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Progesterone/Org inhibits lung adenocarcinoma cell growth via membrane progesterone receptor alpha.

孕酮/Org 通过膜孕酮受体 α 抑制肺腺癌细胞生长。

  • 影响因子:2.17
  • DOI:10.1111/1759-7714.13528
  • 作者列表:"Xiao J","Chen X","Lu X","Xie M","He B","He S","You S","Chen Q
  • 发表时间:2020-06-11
Abstract

BACKGROUND:The aim of this study was to determine whether progesterone could inhibit the growth of lung adenocarcinoma cells via membrane progesterone receptor alpha (mPRα) and elucidate its potential mechanism. The relationship between mPRα expression and the survival prognosis of lung adenocarcinoma patients was studied. METHODS:A mPRα knockdown lung adenocarcinoma cell line was constructed and treated with P4 and Org (a derivative of P4 and specific agonist of mPRα). Cell proliferation was assessed using CCK-8 and plate colony formation assays. Protein expression was detected by western blotting. A nude mouse model of lung adenocarcinoma was established to assess the antitumor effect of P4/Org in vivo. RESULTS:We initially determined that mPRα could promote the development of lung adenocarcinoma through the following lines of evidence. High expression of mPRα both at the mRNA and protein level was significantly associated with the poor prognosis of lung adenocarcinoma patients. The downregulation of mPRα inhibited the proliferation of lung adenocarcinoma cells. We further showed that mPRα mediates the ability of P4 to inhibit the growth of lung adenocarcinoma cells through the following lines of evidence: P4/Org inhibited the proliferation of lung adenocarcinoma cells; mPRα mediated the ability of P4/Org to inhibit lung adenocarcinoma cell proliferation; mPRα mediated the ability of P4/Org to inhibit the PKA (cAMP-dependent protein kinase)/CREB (cAMP responsive element binding protein) and PKA/β-catenin signaling pathways; and P4/Org inhibited the growth of a lung adenocarcinoma tumor model in vivo. CONCLUSIONS:In summary, the results of our study show that progesterone can inhibit lung adenocarcinoma cell growth via mPRα.

摘要

背景: 本研究的目的是确定孕酮是否可以通过膜孕酮受体 α (mpr α) 抑制肺腺癌细胞的生长并阐明其潜在的机制。研究 mpr α 表达与肺腺癌患者生存预后的关系。 方法: 构建 mpr α 敲低的肺腺癌细胞系,用 P4 和 Org (P4 的衍生物和 mpr α 的特异性激动剂) 处理。使用 CCK-8 和平板集落形成试验评估细胞增殖。Western blotting 检测蛋白表达。建立肺腺癌裸鼠模型,评价 P4/Org 的体内抗肿瘤作用。 结果: 我们通过以下证据初步确定 mpr α 可促进肺腺癌的发展。Mpr α 在 mRNA 和蛋白水平的高表达与肺腺癌患者的不良预后显著相关。Mpr α 的下调抑制肺腺癌细胞的增殖。我们通过以下证据进一步表明 mpr α 介导了 P4 抑制肺腺癌细胞生长的能力: P4/Org 抑制肺腺癌细胞的增殖; mpr α 介导 P4/Org 抑制肺腺癌细胞增殖的能力; Mpr α 介导 P4/Org 抑制 PKA 的能力(CAMP 依赖性蛋白激酶)/CREB (cAMP 反应元件结合蛋白) 和 PKA/β-catenin 信号通路; 和 P4/Org 抑制体内肺腺癌肿瘤模型的生长。 结论: 总之,我们的研究结果表明,孕酮可以通过 mpr α 抑制肺腺癌细胞的生长。

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影响因子:1.84
发表时间:2020-01-01
来源期刊:Oncology letters
DOI:10.3892/ol.2019.11149
作者列表:["Das SK","Huang YY","Li B","Yu XX","Xiao RH","Yang HF"]

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