p38 and JNK pathways control E-selectin-dependent extravasation of colon cancer cells by modulating miR-31 transcription

Liu, Zhong; Simoneau, Bryan; Huot, Jacques; Simard, Martin J.

doi:10.18632/oncotarget.13779

Cited by 31 publications

(23 citation statements)

References 30 publications

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“…A critical event of metastatic dissemination to distant sites is the adhesion of circulating malignant cells to vascular endothelial cells [95]. Many studies point to a role for E-selectin displayed on vascular endothelial cells in the recruitment of tumor cells to metastatic sites in breast, bladder, gastric, pancreatic, and colorectal carcinoma, as well as hematological malignancies [95,106,107]. Interestingly, PODXL has been implicated in the interaction of tumor cells to E-selectin as well as to L-selectin [34].…”

Section: Podxl In Metastasismentioning

confidence: 99%

Emerging Role of Podocalyxin in the Progression of Mature B-Cell Non-Hodgkin Lymphoma

Tamayo-Orbegozo

Amo

Díez-García

et al. 2020

Cancers

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Mature B-cell non-Hodgkin lymphoma (B-NHL) constitutes a group of heterogeneous malignant lymphoproliferative diseases ranging from indolent to highly aggressive forms. Although the survival after chemo-immunotherapy treatment of mature B-NHL has increased over the last years, many patients relapse or remain refractory due to drug resistance, presenting an unfavorable prognosis. Hence, there is an urgent need to identify new prognostic markers and therapeutic targets. Podocalyxin (PODXL), a sialomucin overexpressed in a variety of tumor cell types and associated with their aggressiveness, has been implicated in multiple aspects of cancer progression, although its participation in hematological malignancies remains unexplored. New evidence points to a role for PODXL in mature B-NHL cell proliferation, survival, migration, drug resistance, and metabolic reprogramming, as well as enhanced levels of PODXL in mature B-NHL. Here, we review the current knowledge on the contribution of PODXL to tumorigenesis, highlighting and discussing its role in mature B-NHL progression.

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Section: Podxl In Metastasismentioning

confidence: 99%

Emerging Role of Podocalyxin in the Progression of Mature B-Cell Non-Hodgkin Lymphoma

Tamayo-Orbegozo

Amo

Díez-García

et al. 2020

Cancers

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“…The exclusive expression of E-selectin by endothelial cells enables the adhesion and rolling of leukocytes on the endothelium (48). It has been reported that miR-31 directly targets E-selectin to hinder in vitro endothelial adhesion and transendothelial migration of neutrophils (49,50). The transcription of miR-31 depends on IL-1b-induced p38/ JNK/c-Fos/Gata2 pathways (49,50).…”

Section: Mirnas Target Cell Adhesion Moleculesmentioning

confidence: 99%

Endothelial microRNAs regulating the NF‐κB pathway and cell adhesion molecules during inflammation

2018

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The surface of endothelial cells is covered with cell adhesion molecules, including E-selectin, intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM- 1) , that mediate the adhesion and extravasation of leukocytes and play pivotal roles in inflammatory response. microRNAs (miRNAs) regulate the expression of these important cell adhesion molecules through two distinct major mechanisms, namely via modulating the proinflammatory NF-κB pathway, which controls their transcription, and via directly targeting them. The present review highlights the role of various miRNAs in controlling the expression of E-selectin, ICAM-1, and VCAM-1: a type of regulation that can be harnessed for therapeutic prevention of inflammation-associated diseases such as atherosclerosis and sepsis. The roles of secreted miRNAs as paracrine regulators, and cell adhesion molecule-based miRNA delivery are also addressed.-Zhong, L., Simard, M. J., Huot, J. Endothelial microRNAs regulating the NF-κB pathway and cell adhesion molecules during inflammation.

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“…Interestingly, in endothelial cells, p38 controls the transcriptional activation of NFκB and the production of TNFα via phosphorylation of RelA in response to Borrelia burgdoferi antigens [ 84 ]. Moreover, we recently found that activation of endothelial p38 by IL-1β regulates the transcription of miR-31 by activation of c-fos and GATA2 [ 85 ]. In turn, miR-31 represses the expression of E-selectin and thereby adhesion and transendothelial migration of colon cancer cells [ 85 ].…”

Section: The P38 Pathwaysmentioning

confidence: 99%

“…Moreover, we recently found that activation of endothelial p38 by IL-1β regulates the transcription of miR-31 by activation of c-fos and GATA2 [ 85 ]. In turn, miR-31 represses the expression of E-selectin and thereby adhesion and transendothelial migration of colon cancer cells [ 85 ]. Intriguingly, another study indicates that p38 supports the nuclear functions of estrogen receptor by contributing to its phosphorylation [ 86 ].…”

Section: The P38 Pathwaysmentioning

confidence: 99%

“…The miR-31-mediated repression of E-selectin in endothelial cells impairs the metastatic potential of colon cancer cells by decreasing their adhesion to the endothelium. The transcription of miR-31 is activated by IL-1β and depends on p38 and JNK, and their downstream transcription factors GATA2, c-Fos and c-Jun [ 85 ].…”

Section: The Endothelial P38 Pathway As a Major Regulator Of Tumor Prmentioning

confidence: 99%

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The p38 pathway, a major pleiotropic cascade that transduces stress and metastatic signals in endothelial cells

2017

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By gating the traffic of molecules and cells across the vessel wall, endothelial cells play a central role in regulating cardiovascular functions and systemic homeostasis and in modulating pathophysiological processes such as inflammation and immunity. Accordingly, the loss of endothelial cell integrity is associated with pathological disorders that include atherosclerosis and cancer. The p38 mitogen-activated protein kinase (MAPK) cascades are major signaling pathways that regulate several functions of endothelial cells in response to exogenous and endogenous stimuli including growth factors, stress and cytokines. The p38 MAPK family contains four isoforms p38α, p38β, p38γ and p38δ that are encoded by four different genes. They are all widely expressed although to different levels in almost all human tissues. p38α/MAPK14, that is ubiquitously expressed is the prototype member of the family and is referred here as p38. It regulates the production of inflammatory mediators, and controls cell proliferation, differentiation, migration and survival. Its activation in endothelial cells leads to actin remodeling, angiogenesis, DNA damage response and thereby has major impact on cardiovascular homeostasis, and on cancer progression. In this manuscript, we review the biology of p38 in regulating endothelial functions especially in response to oxidative stress and during the metastatic process.

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p38 and JNK pathways control E-selectin-dependent extravasation of colon cancer cells by modulating miR-31 transcription

Cited by 31 publications

References 30 publications

Emerging Role of Podocalyxin in the Progression of Mature B-Cell Non-Hodgkin Lymphoma

Emerging Role of Podocalyxin in the Progression of Mature B-Cell Non-Hodgkin Lymphoma

Endothelial microRNAs regulating the NF‐κB pathway and cell adhesion molecules during inflammation

The p38 pathway, a major pleiotropic cascade that transduces stress and metastatic signals in endothelial cells

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