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<p>Bromodomain adjacent to zinc finger domain 2B (BAZ2B) is involved in chromatin remodeling, non-coding RNA regulation, and aging. However, its role in cancer remains unclear. Using multiple databases (TCGA, GEO, GTEx, TIMER2.0, cBioPortal), we found that <i>BAZ2B</i> is downregulated in many cancers, including breast cancer. Low <i>BAZ2B</i> correlates with poor prognosis, immune infiltration, and diagnostic potential, as shown by ROC and Kaplan–Meier analyses. Functionally, <i>BAZ2B</i> knockdown promoted breast cancer cell proliferation, colony formation, migration, and invasion, but suppressed apoptosis. Western blotting showed that BAZ2B depletion decreased Bax and p53, but increased Bcl-2. <i>BAZ2B</i> deficiency increased lactate production and upregulated glycolytic enzymes (<i>LDHA</i>, <i>HK1</i>, <i>HK2</i>, <i>PKM2</i>, <i>PFK1</i>). This suggests BAZ2B suppresses tumors by inhibiting glycolysis. Multi-omics integration further uncovered <i>BAZ2B</i> loss-induced co-activation of pro-inflammatory factor release and mTOR signaling, concurrent with suppression of apoptotic pathways and dysregulation of DNA repair machinery. Clinical validation using tissue microarrays confirmed reduced BAZ2B expression in tumors versus adjacent tissues, consistent with CPTAC proteomic data from UALCAN and immunohistochemical evidence from HPA. Collectively, BAZ2B constrains breast cancer progression by orchestrating proliferation, apoptosis, EMT, and glycolytic metabolism, positioning it as a promising therapeutic target and multi-cancer biomarker.</p>

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Pan-cancer and multi-omics analyses reveal the diagnostic and prognostic value of BAZ2B in cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月7日

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  • Jimin Guo,
  • Shuqing Wang,
  • Yan Liu,
  • Bin Zhang,
  • Jinghua Zhang,
  • Jinghua Wu,
  • Guijie Qi,
  • Zhihao Shen,
  • Rui Guo,
  • Panyan Du,
  • Ying Zhang,
  • Mingjia Zhao,
  • Liyuan Han,
  • Linfeng Zhou,
  • Yufeng Li,
  • Yating Zhao

摘要

Bromodomain adjacent to zinc finger domain 2B (BAZ2B) is involved in chromatin remodeling, non-coding RNA regulation, and aging. However, its role in cancer remains unclear. Using multiple databases (TCGA, GEO, GTEx, TIMER2.0, cBioPortal), we found that BAZ2B is downregulated in many cancers, including breast cancer. Low BAZ2B correlates with poor prognosis, immune infiltration, and diagnostic potential, as shown by ROC and Kaplan–Meier analyses. Functionally, BAZ2B knockdown promoted breast cancer cell proliferation, colony formation, migration, and invasion, but suppressed apoptosis. Western blotting showed that BAZ2B depletion decreased Bax and p53, but increased Bcl-2. BAZ2B deficiency increased lactate production and upregulated glycolytic enzymes (LDHA, HK1, HK2, PKM2, PFK1). This suggests BAZ2B suppresses tumors by inhibiting glycolysis. Multi-omics integration further uncovered BAZ2B loss-induced co-activation of pro-inflammatory factor release and mTOR signaling, concurrent with suppression of apoptotic pathways and dysregulation of DNA repair machinery. Clinical validation using tissue microarrays confirmed reduced BAZ2B expression in tumors versus adjacent tissues, consistent with CPTAC proteomic data from UALCAN and immunohistochemical evidence from HPA. Collectively, BAZ2B constrains breast cancer progression by orchestrating proliferation, apoptosis, EMT, and glycolytic metabolism, positioning it as a promising therapeutic target and multi-cancer biomarker.