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<p>Metastasis is a major contributor to poor patient survival in lung adenocarcinoma (LUAD); however, the underlying mechanisms remain incompletely understood. Unlike tumorigenesis-associated mutations, recurrent genetic alterations specifically linked to metastasis have not been identified, suggesting that epigenetic mechanisms may play a key role. In this study, we report that histone H2A variant H2A.J expression is significantly down-regulated in LUAD, and that low H2A.J levels are associated with unfavorable survival outcomes. Functional assays revealed that H2A.J overexpression suppresses cancer cell invasion and metastatic potential by modulating the expression of metastasis-associated genes, including TMEM158. Mechanistically, H2A.J is deposited in the promoter region of TMEM158, where it alters the local chromatin status to suppress transcriptional activity. Taken together, our findings suggest that H2A.J functions as an epigenetic suppressor of metastasis in LUAD and highlights its potential as both a prognostic biomarker and a therapeutic target to metastatic progression.</p>

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Histone variant H2A.J is an epigenetic regulator of metastasis in lung adenocarcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月26日

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  • Dong-Gun Kim,
  • Eun-Young Choi,
  • Hye-Mi Ahn,
  • Kyungho Kim,
  • Youn-Jae Kim

摘要

Metastasis is a major contributor to poor patient survival in lung adenocarcinoma (LUAD); however, the underlying mechanisms remain incompletely understood. Unlike tumorigenesis-associated mutations, recurrent genetic alterations specifically linked to metastasis have not been identified, suggesting that epigenetic mechanisms may play a key role. In this study, we report that histone H2A variant H2A.J expression is significantly down-regulated in LUAD, and that low H2A.J levels are associated with unfavorable survival outcomes. Functional assays revealed that H2A.J overexpression suppresses cancer cell invasion and metastatic potential by modulating the expression of metastasis-associated genes, including TMEM158. Mechanistically, H2A.J is deposited in the promoter region of TMEM158, where it alters the local chromatin status to suppress transcriptional activity. Taken together, our findings suggest that H2A.J functions as an epigenetic suppressor of metastasis in LUAD and highlights its potential as both a prognostic biomarker and a therapeutic target to metastatic progression.