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<p>Dysregulation of circadian rhythm genes is related to the increased risk of development of various human cancers. This study investigated the biological roles of Period circadian regulator 3 (PER3) in the development and progression of lung adenocarcinoma and related underlying mechanisms. The expression of PER3 was decreased in lung adenocarcinoma and its low expression was correlated with advanced disease stages. Lentiviral-transduced overexpression of PER3 inhibited but PER3 silencing promoted proliferation, migration and invasion of lung adenocarcinomatous cells, suggesting that it played an anti-carcinogenic role in the development and progression of lung adenocarcinoma. Mechanistically, PER3 overexpression elevated the phosphorylation level of AMPK and reduced the phosphorylation level of mTOR, but PER3 silencing produced the opposite effects. More importantly, the inhibitory effects of PER3 overexpression on cellular proliferation, migration and invasion were partially reversed by the AMPK/mTOR pathway inhibitor. Correspondingly, the promoting effects of PER3 silencing on proliferation, migration and invasion was partially reversed by the AMPK/mTOR pathway activator. These findings collectively suggest that PER3 regulated biological behaviors of lung adenocarcinomatous cells through activating the AMPK/mTOR pathway. PER3 may be a promising biomarker and therapeutic target for lung adenocarcinoma.</p>

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PER3 suppresses lung adenocarcinomatous cell proliferation/migration through activating AMPK/mTOR pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月24日

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  • Guanli Yuan,
  • Yinfeng Liu,
  • Dawei Wu,
  • Jingping Xu

摘要

Dysregulation of circadian rhythm genes is related to the increased risk of development of various human cancers. This study investigated the biological roles of Period circadian regulator 3 (PER3) in the development and progression of lung adenocarcinoma and related underlying mechanisms. The expression of PER3 was decreased in lung adenocarcinoma and its low expression was correlated with advanced disease stages. Lentiviral-transduced overexpression of PER3 inhibited but PER3 silencing promoted proliferation, migration and invasion of lung adenocarcinomatous cells, suggesting that it played an anti-carcinogenic role in the development and progression of lung adenocarcinoma. Mechanistically, PER3 overexpression elevated the phosphorylation level of AMPK and reduced the phosphorylation level of mTOR, but PER3 silencing produced the opposite effects. More importantly, the inhibitory effects of PER3 overexpression on cellular proliferation, migration and invasion were partially reversed by the AMPK/mTOR pathway inhibitor. Correspondingly, the promoting effects of PER3 silencing on proliferation, migration and invasion was partially reversed by the AMPK/mTOR pathway activator. These findings collectively suggest that PER3 regulated biological behaviors of lung adenocarcinomatous cells through activating the AMPK/mTOR pathway. PER3 may be a promising biomarker and therapeutic target for lung adenocarcinoma.