Cooperation between STAT3 and c-Jun suppresses Fas transcription

Vladimir N. Ivanov; Anindita Bhoumik; Mikhail Krasilnikov; Regina Raz; Laurie B. Owen-Schaub; David Levy; Curt M. Horvath; Ze'ev Ronai

doi:10.1016/S1097-2765(01)00199-X

Cooperation between STAT3 and c-Jun suppresses Fas transcription

Vladimir N. Ivanov, Anindita Bhoumik, Mikhail Krasilnikov, Regina Raz, Laurie B. Owen-Schaub, David Levy, Curt M. Horvath, Ze'ev Ronai^*

^*Corresponding author for this work

Molecular Biosciences

Research output: Contribution to journal › Article › peer-review

218 Scopus citations

Abstract

Decreased Fas expression during tumor progression often results in a loss of Fas-ligand (FasL)-mediated apoptosis. Human and mouse melanoma exhibit an inverse correlation between the degree of Fas cell surface expression, tumorigenicity, and metastatic capacity. The expression of dominant negative Stat3 or c-Jun in melanoma cells efficiently increased Fas expression and sensitized cells to FasL-induced apoptosis. Stat3^+/- as well as c-Jun^-/- cells exhibited increased Fas cell surface expression and higher sensitivity to FasL-mediated apoptosis. Suppression of Fas expression by Stat3 and c-Jun is uncoupled from Stat3-mediated transcriptional activation. Our findings indicate that Stat3 oncogenic activities could also be mediated through its cooperation with c-Jun, resulting in downregulation of Fas surface expression, which is implicated in the tumor's ability to resist therapy and metastasize.

Original language	English (US)
Pages (from-to)	517-528
Number of pages	12
Journal	Molecular cell
Volume	7
Issue number	3
DOIs	https://doi.org/10.1016/S1097-2765(01)00199-X
State	Published - Mar 1 2001

Funding

This work was supported by NCI grants CA51995 and TW00960, and the Sharp Foundation grant (to Z.R.) is gratefully acknowledged. We thank Pete Stavropoulos and Rui Qiao for technical assistance and Hans Snoeck and Italas George for assistance in FACS analysis. We also wish to thank Meenhard Herlyn and Ø Fodstad for the melanoma cell lines and Richard Jove for the Stat3β expression vector and Peter Nolan for the Phoenix cells. We thank Tom Maniatis for detailed ChIP protocol. We thank Jim Darnell Jr. for Stat3 constructs and review of this manuscript. We also thank members of the Ronai Lab for advice and discussions.

ASJC Scopus subject areas

Molecular Biology
Cell Biology

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10.1016/S1097-2765(01)00199-X

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title = "Cooperation between STAT3 and c-Jun suppresses Fas transcription",

abstract = "Decreased Fas expression during tumor progression often results in a loss of Fas-ligand (FasL)-mediated apoptosis. Human and mouse melanoma exhibit an inverse correlation between the degree of Fas cell surface expression, tumorigenicity, and metastatic capacity. The expression of dominant negative Stat3 or c-Jun in melanoma cells efficiently increased Fas expression and sensitized cells to FasL-induced apoptosis. Stat3+/- as well as c-Jun-/- cells exhibited increased Fas cell surface expression and higher sensitivity to FasL-mediated apoptosis. Suppression of Fas expression by Stat3 and c-Jun is uncoupled from Stat3-mediated transcriptional activation. Our findings indicate that Stat3 oncogenic activities could also be mediated through its cooperation with c-Jun, resulting in downregulation of Fas surface expression, which is implicated in the tumor's ability to resist therapy and metastasize.",

author = "Ivanov, {Vladimir N.} and Anindita Bhoumik and Mikhail Krasilnikov and Regina Raz and Owen-Schaub, {Laurie B.} and David Levy and Horvath, {Curt M.} and Ze'ev Ronai",

note = "Funding Information: This work was supported by NCI grants CA51995 and TW00960, and the Sharp Foundation grant (to Z.R.) is gratefully acknowledged. We thank Pete Stavropoulos and Rui Qiao for technical assistance and Hans Snoeck and Italas George for assistance in FACS analysis. We also wish to thank Meenhard Herlyn and {\O} Fodstad for the melanoma cell lines and Richard Jove for the Stat3β expression vector and Peter Nolan for the Phoenix cells. We thank Tom Maniatis for detailed ChIP protocol. We thank Jim Darnell Jr. for Stat3 constructs and review of this manuscript. We also thank members of the Ronai Lab for advice and discussions.",

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doi = "10.1016/S1097-2765(01)00199-X",

language = "English (US)",

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T1 - Cooperation between STAT3 and c-Jun suppresses Fas transcription

AU - Ivanov, Vladimir N.

AU - Bhoumik, Anindita

AU - Krasilnikov, Mikhail

AU - Raz, Regina

AU - Owen-Schaub, Laurie B.

AU - Levy, David

AU - Horvath, Curt M.

AU - Ronai, Ze'ev

N1 - Funding Information: This work was supported by NCI grants CA51995 and TW00960, and the Sharp Foundation grant (to Z.R.) is gratefully acknowledged. We thank Pete Stavropoulos and Rui Qiao for technical assistance and Hans Snoeck and Italas George for assistance in FACS analysis. We also wish to thank Meenhard Herlyn and Ø Fodstad for the melanoma cell lines and Richard Jove for the Stat3β expression vector and Peter Nolan for the Phoenix cells. We thank Tom Maniatis for detailed ChIP protocol. We thank Jim Darnell Jr. for Stat3 constructs and review of this manuscript. We also thank members of the Ronai Lab for advice and discussions.

PY - 2001/3/1

Y1 - 2001/3/1

N2 - Decreased Fas expression during tumor progression often results in a loss of Fas-ligand (FasL)-mediated apoptosis. Human and mouse melanoma exhibit an inverse correlation between the degree of Fas cell surface expression, tumorigenicity, and metastatic capacity. The expression of dominant negative Stat3 or c-Jun in melanoma cells efficiently increased Fas expression and sensitized cells to FasL-induced apoptosis. Stat3+/- as well as c-Jun-/- cells exhibited increased Fas cell surface expression and higher sensitivity to FasL-mediated apoptosis. Suppression of Fas expression by Stat3 and c-Jun is uncoupled from Stat3-mediated transcriptional activation. Our findings indicate that Stat3 oncogenic activities could also be mediated through its cooperation with c-Jun, resulting in downregulation of Fas surface expression, which is implicated in the tumor's ability to resist therapy and metastasize.

AB - Decreased Fas expression during tumor progression often results in a loss of Fas-ligand (FasL)-mediated apoptosis. Human and mouse melanoma exhibit an inverse correlation between the degree of Fas cell surface expression, tumorigenicity, and metastatic capacity. The expression of dominant negative Stat3 or c-Jun in melanoma cells efficiently increased Fas expression and sensitized cells to FasL-induced apoptosis. Stat3+/- as well as c-Jun-/- cells exhibited increased Fas cell surface expression and higher sensitivity to FasL-mediated apoptosis. Suppression of Fas expression by Stat3 and c-Jun is uncoupled from Stat3-mediated transcriptional activation. Our findings indicate that Stat3 oncogenic activities could also be mediated through its cooperation with c-Jun, resulting in downregulation of Fas surface expression, which is implicated in the tumor's ability to resist therapy and metastasize.

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Cooperation between STAT3 and c-Jun suppresses Fas transcription

Abstract

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