2025 年 71 巻 5 号 p. 298-301
This study explores the potential of targeting epigenetics and cellular senescence as novel therapeutic strategies for cancer, with a focus on thoracic malignancies. Despite significant advances in cancer treatment, including molecularly targeted therapies and immune checkpoint inhibitors, challenges such as drug resistance and side effects remain. Recent research has highlighted the role of epigenetic abnormalities, such as histone modifications, in regulating gene expression and promoting cancer progression. In particular, inhibition of SETD1A, a histone methyltransferase involved in H3K4 methylation, has been shown to suppress tumor growth and metastasis in vivo. In addition, SETD1A inhibition also induces cellular senescence as evidenced by cell cycle arrest and increased expression of senescence markers. These findings suggest that the epigenetic regulation of tumor suppressor genes and the induction of cellular senescence could represent a new approach to cancer therapy. While traditional anticancer drugs primarily induce apoptosis, targeting cellular senescence may provide a more stable, long-term suppression of tumor growth. These findings highlight the need for further research into epigenetic mechanisms and their role in cancer progression. A better understanding of these processes may lead to the development of more effective, targeted therapies for the treatment of thoracic and other malignancies.