed. The effect of PTEN on the growth and proliferation of CA46 and RAJI cells was analyzed using a Cell Counting Kit‑8 assay. Apoptosis was detected by Hoechst 33342 and propidium iodide double staining. Flow cytometry was used to analyze the cell cycle. A Transwell chamber was used to detect cell migration and invasion abilities. Western blot analysis was used to detect related protein changes. The mechanism of the effect of PTEN on the biological characteristics of Burkitt's lymphoma cells was subsequently analyzed. The results revealed that PTEN inhibited the proliferation of CA46 and RAJI cells by downregulating the expression of p‑AKT, It was indicated that the upregulation of proapoptotic proteins (including Bad and Bax) induced apoptosis, regulated cyclin (including P53, P21, CDK4, CDK6, cyclin D3 and cyclin H) to inhibit cell cycle progression, and mediated epithelial‑mesenchymal transition‑like cell markers (including E‑cadherin, N‑cadherin, β‑catenin, TCF‑8, vimentin, Slug and Snail) to inhibit cell migration and invasion. In conclusion, the tumor‑suppressor gene PTEN inhibited the phosphoinositide 3‑kinase/protein kinase B (PI3K/AKT) signaling pathway and inhibited the proliferation and migration of Burkitt's lymphoma cells, induced apoptosis and cell cycle arrest, thus playing a crucial role in the pathogenesis of Burkitt's lymphoma.

摘要

本研究旨在探讨磷酸酶和张力蛋白同源物 (PTEN) 在伯基特淋巴瘤发病中的可能机制。并提供了新的信息,可用于这种疾病的靶向治疗。构建 PTEN 慢病毒过表达载体和短发夹 PTEN 沉默载体。使用细胞计数 kit ‑ 8 试验分析 PTEN 对 CA46 和 RAJI 细胞生长和增殖的影响。通过 Hoechst 33342 和碘化丙啶双染色法检测细胞凋亡。流式细胞仪分析细胞周期。使用 Transwell 小室检测细胞迁移和侵袭能力。Western blot 分析检测相关蛋白变化。随后分析 PTEN 对伯基特淋巴瘤细胞生物学特性影响的机制。结果表明,PTEN 通过下调 p ‑ akt 的表达抑制 CA46 和 RAJI 细胞的增殖,表明促凋亡蛋白 (包括 Bad 和 Bax) 的上调诱导了细胞凋亡, 调节细胞周期蛋白 (包括 P53 、 P21 、 CDK4 、 CDK6 、 cyclin D3 和 cyclin H)抑制细胞周期进程,并介导上皮-间质转化样细胞标志物 (包括 e ‑ cadherin 、 n ‑ cadherin 、 β ‑ catenin 、 tfc ‑ 8 、 vimentin 、 Slug 和 Snail) 抑制细胞迁移和侵袭。总之,肿瘤抑制基因 PTEN 抑制磷酸肌醇 3 ‑ 激酶/蛋白激酶 B (PI3K/AKT) 信号通路,抑制伯基特淋巴瘤细胞的增殖和迁移, 诱导细胞凋亡和细胞周期阻滞,从而在伯基特淋巴瘤的发病机制中发挥至关重要的作用。

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关键词: 暂无
翻译标题与摘要 下载文献
影响因子:3.07
发表时间:2020-02-01
来源期刊:Oncology reports
DOI:10.3892/or.2020.7457
作者列表:["Li C","Xu Y","Xin P","Zheng Y","Zhu X"]

METHODS:The aim of the present study was to explore the possible mechanisms of phosphatase and tensin homolog (PTEN) in the pathogenesis of Burkitt's lymphoma, and provide novel information that can be used in the targeted treatment of this disease. PTEN lentiviral overexpression vector and short‑hairpin PTEN silencing vectors were constructed. The effect of PTEN on the growth and proliferation of CA46 and RAJI cells was analyzed using a Cell Counting Kit‑8 assay. Apoptosis was detected by Hoechst 33342 and propidium iodide double staining. Flow cytometry was used to analyze the cell cycle. A Transwell chamber was used to detect cell migration and invasion abilities. Western blot analysis was used to detect related protein changes. The mechanism of the effect of PTEN on the biological characteristics of Burkitt's lymphoma cells was subsequently analyzed. The results revealed that PTEN inhibited the proliferation of CA46 and RAJI cells by downregulating the expression of p‑AKT, It was indicated that the upregulation of proapoptotic proteins (including Bad and Bax) induced apoptosis, regulated cyclin (including P53, P21, CDK4, CDK6, cyclin D3 and cyclin H) to inhibit cell cycle progression, and mediated epithelial‑mesenchymal transition‑like cell markers (including E‑cadherin, N‑cadherin, β‑catenin, TCF‑8, vimentin, Slug and Snail) to inhibit cell migration and invasion. In conclusion, the tumor‑suppressor gene PTEN inhibited the phosphoinositide 3‑kinase/protein kinase B (PI3K/AKT) signaling pathway and inhibited the proliferation and migration of Burkitt's lymphoma cells, induced apoptosis and cell cycle arrest, thus playing a crucial role in the pathogenesis of Burkitt's lymphoma.

关键词: 暂无
翻译标题与摘要 下载文献
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