Elevated expression of NFE2L3 promotes the development of gastric cancer through epithelial-mesenchymal transformation.
Elevated expression of NFE2L3 promotes the development of gastric cancer through epithelial-mesenchymal transformation.
复制标题
NFE2L3表达升高通过上皮间质转化促进胃癌的发生
DOI：
10.1080/21655979.2021.2005915
复制
发表时间：
2021-12
期刊：
影响因子：
4.9
通讯作者：
Li Y
中科院分区：
文献类型：
--
作者：
Wang X;Li Y;Fang Z;Li Y
胃癌是一种死亡率较高的恶性肿瘤，但对其分子机制的研究还很有限。本研究首次探讨核因子NFE2L3(核因子，红系2样蛋白3)在胃癌中的生物学作用。用Western印迹和RT-qPCR检测基因在蛋白和mRNA水平的表达。用短发夹状RNA(ShRNA)表达抑制NFE2L3的表达。CCK-8和集落形成实验检测细胞增殖。用Transwell法和流式细胞仪检测细胞的迁移、侵袭、细胞周期和细胞凋亡。结果表明，NFE2L3在胃癌组织中高表达，促进了胃癌细胞的增殖和转移。抑制NFE2L3的表达可阻断细胞周期，增加细胞凋亡率，而抑制NFE2L3的表达可促进上皮-间充质转化(EMT)过程。综上所述，NFE2L3在胃癌中高表达，促进了胃癌细胞的增殖和转移，促进了EMT过程。
Gastric cancer (GC) is a malignant tumor with high mortality, but research on its molecular mechanisms remain limited. This study is the first to explore the biological role of nuclear factor NFE2L3 (nuclear factor, erythroid 2 like 3) in GC. We used Western blot and RT–qPCR to detect gene expression at the protein or mRNA level. Short hairpin RNA (shRNA) transfection was used to inhibit NFE2L3 expression. CCK-8 and colony formation assays were used to detect cell proliferation. Cell migration, invasion, cell cycle and apoptosis were detected by Transwell assays and flow cytometry. The results showed that NFE2L3 was highly expressed in gastric cancer tissues and promoted gastric cancer cell proliferation and metastasis. Inhibiting NFE2L3 expression blocks the cell cycle and increases the proportion of apoptotic cells, whereas NFE2L3 expression promotes the epithelial-mesenchymal transformation (EMT) process. In summary, NFE2L3 is highly expressed in gastric cancer and promotes gastric cancer cell proliferation and metastasis and the EMT process.
登录
查看更多内容
影响因子：
4.8
作者：
Kokot, Agatha;Metze, Dieter;Boehm, Markus
通讯作者：
Boehm, Markus
影响因子：
3.3
作者：
Liou GY;Storz P
通讯作者：
Storz P
影响因子：
5.3
作者：
Chen, Dehu;Cao, Gan;Liu, Qinghong
通讯作者：
Liu, Qinghong
影响因子：
5.3
作者：
Derjuga, A;Gourley, TS;Blank, V
通讯作者：
Blank, V
影响因子：
3.9
作者：
Ren Y;Wang Y;Hao S;Yang Y;Xiong W;Qiu L;Tao J;Tang A
通讯作者：
Tang A