AI Article Synopsis

  • FGL2 is found to be upregulated in colorectal cancer tissues and cell lines, suggesting its potential role in colorectal carcinogenesis.
  • The study used various assays to evaluate how FGL2 influences the proliferation, migration, and invasion of specific cancer cell lines (LOVO and SW620).
  • Results indicate that the MAPK signaling pathway activates FGL2, and reducing FGL2 levels leads to decreased cancer cell activity, highlighting its importance in cancer progression.

Article 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.

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Source
http://dx.doi.org/10.1002/cbin.11198DOI Listing

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