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<p>Lung squamous cell carcinoma (LUSC) is a subtype of non-small cell lung cancer (NSCLC). Compared to lung adenocarcinoma (LUAD), LUSC is characterized by a greater propensity for recurrence and metastasis, poorer prognosis, and shorter survival. Therefore, further research into the pathogenesis of LUSC and the identification of new therapeutic targets are essential to advance clinical treatment options for this aggressive cancer. FAM111B, a serine protease and cancer-associated nuclear protein, has been implicated in various cancers. Previous studies have shown that FAM111B is closely associated with the progression of LUAD. However, our pan-cancer analysis suggests that FAM111B is highly expressed in LUSC and plays an oncogenic role, which is consistent with its higher expression in LUSC compared to LUAD in clinical samples. To investigate the functional role of FAM111B in LUSC, we developed both in vitro and in vivo knockdown models. Our results demonstrate that knocking down FAM111B significantly inhibits the proliferation, migration, and invasion of LUSC cells. Additionally, FAM111B knockdown induces cell cycle arrest in the S phase, further underscoring its role in LUSC progression. Mechanistically, FAM111B promotes LUSC migration and invasion by facilitating epithelial-mesenchymal transition (EMT). Moreover, the proliferation and cell cycle processes in LUSC may be regulated through the PI3K signaling pathway. In conclusion, our study elucidates the clinical relevance and molecular mechanisms of FAM111B in LUSC, highlighting its potential as a novel therapeutic target for this challenging cancer subtype.</p>

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FAM111B may promote the progression of lung squamous cell carcinoma through PI3K signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月2日

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  • Yajuan Chen,
  • Shiwei Chai,
  • Huimin Wang,
  • Yunyi Chen,
  • Yanting Bi,
  • Yifei Ma,
  • Ruotian Li,
  • Ruiyi Liu,
  • Zaoxiu Hu,
  • Shaoxiang Wan

摘要

Lung squamous cell carcinoma (LUSC) is a subtype of non-small cell lung cancer (NSCLC). Compared to lung adenocarcinoma (LUAD), LUSC is characterized by a greater propensity for recurrence and metastasis, poorer prognosis, and shorter survival. Therefore, further research into the pathogenesis of LUSC and the identification of new therapeutic targets are essential to advance clinical treatment options for this aggressive cancer. FAM111B, a serine protease and cancer-associated nuclear protein, has been implicated in various cancers. Previous studies have shown that FAM111B is closely associated with the progression of LUAD. However, our pan-cancer analysis suggests that FAM111B is highly expressed in LUSC and plays an oncogenic role, which is consistent with its higher expression in LUSC compared to LUAD in clinical samples. To investigate the functional role of FAM111B in LUSC, we developed both in vitro and in vivo knockdown models. Our results demonstrate that knocking down FAM111B significantly inhibits the proliferation, migration, and invasion of LUSC cells. Additionally, FAM111B knockdown induces cell cycle arrest in the S phase, further underscoring its role in LUSC progression. Mechanistically, FAM111B promotes LUSC migration and invasion by facilitating epithelial-mesenchymal transition (EMT). Moreover, the proliferation and cell cycle processes in LUSC may be regulated through the PI3K signaling pathway. In conclusion, our study elucidates the clinical relevance and molecular mechanisms of FAM111B in LUSC, highlighting its potential as a novel therapeutic target for this challenging cancer subtype.