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MAPK‐mediated upregulation of fibrinogen‐like protein 2 promotes proliferation, migration, and invasion of colorectal cancer cells

机译:MAPK介导的纤维蛋白原蛋白2的上调促进了结直肠癌细胞的增殖,迁移和侵袭

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Abstract Fibrinogen‐like protein 2 (FGL2) has been reported to play a key role in the development of human cancers. However, it is still unmasked whether FGL2 plays a potential role in colorectal carcinogenesis. In this study, the messenger RNA and protein expression levels were measured by quantitative real‐time polymerase chain reaction and western blot. Cell counting kit‐8 assay, transwell migration, and invasion assay were carried out to evaluate the proliferation, migration, and invasion of LOVO and SW620 cells. FGL2 was upregulated in colorectal cancer (CRC) tissues, as well as cell lines. Mitogen‐activated protein kinase (MAPK) signaling was activated in CRC tissues and cell lines. FGL2 was confirmed to be downregulated by MAPK signaling inhibitor U0126. Further, we determined that knockdown of FGL2 caused a reduction of proliferation, migration, and invasion in LOVO and SW620 cells. Consistently, treatment of LOVO and SW620 cells with U0126 led to a decrease in cell proliferation, migration, and invasion. However, these changes initiated by U0126 were abolished by FGL2 overexpression. To conclude, MAPK‐mediated upregulation of FGL2 promotes the proliferation, migration, and invasion of CRC cells.
机译:据报道,摘要纤维蛋白胶样蛋白2(FGL2)在人类癌症的发展中发挥着关键作用。然而,它仍然揭示FL2是否在结肠直肠癌中发挥潜在作用。在该研究中,通过定量实时聚合酶链反应和蛋白质印迹测量信使RNA和蛋白质表达水平。进行细胞计数试剂盒测定,进行Transwell迁移和侵袭测定,以评估Lovo和SW620细胞的增殖,迁移和侵袭。 FGL2在结肠直肠癌(CRC)组织中上调,以及细胞系。在CRC组织和细胞系中激活丝分裂剂活化的蛋白激酶(MAPK)信号传导。确认FGL2通过MAPK信号抑制剂U0126下调。此外,我们确定FL2的敲低导致Lovo和SW620细胞中的增殖,迁移和侵袭降低。始终如一地,使用U0126治疗LOVO和SW620细胞导致细胞增殖,迁移和侵袭的降低。然而,U0126发起的这些变化由FGL2过表达废除。为了得出结论,MAPK介导的FGL2的上调促进了CRC细胞的增殖,迁移和侵袭。

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