南美超级胎牛血清999尝鲜特惠
转染试剂低至5折
基质胶阶梯特惠
积分商城,好礼送不停
南美超级胎牛血清999尝鲜特惠
转染试剂低至5折
基质胶阶梯特惠
积分商城,好礼送不停
分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

SOCS4上调促进食管鳞状细胞癌细胞增殖和迁移的研究

Up-regulation of SOCS4 promotes cell proliferation and migration in esophageal squamous cell carcinoma

Jie Ying, Huan-Huan Huang, Miao-Miao Zhang, Jin-Fei Chen

Journal:Translational Cancer Research

IF:1.24

DOI:10.21037/tcr-21-700

PMID:35116557

Published:2021-05-01

research field:分子生物学免疫学病毒学

Abstract

Background Suppressors of cytokine signaling family member 4 (SOCS4) was shown to serve critical and multifaceted roles in the progression of numerous cancers, including hepatocellular carcinoma, thyroid cancer, breast cancer, and lung adenocarcinoma. While, the expression and the roles of SOCS4 in esophageal squamous cell carcinoma (ESCC) remain elusive. The current study is aimed to investigate the expression pattern and functions of SOCS4 in ESCC. Methods The relationship between SOCS4 and the clinicopathological features of ESCC was analyzed. SOCS4 expression in ESCC tissues was measured by western blot, quantitative real-time polymerase chain reaction (qRT-PCR), and immunohistochemical (IHC) staining. The roles of SOCS4 in modulating ESCC cell behaviors were examined using a series of assays, including cell proliferation assay, cell counting kit-8 (CCK-8) assay, cell cycle analysis, and wound-healing assay. Results In human ESCC tissues, SOCS4 expression was up-regulated and correlated with tumor size and lymph node metastasis, however was not correlated with the overall survival (OS) of patients. SOCS4 silencing in ESCC cells resulted in the suppression of cell growth, which was related to the cell cycle. SOCS4 knockdown also inhibited nuclear factor-kappa B (NF-κB) signaling and decreased the migratory potential of ESCC cells. Conclusions These findings revealed that increased expression of SOCS4 in ESCC may promote the progression, proliferation, and migration by NF-κB signaling. Inhibition of SOCS4 may be a promising therapeutic strategy for ESCC.

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