Where Sin3a Meets STAT3: Balancing STAT3-Mediated Transcriptional Activation and Repression

Where Sin3a Meets STAT3: Balancing STAT3-Mediated Transcriptional Activation and Repression

STAT3 can mediate epigenetic silencing of tumor suppressor genes (TSG). However, little is known about the molecular mechanisms involved, except that this action is mediated by DNA methylation and requires STAT3 acetylation. In this issue of , Gambi and colleagues confirm that oncogene-driven consti...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Vol. 79; no. 12; pp. 3031 - 3033
Main Authors: Monteleone, Emanuele, Poli, Valeria
Format: Journal Article
Language:English
Published: United States 15-06-2019
Subjects:
DNA Methylation
Promoter Regions, Genetic
Repressor Proteins - genetics
STAT3 Transcription Factor - genetics
Transcriptional Activation
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Summary:STAT3 can mediate epigenetic silencing of tumor suppressor genes (TSG). However, little is known about the molecular mechanisms involved, except that this action is mediated by DNA methylation and requires STAT3 acetylation. In this issue of , Gambi and colleagues confirm that oncogene-driven constitutive STAT3 acetylation is responsible for TSG silencing. Furthermore, they show that the Sin3a transcriptional repressor complex is an obligatory partner of STAT3 on the promoters of the repressed genes, shedding light on the mechanisms involved in STAT3-mediated transcriptional repression, and more importantly, identifying that the STAT3-Sin3a axis is a potential selective therapeutic target in STAT3-dependent tumors. .
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ISSN:0008-5472
1538-7445
DOI:10.1158/0008-5472.CAN-19-0927