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<p>Gastric cancer (GC) poses a persistent global health burden, largely attributed to its asymptomatic early stages and limited efficacy of existing therapies. PHF23, which has been primarily studied in hematologic malignancies and degenerative joint diseases, has not been explored in gastric cancer. In this study, PHF23 expression was assessed in GC tissues through immunohistochemistry and public dataset analysis. Functional assays, including proliferation, migration, invasion, and apoptosis, were performed following PHF23 knockdown in GC cell lines. Tumorigenic effects were evaluated in nude mouse models, and potential downstream pathways were explored by enrichment analysis and Western blot. PHF23 was markedly overexpressed in GC tissues and significantly correlated with adverse clinical parameters such as advanced invasion depth, lymphatic spread, and TNM stage. High PHF23 levels were associated with reduced overall survival, and multivariate Cox analysis identified PHF23 as an independent prognostic factor. Silencing PHF23 impaired tumor cell proliferation, motility, and survival in vitro, and reduced tumor growth in vivo. Preliminary molecular analysis indicated that PHF23 knockdown is correlated with reduced phosphorylation levels of JAK2 and STAT3, suggesting a potential involvement of the JAK/STAT pathway. These results highlight PHF23 as a biologically relevant contributor to GC progression, with potential value in prognosis and therapeutic targeting.</p>

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Oncogenic role of PHF23 in gastric cancer progression

  • 期刊论文

  • 发表日期：

    2026年3月4日

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  • Wenhao Qu,
  • Jiaqi Jia,
  • Ning Zhang,
  • Rumeng Wang,
  • Yang Liu,
  • Shuyu Zhang,
  • Hangbo Gao,
  • Yuyue Tao,
  • Lizhou Jia,
  • Yugang Liu,
  • Jianguo Zhao

摘要

Gastric cancer (GC) poses a persistent global health burden, largely attributed to its asymptomatic early stages and limited efficacy of existing therapies. PHF23, which has been primarily studied in hematologic malignancies and degenerative joint diseases, has not been explored in gastric cancer. In this study, PHF23 expression was assessed in GC tissues through immunohistochemistry and public dataset analysis. Functional assays, including proliferation, migration, invasion, and apoptosis, were performed following PHF23 knockdown in GC cell lines. Tumorigenic effects were evaluated in nude mouse models, and potential downstream pathways were explored by enrichment analysis and Western blot. PHF23 was markedly overexpressed in GC tissues and significantly correlated with adverse clinical parameters such as advanced invasion depth, lymphatic spread, and TNM stage. High PHF23 levels were associated with reduced overall survival, and multivariate Cox analysis identified PHF23 as an independent prognostic factor. Silencing PHF23 impaired tumor cell proliferation, motility, and survival in vitro, and reduced tumor growth in vivo. Preliminary molecular analysis indicated that PHF23 knockdown is correlated with reduced phosphorylation levels of JAK2 and STAT3, suggesting a potential involvement of the JAK/STAT pathway. These results highlight PHF23 as a biologically relevant contributor to GC progression, with potential value in prognosis and therapeutic targeting.