凝胶蛋白通过调节上皮-间质转化抑制食管鳞状细胞癌的恶性进展。
Transgelin Inhibits the Malignant Progression of Esophageal Squamous Cell Carcinomas by Regulating Epithelial-Mesenchymal Transition.
作者信息
Yang Boli, Chen Qiuyu, Wan Changshan, Sun Siyuan, Zhu Lanping, Zhao Zhizhong, Zhong Weilong, Wang Bangmang
机构信息
Department of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, Tianjin Institute of Digestive Disease, Tianjin, China.
Department of Digestive Diseases, General Hospital of Jincheng, Tianjin, China.
出版信息
Front Oncol. 2021 Aug 26;11:709486. doi: 10.3389/fonc.2021.709486. eCollection 2021.
OBJECTIVE
This article investigates the role of Transgelin (TAGLN) in the epithelial-mesenchymal transition (EMT) of esophageal squamous cell carcinomas (ESCC) and its possible mechanism of inhibiting the invasion of these cancers.
METHODS
Tissue specimens and clinical information of patients with ESCC were collected to analyze the relationship between Transgelin expression level and prognosis of patients with ESCC. Transgelin siRNA was used to knock down Transgelin expression. The expression of Transgelin in Eca-109 and KYSE-150 cells was overexpressed by Transgelin-overexpressing plasmid. The effects of Transgelin overexpression and knockdown on the proliferation of Eca-109 and KYSE-150 cells were examined by Transwell chamber, scratch assay, and CCK-8 cell activity assay. RT-PCR and Western blot were used to detect the effect of Transgelin overexpression or knockdown on the mRNA and protein expressions of E-cadherin and Vimentin. TCGA data were used to analyze Transgelin co-expressed genes and further study the GO and KEGG enrichment analysis results under the influence of Transgelin.
RESULTS
The expression of Transgelin was low in ESCC, and its expression level was positively correlated with the prognosis of patients with ESCC. The targeted Transgelin siRNA and Transgelin-overexpressing plasmid can effectively regulate the expression of Transgelin mRNA and protein in Eca-109 and KYSE-150 cells. After overexpression of Transgelin, the invasion and proliferation abilities of Eca-109 and KYSE-150 cells were significantly decreased compared with those of the control group (P < 0.05). However, Transgelin knockdown could promote the proliferation, migration, and invasion of ESCC cells. The overexpression of Transgelin inhibits EMT in ESCC. With the increase of Transgelin expression in Eca-109 and KYSE-150 cells, the expression of E-cadherin increased, while the expression of Vimentin decreased, and the difference was statistically significant (P < 0.05).
CONCLUSION
Transgelin can inhibit the malignant progression of ESCC by inhibiting the occurrence of EMT.
目的
本文旨在研究原肌球蛋白（TAGLN）在食管鳞状细胞癌（ESCC）上皮-间质转化（EMT）中的作用及其抑制这些癌症侵袭的可能机制。
方法
收集ESCC患者的组织标本和临床信息，分析原肌球蛋白表达水平与ESCC患者预后的关系。使用原肌球蛋白siRNA敲低原肌球蛋白表达。通过原肌球蛋白过表达质粒使Eca-109和KYSE-150细胞中原肌球蛋白的表达过表达。通过Transwell小室、划痕试验和CCK-8细胞活性试验检测原肌球蛋白过表达和敲低对Eca-109和KYSE-150细胞增殖的影响。采用RT-PCR和蛋白质印迹法检测原肌球蛋白过表达或敲低对E-钙黏蛋白和波形蛋白mRNA及蛋白表达的影响。利用TCGA数据分析原肌球蛋白共表达基因，并进一步研究原肌球蛋白影响下的基因本体（GO）和京都基因与基因组百科全书（KEGG）富集分析结果。
结果
ESCC中原肌球蛋白表达较低，其表达水平与ESCC患者的预后呈正相关。靶向原肌球蛋白的siRNA和原肌球蛋白过表达质粒可有效调节Eca-109和KYSE-150细胞中原肌球蛋白mRNA和蛋白的表达。原肌球蛋白过表达后，与对照组相比，Eca-109和KYSE-150细胞的侵袭和增殖能力显著降低（P<0.05）。然而，原肌球蛋白敲低可促进ESCC细胞的增殖、迁移和侵袭。原肌球蛋白的过表达抑制ESCC中的EMT。随着Eca-109和KYSE-150细胞中原肌球蛋白表达的增加，E-钙黏蛋白的表达增加，而波形蛋白的表达降低，差异具有统计学意义（P<0.05）。
结论
原肌球蛋白可通过抑制EMT的发生来抑制ESCC的恶性进展。
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