通过IL-6/JAK2/STAT3 途径,SOCS2的高表达抑制了宫颈癌中的EMT和M2巨噬细胞极化。
Overexpression of SOCS2 Inhibits EMT and M2 Macrophage Polarization in Cervical Cancer via IL-6/JAK2/STAT3 Pathway.
发表日期:2023 Aug 18
作者:
Dan Li, Yandan Huang, Min Wei, Bin Chen, Yan Lu
来源:
CYTOKINE & GROWTH FACTOR REVIEWS
摘要:
SOCS2是压制细胞因子信号(SOCS)蛋白家族的成员,与多种癌症的发生和发展有关。本研究揭示了SOCS2在宫颈癌中的表达和分子机制。本研究使用RT-qPCR、Western Blot和免疫组化方法检测宫颈癌组织和肿瘤细胞中SOCS2的表达水平。通过慢病毒过表达SOCS2在SiHa细胞中。通过体外实验研究了SOCS2过表达前后宫颈癌细胞增殖、迁移和侵袭能力的变化。使用Western Blot检测IL-6/JAK2/STAT3通路和EMT相关蛋白的表达。将M0巨噬细胞与肿瘤条件培养基共培养,通过RT-qPCR检测SOCS2对巨噬细胞极化的影响。宫颈癌组织中SOCS2的表达水平显著下调。SOCS2与CD163+M2巨噬细胞呈负相关。SOCS2的过表达抑制了宫颈癌细胞的增殖、迁移和侵袭。Twist-2、N-钙粘蛋白和Vimentin的表达下调,而E-钙粘蛋白的表达上调。此外,IL-6、p-JAK2和p-STAT3的表达下调。添加RhIL-6后,LV-SOCS2组中E-钙粘蛋白蛋白表达发生逆转。LV-SOCS2组的CM抑制了M2巨噬细胞的极化。SOCS2通过IL-6/JAK2/STAT3通路作用于宫颈癌,具有新的生物学靶点和抑制剂作用。版权所有© Bentham Science Publishers; 如有任何问题,请发送邮件至epub@benthamscience.net。
SOCS2 is a member of the suppressor of cytokine signaling (SOCS) protein family associated with the occurrence and development of multiple cancers. This study revealed the expression and molecular mechanisms of SOCS2 in cervical cancer.In this study, RT-qPCR, Western Blot, and immunohistochemistry were used to detect the expression level of SOCS2 in cervical cancer tissues and tumor cells. We overexpressed SOCS2 in SiHa cells via lentivirus. In-vitro experiments were used to investigate the changes in cervical cancer cell proliferation, migration, and invasion ability before and after SOCS2 overexpression. Western Blot was used to detect the expression of IL-6/JAK2/STAT3 pathway and EMT-related proteins. M0 macrophages were co-cultured with the tumor-conditioned medium. The effect of SOCS2 on macrophage polarization was examined by RT-qPCR.SOCS2 expression level was significantly downregulated in cervical cancer tissues. SOCS2 was negatively correlated with CD163+M2 macrophages. Overexpression of SOCS2 inhibited the proliferation, migration, and invasion of cervical cancer cells. The expressions of Twist-2, N-cadherin, and Vimentin were decreased, while the expression of E-cadherin was increased. Moreover, the expression of IL-6, p-JAK2, and p-STAT3 were decreased. After the addition of RhIL-6, the expression of E-cadherin protein in the LV-SOCS2 group was reversed. CM in the LV-SOCS2 group inhibited the polarization of M2 macrophages.SOCS2 acts as a novel biological target and suppressor of cervical cancer through IL-6/JAK2/STAT3 pathway.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.