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 () and In-Hoo Kim
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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: 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: 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: Graduate School of Cancer Science and Policy, National Cancer Center

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Although several somatic single nucleotide variations in histone H3.3 have been investigated as cancer drivers, other types of aberration have not been well studied. Here, we demonstrate that overexpression of H3F3A, encoding H3.3, is associated with lung cancer progression and promotes lung cancer cell migration by activating metastasis-related genes. H3.3 globally activates gene expression through the occupation of intronic regions in lung cancer cells. Moreover, H3.3 binding regions show characteristics of regulatory DNA elements. We show that H3.3 is deposited at a specific intronic region of GPR87, where it modifies the chromatin status and directly activates GPR87 transcription. The expression levels of H3F3A and GPR87, either alone or in combination, are robust prognostic markers for early-stage lung cancer, and may indicate potential for the development of treatments involving GPR87 antagonists. In summary, our results demonstrate that intronic regulation by H3F3A may be a target for the development of novel therapeutic strategies.

Date: 2016
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DOI: 10.1038/ncomms12914

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