Interruption of aberrant chromatin looping is required for regenerating RB1 function and suppressing tumorigenesis

Xuyang Wen; Tianyi Ding; Fang Li; Jiayan Fan; Xianqun Fan; Renbing Jia; He Zhang

doi:10.1038/s42003-022-04007-2

Communications Biology (Sep 2022)

Interruption of aberrant chromatin looping is required for regenerating RB1 function and suppressing tumorigenesis

Xuyang Wen,
Tianyi Ding,
Fang Li,
Jiayan Fan,
Xianqun Fan,
Renbing Jia,
He Zhang

Affiliations

Xuyang Wen: Institute for Regenerative Medicine, Shanghai East Hospital, Frontier Science Research Center for Stem Cells, School of Life Science and Technology, Tongji University
Tianyi Ding: Institute for Regenerative Medicine, Shanghai East Hospital, Frontier Science Research Center for Stem Cells, School of Life Science and Technology, Tongji University
Fang Li: Department of Ophthalmology, Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine
Jiayan Fan: Department of Ophthalmology, Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine
Xianqun Fan: Department of Ophthalmology, Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine
Renbing Jia: Department of Ophthalmology, Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine
He Zhang: Institute for Regenerative Medicine, Shanghai East Hospital, Frontier Science Research Center for Stem Cells, School of Life Science and Technology, Tongji University

DOI: https://doi.org/10.1038/s42003-022-04007-2
Journal volume & issue: Vol. 5, no. 1
pp. 1 – 11

Abstract

Read online

A CTCF mediated intrachromosomal looping of RB1 promoter and its downstream silencer served as a regulatory inducer to inactivate RB1, revealing a novel transcriptional mechanism underlying RB1 dysfunction independent of gene mutation.

Published in Communications Biology

ISSN: 2399-3642 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science: Biology (General)
Website: https://www.nature.com/commsbio/

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