Conversion of TNFα from Antiproliferative to Proliferative Ligand in Mouse Intestinal Epithelial Cells by Regulating Mitogen-Activated Protein Kinase

Kaiser, G. C.; Yan, Fang; Polk, D. Brent

doi:10.1006/excr.1999.4488

Cited by 42 publications

(30 citation statements)

References 44 publications

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“…It remains to be determined whether Spry2 is indeed dysregulated in IBD. Interestingly, multiple mechanisms of Spry2 regulation have been reported: We reported a decrease in Spry2 only at the protein, not message, a stimulus, [15][16][17] and may all be separately regulated. Whether Spry2 can selectively alter these parameters of MAPK signaling in colon epithelial cells remains to be determined.…”

Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tmentioning

confidence: 70%

Sprouty keeps bowel kinases regular in colon cancer, while miR-21 targets Sprouty

Frey

Carraro

Batra³

et al. 2011

Cancer Biology & Therapy

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Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tmentioning

confidence: 70%

Sprouty keeps bowel kinases regular in colon cancer, while miR-21 targets Sprouty

Frey

Carraro

Batra³

et al. 2011

Cancer Biology & Therapy

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“…Thus, although EGFR is not necessary for TNF-stimulated MAPK activation in intestinal epithelial cells, neither is MAPK activation sufficient to promote cell survival after TNF stimulation (6). Our previous studies showed that TNF regulates proliferation through ERK1/2 activation (25,26). Together these findings suggest that EGFR/ ErbB2 may not be required for TNF-stimulated MAPK activation to regulate intestinal epithelial cell proliferation.…”

Section: Fig 4 Suppression Of Egfr and Erbb2 Expression Promotes Apmentioning

confidence: 90%

Transactivation of EGF receptor and ErbB2 protects intestinal epithelial cells from TNF-induced apoptosis

Yamaoka¹,

Yan²,

Cao³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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101

114

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TNF is a pleiotropic cytokine that activates both anti-and proapoptotic signaling pathways, with cell fate determined by the balance between these two pathways. Activation of ErbB family members, including EGF receptor (EGFR/ErbB1), promotes cell survival and regulates several signals that overlap with those stimulated by TNF. This study was undertaken to determine the effects of TNF on EGFR and ErbB2 activation and intestinal epithelial cell survival. Mice, young adult mouse colon epithelial cells, and EGFR knockout mouse colon epithelial cells were treated with TNF. Activation of EGFR, ErbB2, Akt, Src, and apoptosis were determined in vivo and in vitro. TNF stimulated EGFR phosphorylation in young adult mouse colon epithelial cells, and loss of EGFR expression or inhibition of kinase activity increased TNF-induced apoptosis, which was prevented in WT but not by kinase-inactive EGFR expression. Similarly, TNF injection stimulated apoptosis in EGFR-kinasedefective mice (EGFR wa2 ) compared with WT mice. TNF also activated ErbB2, and loss of ErbB2 expression increased TNF-induced apoptosis. Furthermore, Src-kinase activity and the expression of both EGFR and ErbB2 were required for TNF-induced cell survival. Akt was shown to be a downstream target of TNF-activated EGFR and ErbB2. These findings demonstrate that EGFR and ErbB2 are critical mediators of TNF-regulated antiapoptotic signals in intestinal epithelial cells. Given evidence for TNF signaling in the development of colitis-associated carcinoma, this observation has significant implications for understanding the role of EGFR in maintaining intestinal epithelial cell homeostasis during cytokinemediated inflammatory responses.

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“…48,49 TNFR1 induces growth arrest through sustained mitogen-activated protein kinase activity, 50 whereas TNF-␣ stimulates proliferation via TNFR2. 51 It was found in this study that each neutralization antibody against TNFR1 or TNFR2 suppressed considerably but not completely the expression of CXCR4 mRNA.…”

Section: Discussionmentioning

confidence: 99%

Possible Regulation of Migration of Intrahepatic Cholangiocarcinoma Cells by Interaction of CXCR4 Expressed in Carcinoma Cells with Tumor Necrosis Factor-α and Stromal-Derived Factor-1 Released in Stroma

Ohira

Sasaki

Harada

et al. 2006

The American Journal of Pathology

109

114

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Conversion of TNFα from Antiproliferative to Proliferative Ligand in Mouse Intestinal Epithelial Cells by Regulating Mitogen-Activated Protein Kinase

Cited by 42 publications

References 44 publications

Sprouty keeps bowel kinases regular in colon cancer, while miR-21 targets Sprouty

Sprouty keeps bowel kinases regular in colon cancer, while miR-21 targets Sprouty

Transactivation of EGF receptor and ErbB2 protects intestinal epithelial cells from TNF-induced apoptosis

Possible Regulation of Migration of Intrahepatic Cholangiocarcinoma Cells by Interaction of CXCR4 Expressed in Carcinoma Cells with Tumor Necrosis Factor-α and Stromal-Derived Factor-1 Released in Stroma

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