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

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...

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Published inCell biology international Vol. 43; no. 12; pp. 1483 - 1491
Main Authors Liu, Xiaochuan, Chu, Yunxiang, Wang, Dongsheng, Weng, Yan, Jia, Zhiwei
Format Journal Article
LanguageEnglish
Published England Wiley Subscription Services, Inc 01.12.2019
Subjects
Carcinogenesis
Cell migration
Cell proliferation
Colorectal cancer
Colorectal carcinoma
Fibrinogen
fibrinogen‐like protein 2
Gene expression
Kinases
MAP kinase
metastasis
mitogen‐activated protein kinase
Polymerase chain reaction
Protein kinase
Proteins
Up-regulation
mitogen-activated protein kinase
colorectal cancer
metastasis
fibrinogen-like protein 2
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Summary: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.
ISSN:1065-6995
1095-8355
DOI:10.1002/cbin.11198