SINHCAF/FAM60A and SIN3A specifically repress HIF 2α expression

John Biddlestone; Michael Batie; Daniel Bandarra; Ivan Munoz; Sonia Rocha

doi:10.1042/BCJ20170945

SINHCAF/FAM60A and SIN3A specifically repress HIF 2α expression

John Biddlestone, Michael Batie, Daniel Bandarra, Ivan Munoz, Sonia Rocha (Lead / Corresponding author)

MRC PPU

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14 Citations (Scopus)

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Abstract

The SIN3A-HDAC complex is a master transcriptional repressor, required for development but often deregulated in disease. Here, we report that the recently identified new component of this complex, SINHCAF/FAM60A, links the SIN3A-HDAC co-repressor complex function to the hypoxia response. We show that SINHCAF specifically repress HIF 2α mRNA and protein expression, via its interaction with the transcription factor SP1, and recruitment of HDAC1 to the HIF 2α promoter. SINHCAF control over HIF 2α results in functional cellular changes in in vitro angiogenesis, and viability. Our analysis reveals an unexpected link between SINHCAF and the regulation of the hypoxia response.

Original language	English
Pages (from-to)	2073-2090
Number of pages	18
Journal	Biochemical Journal
Volume	475
Issue number	12
Early online date	21 May 2018
DOIs	https://doi.org/10.1042/BCJ20170945
Publication status	Published - 29 Jun 2018

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Cell Biology

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10.1042/BCJ20170945Licence: CC BY

Final Published VersionFinal published version, 1.98 MBLicence: CC BY

Strategic Award: Wellcome Trust Technology Platform
Blow, J. (Investigator), Lamond, A. (Investigator) & Owen-Hughes, T. (Investigator)
1/01/13 → 30/09/18
Project: Research
Mechanisms of Inflammation and Hypoxia-Induced Responses Mediated by HIF and NF-KB in Cancer (Senior Research Fellowship)
Lamond, A. (Investigator) & Rocha, S. (Investigator)
1/08/11 → 1/08/17
Project: Research

Cite this

@article{220d6e1ee2b0474d981d5e9c3ca0701e,

title = "SINHCAF/FAM60A and SIN3A specifically repress HIF 2α expression",

abstract = "The SIN3A-HDAC complex is a master transcriptional repressor, required for development but often deregulated in disease. Here, we report that the recently identified new component of this complex, SINHCAF/FAM60A, links the SIN3A-HDAC co-repressor complex function to the hypoxia response. We show that SINHCAF specifically repress HIF 2α mRNA and protein expression, via its interaction with the transcription factor SP1, and recruitment of HDAC1 to the HIF 2α promoter. SINHCAF control over HIF 2α results in functional cellular changes in in vitro angiogenesis, and viability. Our analysis reveals an unexpected link between SINHCAF and the regulation of the hypoxia response.",

author = "John Biddlestone and Michael Batie and Daniel Bandarra and Ivan Munoz and Sonia Rocha",

note = "J.B was funded by a Cancer Research UK clinical fellowship; D.B. was funded by a PhD studentship from the Portuguese Science Foundation and Graduate Program in Areas of Basic and Applied Biology (GABBA); M.B. is funded by a MRC PhD studentship. S.R.was funded by a Cancer Research UK Senior Research Fellowship C99667/A12918; This work was also supported by a Wellcome Trust Strategic Award (097945/B/11/Z) and additionally supported by a small grant from the Anne and Normile Baxter prize for cancer research 2014.",

year = "2018",

month = jun,

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doi = "10.1042/BCJ20170945",

language = "English",

volume = "475",

pages = "2073--2090",

journal = "Biochemical Journal",

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T1 - SINHCAF/FAM60A and SIN3A specifically repress HIF 2α expression

AU - Biddlestone, John

AU - Batie, Michael

AU - Bandarra, Daniel

AU - Munoz, Ivan

AU - Rocha, Sonia

N1 - J.B was funded by a Cancer Research UK clinical fellowship; D.B. was funded by a PhD studentship from the Portuguese Science Foundation and Graduate Program in Areas of Basic and Applied Biology (GABBA); M.B. is funded by a MRC PhD studentship. S.R.was funded by a Cancer Research UK Senior Research Fellowship C99667/A12918; This work was also supported by a Wellcome Trust Strategic Award (097945/B/11/Z) and additionally supported by a small grant from the Anne and Normile Baxter prize for cancer research 2014.

PY - 2018/6/29

Y1 - 2018/6/29

N2 - The SIN3A-HDAC complex is a master transcriptional repressor, required for development but often deregulated in disease. Here, we report that the recently identified new component of this complex, SINHCAF/FAM60A, links the SIN3A-HDAC co-repressor complex function to the hypoxia response. We show that SINHCAF specifically repress HIF 2α mRNA and protein expression, via its interaction with the transcription factor SP1, and recruitment of HDAC1 to the HIF 2α promoter. SINHCAF control over HIF 2α results in functional cellular changes in in vitro angiogenesis, and viability. Our analysis reveals an unexpected link between SINHCAF and the regulation of the hypoxia response.

AB - The SIN3A-HDAC complex is a master transcriptional repressor, required for development but often deregulated in disease. Here, we report that the recently identified new component of this complex, SINHCAF/FAM60A, links the SIN3A-HDAC co-repressor complex function to the hypoxia response. We show that SINHCAF specifically repress HIF 2α mRNA and protein expression, via its interaction with the transcription factor SP1, and recruitment of HDAC1 to the HIF 2α promoter. SINHCAF control over HIF 2α results in functional cellular changes in in vitro angiogenesis, and viability. Our analysis reveals an unexpected link between SINHCAF and the regulation of the hypoxia response.

U2 - 10.1042/BCJ20170945

DO - 10.1042/BCJ20170945

M3 - Article

C2 - 29784889

SN - 0264-6021

VL - 475

SP - 2073

EP - 2090

JO - Biochemical Journal

JF - Biochemical Journal

IS - 12

ER -

SINHCAF/FAM60A and SIN3A specifically repress HIF 2α expression

Abstract

ASJC Scopus subject areas

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Projects

Strategic Award: Wellcome Trust Technology Platform

Mechanisms of Inflammation and Hypoxia-Induced Responses Mediated by HIF and NF-KB in Cancer (Senior Research Fellowship)

Cite this