The cell-membrane prothrombinase, fibrinogen-like protein 2, promotes angiogenesis and tumor development

Rabizadeh, Esther; Cherny, Izhack; Lederfein, Doron; Sherman, Shany; Binkovsky, Natalia; Rosenblat, Yevgenia; Inbal, Aida

doi:10.1016/j.thromres.2014.11.023

Cited by 27 publications

(28 citation statements)

References 35 publications

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“…However, the regulative mechanism and influential factors of ectopic expression of FGL2, especially in CRC, remain largely unknown. We found that FGL2 depletion suppressed the proliferation, migration, and invasion of LOVO and SW620 cells, which is consistent with a previous report (Rabizadeh et al, ). Therefore, our findings provide a strong support for the role of FGL2 as an oncogene in CRC progression.…”

Section: Discussionsupporting

confidence: 93%

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

Liu

Chu

Wang

et al. 2019

Cell Biology International

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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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Section: Discussionsupporting

confidence: 93%

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

Liu

Chu

Wang

et al. 2019

Cell Biology International

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“…This indicates that FGL2 is involved in controlling the immunopathological damage through PD-1 signaling, which is associated with various types of cancer [ 35 ]. Also, mFGL-2 appears to promote angiogenesis and tumorigenesis through the FGF-2/ERK (fibroblast growth factor-2/extracellular signal-regulated kinases) signaling pathway, but not by thrombin-mediated mechanism [ 36 ]. Importantly, FGL2 is over-expressed in colorectal carcinoma (CRC) and clear cell renal cell carcinoma (ccRCC) tumors compared to non-tumor tissues [ 25 , 37 ], and the expression levels are associated with cell proliferation and invasion in vitro and with CRC progression and metastasis in vivo [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Soluble fibrinogen-like protein 2 levels in patients with hepatitis B virus-related liver diseases

Tong

Hoàn

et al. 2018

BMC Infect Dis

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BackgroundClinical progression of HBV-related liver diseases is largely associated with the activity of HBV-specific T cells. Soluble fibrinogen-like protein 2 (sFGL2), mainly secreted by T cells, is an important effector molecule of the immune system.MethodssFGL2 levels were determined by ELISA assays in sera of 296 HBV patients clinically classified into the subgroups of acute hepatitis B (AHB), chronic hepatitis B (CHB), liver cirrhosis (LC), hepatocellular carcinoma (HCC) and patients with LC plus HCC. As control group, 158 healthy individuals were included. FGL2 mRNA was quantified by qRT-PCR in 32 pairs of tumor and adjacent non-tumor liver tissues.ResultssFGL2 levels were elevated in HBV patients compared to healthy controls (P < 0.0001). In the patient group, sFGL2 levels were increased in AHB compared to CHB patients (P = 0.017). sFGL2 levels were higher in LC patients compared to those without LC (P = 0.006) and were increased according to the development of cirrhosis as staged by Child-Pugh scores (P = 0.024). Similarly, HCC patients had increased sFGL2 levels compared to CHB patients (P = 0.033) and FGL2 mRNA was up-regulated in tumor tissues compared to adjacent non-tumor tissues (P = 0.043). In addition, sFGL2 levels were positively correlated with HBV-DNA loads and AST (Spearman’s rho = 0.21, 0.25 and P = 0.006, 0.023, respectively), but reversely correlated with platelet counts and albumin levels (Spearman’s rho = − 0.27, − 0.24 and P = 0.014, 0.033, respectively).ConclusionssFGL2 levels are induced by HBV infection and correlated with the progression and clinical outcome of HBV-related liver diseases. Thus, sFGL2 may serve as a potential indicator for HBV-related liver diseases.

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“…Fibrinogen-like protein 2 (FGL2) was significantly overexpressed in non-carriers, compared to both naïve animals as well as compared to persistently FMDV-infected carriers. Secretory FGL2 is an immunosuppressive effector molecule of T reg cells, whereas membrane-associated FGL2 has prothrombinase activity [ 95 ]. Since the pattern of FGL2 expression in our dataset was diametrically opposed to the expression of many other T reg genes ( Fig 5 ), it likely represents the membrane-bound protein which is found on endothelial cells and activated macrophages.…”

Section: Discussionmentioning

confidence: 99%

Transcriptomic Analysis of Persistent Infection with Foot-and-Mouth Disease Virus in Cattle Suggests Impairment of Apoptosis and Cell-Mediated Immunity in the Nasopharynx

et al. 2016

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In order to investigate the mechanisms of persistent foot-and-mouth disease virus (FMDV) infection in cattle, transcriptome alterations associated with the FMDV carrier state were characterized using a bovine whole-transcriptome microarray. Eighteen cattle (8 vaccinated with a recombinant FMDV A vaccine, 10 non-vaccinated) were challenged with FMDV A24 Cruzeiro, and the gene expression profiles of nasopharyngeal tissues collected between 21 and 35 days after challenge were compared between 11 persistently infected carriers and 7 non-carriers. Carriers and non-carriers were further compared to 2 naïve animals that had been neither vaccinated nor challenged. At a controlled false-discovery rate of 10% and a minimum difference in expression of 50%, 648 genes were differentially expressed between FMDV carriers and non-carriers, and most (467) had higher expression in carriers. Among these, genes associated with cellular proliferation and the immune response–such as chemokines, cytokines and genes regulating T and B cells–were significantly overrepresented. Differential gene expression was significantly correlated between non-vaccinated and vaccinated animals (biological correlation +0.97), indicating a similar transcriptome profile across these groups. Genes related to prostaglandin E2 production and the induction of regulatory T cells were overexpressed in carriers. In contrast, tissues from non-carrier animals expressed higher levels of complement regulators and pro-apoptotic genes that could promote virus clearance. Based on these findings, we propose a working hypothesis for FMDV persistence in nasopharyngeal tissues of cattle, in which the virus may be maintained by an impairment of apoptosis and the local suppression of cell-mediated antiviral immunity by inducible regulatory T cells.

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The cell-membrane prothrombinase, fibrinogen-like protein 2, promotes angiogenesis and tumor development

Cited by 27 publications

References 35 publications

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

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

Soluble fibrinogen-like protein 2 levels in patients with hepatitis B virus-related liver diseases

Transcriptomic Analysis of Persistent Infection with Foot-and-Mouth Disease Virus in Cattle Suggests Impairment of Apoptosis and Cell-Mediated Immunity in the Nasopharynx

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