唐进亮,范学科,王鹏帅.中胚层特异性转录物通过细胞外基质重塑促进胃癌细胞的侵袭[J].安徽医药,2024,28(11):2231-2235. |
中胚层特异性转录物通过细胞外基质重塑促进胃癌细胞的侵袭 |
Mesoderm-specific transcripts promote invasion of gastric cancer cells through extracellular matrix remodeling |
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DOI:10.3969/j.issn.1009-6469.2024.11.024 |
中文关键词: 胃肿瘤 中胚层 中胚层特异性转录物 上皮 -间质转化 |
英文关键词: Stomach neoplasms Mesoderm Mesoderm-specific transcript Epithelial-mesenchymal transition |
基金项目:山西省卫健委课题( 2022003) |
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中文摘要: |
目的探索中胚层特异性转录物(MEST)通过细胞外基质重塑促进胃癌细胞的侵袭的作用及其生物学机制。方法选取 2022年 7―8月在晋城市人民医院确诊为胃癌的病人 27例。以蛋白质印迹法检测胃癌组织和细胞中 MEST的表达。在 AGS和 SGC-7901中分别建立了 MEST沉默细胞系,研究 MEST对细胞增殖、迁移、侵袭和上皮间质转化的影响。蛋白质印迹法检测 Wnt/β-catenin/Twist-1信号通路相关蛋白的表达水平。在裸鼠体内种植定感染了表达 sh-MEST的慢病毒的胃癌细胞系 MK-45,接种后观察肿瘤生长并记录数据。结果 MEST在胃癌组织和细胞系中升高。与正常胃黏膜组织相比,胃癌组织中 MEST蛋白水平显著升高[( 100.00±9.03)%比( 824.27±70.15)%,t=83.43,P<0.001]; MEST的沉默阻碍了细胞增殖、迁移和侵袭以及上皮-间质转化。蛋白质印迹法结果显示, MEST沉默后胃癌细胞 E-cadherin上皮细胞标志物蛋白被上调,神经钙黏素( N-cadherin)、波形蛋白( Vimentin)、 Wnt、β-catenin、Snail和 Twist1等间质细胞标志蛋白的表达与之相反。转染 sh-MEST抑制了胃癌细胞在活生物体内的生长。结论 MEST通过 Wnt/β-catenin/Twist-1信号在胃癌中发挥致癌功能, MEST可能代表了胃癌治疗的一个潜在靶标。 |
英文摘要: |
Objective To explore the role of mesoderm-specific transcripts (MEST) in promoting the invasion of gastric cancer cellsthrough extracellular matrix remodeling and its biological mechanism.Methods The expression of MEST in gastric cancer tissues and cells was detected by western-blotting. MEST-shRNAs transfered in AGS and SGC-7901 respectively to study the effects of MEST oncell proliferation, migration, invasion and epithelial mesenchymal transition. Western-blotting was used to detect the expression levels of proteins related to the Wnt/β-catenin/Twist-1 signaling pathway. GC cell line MK-45 infected with MEST-shRNA was grown in nude mice, and tumor growth was observed and data recorded after inoculation.Results MEST was elevated in gastric cancer tissues and cell lines[(100.00±9.03)% vs. (824.27±70.15)%,t=83.43, P<0.001]. silencing of MEST impeded cell proliferation, migration and invasion, and epithelial-mesenchymal transition. Western-blotting showed that E-cadherin epithelial cell marker protein was upregulated ingastric cancer cells after MEST silencing, in contrast to the expression of mesenchymal cell marker proteins such as N-cadherin, Vimentin, Wnt, β-catenin, Snail and Twist1. Transfection of sh-MEST inhibited the growth of gastric cancer cells in living organisms.Con? clusion Our data confirm that MEST exerts oncogenic functions in gastric cancer via MEST via Wnt/β-catenin/Twist-1 signaling, and that MEST may represent a potential target for gastric cancer therapy. |
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