MIF, secreted by human hepatic sinusoidal endothelial cells, promotes chemotaxis and outgrowth of colorectal cancer in liver prometastasis

Hu, Chun-Ting; Guo, Lili; Feng, Na; Zhang, Lei; Zhou, Na; Ma, Lili; Shen, Lan; Tong, Guihui; Yan, Qianwen; Zhu, Shijie; Bian, Xiu‐Wu; Lai, Maode; Deng, Yao; Ding, Yan‐Qing

doi:10.18632/oncotarget.4198

Cited by 48 publications

(43 citation statements)

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“…Our findings are consistent with recent evidence suggesting the potential value of cofilin in the context of the actin cytoskeleton in the development of prostate cancer and lymph node metastasis [34]. Phosphorylation of cofilin in colorectal cancer cells caused by migration inhibitory factor accelerated mobility of cancer cells toward an invasive and metastatic phenotype [35]. Moreover, our results demonstrate a significant association between EMT and increased nuclear cofilin levels and bladder cancer–related death.…”

Section: Discussionsupporting

confidence: 92%

Association of epithelial-mesenchymal transition and nuclear cofilin with advanced urothelial cancer

et al. 2016

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Summary Tumor epithelial cells undergo a morphologic shift through the process of EMT with characteristic loss of cell polarity, conferring invasive and metastatic properties during cancer progression. Signaling by transforming growth factor-β mediates EMT programming and its phenotypic reversal to mesenchymal-epithelial transition. The role of EMT in bladder cancer progression to advanced disease is poorly understood. In this study, we conducted a retrospective analysis of the EMT landscape and actin cytoskeleton remodeling in a series of human bladder cancer specimens. Immunoreactivity for E-cadherin, N-cadherin, and vimentin protein expression was performed toward establishing an EMT signature in human bladder cancer. Serial sections were assessed for the primary regulator of the actin cytoskeleton remodeling and transforming growth factor-β signaling effector, cofilin. Our results demonstrate that EMT induction in clinical bladder cancer specimens is significantly associated with bladder cancer progression to high-grade, invasive disease. Evaluation of expression and cellular localization of the cytoskeleton regulator cofilin revealed a significant association between overexpression of nuclear cofilin with bladder cancer progression. This study is of translational significance in defining the value of EMT signature and cytoskeletal cofilin as potential tumor markers and targetable platforms for the treatment of invasive bladder cancer.

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Section: Discussionsupporting

confidence: 92%

Association of epithelial-mesenchymal transition and nuclear cofilin with advanced urothelial cancer

et al. 2016

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“…In contrast, bone marrow chimeric mice expressing WT bone marrow on a Mif−/− background were protected from ethanol-induced liver injury. While these studies cannot exclude a potential contribution of MIF in other hepatic cell types, such as endothelial cells[32] or hepatic stellate cells[33], they are consistent with a likely role of hepatocytes as an important cellular source of MIF in the liver.…”

Section: Discussionmentioning

confidence: 71%

Hepatocyte-derived macrophage migration inhibitory factor mediates alcohol-induced liver injury in mice and patients

Marin

Poulsen²,

Òdena

et al. 2017

Journal of Hepatology

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Background & aims Macrophage migration inhibitory factor (MIF) is a multi-potent cytokine that contributes to the inflammatory response to injury. MIF is expressed by multiple cell types; however, the cellular source and actions of MIF in alcoholic liver disease (ALD) are not well known. Here we tested the hypothesis that non-myeloid cells, specifically hepatocytes, are an important cellular source of MIF in ALD. Methods MIF expression was measured in HuH7 and differentiated THP-1 cells in response to ethanol. Ethanol-induced liver injury was assessed in C57BL/6 (WT) and Mif−/− bone marrow chimeras. MIF was measured in peripheral and suprahepatic serum, as well as visualized by immunohistochemistry in liver biopsies, from patients with alcoholic hepatitis (AH). Results HuH7 hepatocytes, but not THP-1 macrophages, released MIF in response to challenge with ethanol in culture. In chimeric mice expressing MIF in non-myeloid cells (Mif−/− →WT), chronic ethanol feeding increased ALT/AST, hepatic steatosis, and expression of cytokine/chemokine mRNA. In contrast, chimeric mice not expressing MIF in non-myeloid cells (WT→ Mif−/−) were protected from ethanol-induced liver injury. Immunohistochemical staining of liver biopsies from patients with AH revealed a predominant localization of MIF to hepatocytes. Interestingly, the concentration of MIF in suprahepatic serum, but not peripheral serum, was positively correlated with clinical indicators of disease severity and with an increased risk of mortality in patients with AH. Conclusions Taken together, these data provide evidence that hepatocyte-derived MIF is critical to the pathogenesis of ALD in mice and likely contributes to liver injury in patients with AH.

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“…Keshamouni et al found that MIF was up‐regulated during TGF‐β induced EMT via temporal quantitative proteomic analysis in lung adenocarcinoma cells. Hu et al validated that MIF could promote migration, proliferation, and EMT, and MIF facilitated colorectal cancer cells transfer to liver and the level of MIF was related to the size of hepatic metastases. Zeng et al noted that inhibition of MIF through siRNA could repress biological behavior of oral squamous cell carcinoma (OSCC) cells, and the level of Twist was decreased in the MIF‐knockdown OSCC cells, simultaneously.…”

Section: Discussionmentioning

confidence: 99%

MIF promotes perineural invasion through EMT in salivary adenoid cystic carcinoma

Zhang

Wang

et al. 2019

Molecular Carcinogenesis

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Macrophage migration inhibitory factor (MIF) is a prominent orchestrator during the onset and progression of cancer. Recently, MIF was detected in salivary adenoid cystic carcinoma (SACC). However, its functional effect in perineural invasion (PNI) of SACC remained unknown. To illuminate the effect of MIF in genesis of PNI in SACC, we examined the expression of MIF, epithelial‐to‐mesenchymal transition (EMT)‐related markers, and Schwann cell markers by immunohistochemical analysis in 158 cases of SACC samples. Meanwhile, the correlation between MIF and PNI of SACC species was analyzed. Our data indicated that MIF expression was associated with PNI of SACC significantly. In vitro, the silence and overexpression experiments of MIF were performed in SACC cell lines. The ability of migration, invasion and PNI could be inhibited significantly by siRNA‐mediated MIF silence, and the occurrence of EMT and Schwann‐like cell differentiation was also inhibited by MIF silence in SACC‐LM cells. Overexpression of MIF in SACC‐83 cells using expressive plasmid showed the opposite effects. Our findings identified that an association between PNI and MIF expression existed. MIF may promote PNI of SACC by participating in cytoskeletal reorganization and pseudo foot formation induced by EMT and the Schwann‐like cell differentiation of SACC cells.

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MIF, secreted by human hepatic sinusoidal endothelial cells, promotes chemotaxis and outgrowth of colorectal cancer in liver prometastasis

Cited by 48 publications

References 50 publications

Association of epithelial-mesenchymal transition and nuclear cofilin with advanced urothelial cancer

Association of epithelial-mesenchymal transition and nuclear cofilin with advanced urothelial cancer

Hepatocyte-derived macrophage migration inhibitory factor mediates alcohol-induced liver injury in mice and patients

MIF promotes perineural invasion through EMT in salivary adenoid cystic carcinoma

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