Histone variant H3F3A promotes lung cancer cell migration through intronic regulation

Seong-Min Park; Eun-Young Choi; Mingyun Bae; Sunshin Kim; Jong Bae Park; Heon Yoo; Jung Kyoon Choi; Youn-Jae Kim; Seung-Hoon Lee; In-Hoo Kim

doi:10.1038/ncomms12914

Nature Communications (Oct 2016)

Histone variant H3F3A promotes lung cancer cell migration through intronic regulation

Seong-Min Park,
Eun-Young Choi,
Mingyun Bae,
Sunshin Kim,
Jong Bae Park,
Heon Yoo,
Jung Kyoon Choi,
Youn-Jae Kim,
Seung-Hoon Lee,
In-Hoo Kim

Affiliations

Seong-Min Park: Specific Organs Cancer Branch, Research Institute, National Cancer Center
Eun-Young Choi: Specific Organs Cancer Branch, Research Institute, National Cancer Center
Mingyun Bae: Department of Bio and Brain Engineering, KAIST
Sunshin Kim: Precision Medicine Branch, Research Institute, National Cancer Center
Jong Bae Park: Specific Organs Cancer Branch, Research Institute, National Cancer Center
Heon Yoo: Specific Organs Cancer Branch, Research Institute, National Cancer Center
Jung Kyoon Choi: Department of Bio and Brain Engineering, KAIST
Youn-Jae Kim: Specific Organs Cancer Branch, Research Institute, National Cancer Center
Seung-Hoon Lee: Specific Organs Cancer Branch, Research Institute, National Cancer Center
In-Hoo Kim: Department of System Cancer Science, Graduate School of Cancer Science and Policy, National Cancer Center

DOI: https://doi.org/10.1038/ncomms12914
Journal volume & issue: Vol. 7, no. 1
pp. 1 – 14

Abstract

Read online

Histone variants act as transcriptional activators and repressors and have been linked to cancer progression. Park and Choi et al. show that the histone H3.3 overexpression is associated with early-stage lung cancer, and promotes cancer cell migration by upregulating a G-protein-coupled receptor.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

About the journal