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首页> 外文期刊>Cancer Management and Research >STIP1 Regulates Proliferation and Migration of Lung Adenocarcinoma Through JAK2/STAT3 Signaling Pathway
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STIP1 Regulates Proliferation and Migration of Lung Adenocarcinoma Through JAK2/STAT3 Signaling Pathway

机译：STIP1通过JAK2 / Stat3信号通路调节肺腺癌的增殖和迁移

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Purpose: Recent studies have shown that STIP1 is associated with proliferation and migration in numerous types of tumors; however, the role of STIP1 in lung adenocarcinoma is still poorly understood. Therefore, the aim of this study was to evaluate the role of STIP1 in lung adenocarcinoma, in vitro and in vivo. Methods: The expression of STIP1 in lung adenocarcinoma was assessed by immunohistochemistry, RT-qPCR, and Western blot. The effects of STIP1 on the proliferation of lung adenocarcinoma cells were detected by the cell counting kit-8 assay; the effect of STIP1 on adhesion of lung adenocarcinoma cells was detected by Giemsa staining, while the cell scratch and Transwell assays were employed to examine the effect of STIP1 on the migratory ability of lung adenocarcinoma cells. Finally, apoptosis was evaluated by Hoechst staining and flow cytometry. Results: The expression level of STIP1 in lung adenocarcinoma tissue was significantly higher than that in adjacent normal tissue ( P 0.05). Compared with that in nontransfected controls, cell proliferation, adhesion, and migration, as well as vimentin protein expression and levels of phosphorylated JAK2/STAT3, were significantly decreased ( P 0.05) in A549 lung adenocarcinoma cells transfected with STIP1 shRNA, whereas E-cadherin protein expression and rates of apoptosis were significantly increased in these cells ( P 0.05). Conclusion: Elevated expression of STIP1 in lung adenocarcinoma may enhance the proliferative, adhesive, and migratory ability, and reduce the apoptosis of lung adenocarcinoma cells through the JAK2/STAT3 signaling pathway and epithelial-mesenchymal transition (EMT), thereby promoting the recurrence and metastatic potential of this cancer. The results indicate that STIP1 may be an effective therapeutic target for the treatment of lung adenocarcinoma.
机译：目的：最近的研究表明，STIP1与许多类型的肿瘤中的增殖和迁移有关;然而，STIP1在肺腺癌中的作用仍然很糟糕。因此，本研究的目的是评估STIP1在肺腺癌，体外和体内的作用。方法：通过免疫组织化学，RT-QPCR和Western印迹评估肺腺癌STIP1的表达。细胞计数试剂盒-8测定检测STIP1对肺腺癌细胞增殖的影响; Giemsa染色检测到STIP1对肺腺癌细胞粘附的影响，而MEMSA染色检测到细胞划痕和转发测定检查STIP1对肺腺癌细胞迁徙能力的影响。最后，通过Hoechst染色和流式细胞术评估细胞凋亡。结果：肺腺癌组织中STIP1的表达水平显着高于相邻正常组织中的表达水平（P <0.05）。与非扫描的对照，细胞增殖，粘附和迁移，以及Vimentin蛋白表达和磷酸化JAK2 / Stat3的水平相比，在用STIP1 shRNA转染的A549肺腺癌细胞中显着降低（P <0.05），而E-在这些细胞中，钙粘蛋白蛋白表达和细胞凋亡的速率显着增加（P <0.05）。结论：肺腺癌中STIP1的表达升高可提高通过JAK2 / Stat3信号通路和上皮间充质转换（EMT）降低肺腺癌细胞的凋亡，从而促进复发和转移这种癌症的潜力。结果表明，STIP1可以是治疗肺腺癌的有效治疗靶标。

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