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<p>FAM83D plays a crucial role in cervical cancer (CC) metastasis, though its exact mechanism remains unclear. This study found that FAM83D was significantly upregulated in CC tissues, particularly in metastatic cases, and correlated with advanced tumor stage and poor prognosis. While it did not affect CC cell proliferation, chemosensitivity, or tumorigenesis, FAM83D overexpression enhanced migration and invasion, whereas its knockdown suppressed these effects. In vivo, silencing FAM83D markedly reduced lung and liver metastases in mice. Mechanistically, FAM83D upregulated EMT-like changes and Snail stability by directly interacting with GSK3β and promoting its Ser9 phosphorylation, thereby activating GSK3β/Snail signaling. Furthermore, AKT and PKA served as key upstream kinases in FAM83D-mediated GSK3β inactivation. Inhibition of GSK3β reversed the anti-metastatic effects of FAM83D knockdown. These results identify FAM83D as a key metastasis driver in CC, functioning through GSK3β/Snail/EMT axis, and suggest its potential as a therapeutic target to inhibit CC progression.</p>

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FAM83D facilitates EMT and metastasis of cervical cancer via interaction with GSK3β and inactivation of GSK3β/stabilization of Snail signaling

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月25日

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  • Jiaofeng Li,
  • Fengtian Li,
  • Xia Meng,
  • Zhiling Yang,
  • Zhengguang Li,
  • Hualong Tang,
  • Wanglong Zhu,
  • Haoming Li,
  • Xingqiang He,
  • Xinyue Lin,
  • Zhengyu Han,
  • Mei Chen,
  • Yuhan Yang,
  • Jingyi Wang,
  • Kun Zhang

摘要

FAM83D plays a crucial role in cervical cancer (CC) metastasis, though its exact mechanism remains unclear. This study found that FAM83D was significantly upregulated in CC tissues, particularly in metastatic cases, and correlated with advanced tumor stage and poor prognosis. While it did not affect CC cell proliferation, chemosensitivity, or tumorigenesis, FAM83D overexpression enhanced migration and invasion, whereas its knockdown suppressed these effects. In vivo, silencing FAM83D markedly reduced lung and liver metastases in mice. Mechanistically, FAM83D upregulated EMT-like changes and Snail stability by directly interacting with GSK3β and promoting its Ser9 phosphorylation, thereby activating GSK3β/Snail signaling. Furthermore, AKT and PKA served as key upstream kinases in FAM83D-mediated GSK3β inactivation. Inhibition of GSK3β reversed the anti-metastatic effects of FAM83D knockdown. These results identify FAM83D as a key metastasis driver in CC, functioning through GSK3β/Snail/EMT axis, and suggest its potential as a therapeutic target to inhibit CC progression.