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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.

Histone variant H3F3A promotes lung cancer cell migration through intronic regulation