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<p><i>BYSL</i>, located on chromosome 6p21.1, is implicated in tumor progression, but its role in acute myeloid leukemia (AML) remains unclear. <i>BYSL</i> expression was analyzed using public databases and AML clinical samples. A prognostic model incorporating <i>BYSL</i> was constructed and validated. Functional assays were performed by knocking down <i>BYSL</i> in AML cell lines to evaluate proliferation, apoptosis, and cell cycle regulation. To investigate the underlying mechanism, Gene set enrichment analysis (GSEA), Western blotting and chromatin immunoprecipitation-quantitative polymerase chain reaction (ChIP-qPCR) assays were performed. <i>BYSL</i> was significantly overexpressed in AML, with high expression correlating with severe anemia and poor overall survival. A risk model incorporating <i>BYSL</i> along with clinical factors (age, cytogenetic risk, transplantation, gene mutations) demonstrated strong predictive accuracy (c-index = 0.754). Functional assays showed that <i>BYSL</i> knockdown significantly inhibited cell proliferation, reduced colony-forming ability, and induced cell cycle arrest at the G0/G1 phase. Mechanistically, <i>BYSL</i> suppression notably decreased PI3K and AKT phosphorylation, implicating this signaling pathway. Additionally, ChIP-qPCR experiments confirmed that <i>BYSL</i> is transcriptionally regulated by <i>c-MYC</i> through direct promoter binding. Our findings support a role for <i>BYSL</i> in AML pathogenesis, potentially through modulation of the PI3K/AKT signaling pathway. Transcriptionally regulated by <i>c-MYC</i>, <i>BYSL</i> may serve as a prognostic biomarker and warrants further investigation as a potential therapeutic target.</p>

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Investigation of the expression and potential mechanistic role of BYSL in acute myeloid leukemia

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月19日

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  • Jie Gao,
  • Fujue Wang,
  • Yingying Chen,
  • Pengqiang Wu,
  • Yongqian Jia,
  • Xianmin Song

摘要

BYSL, located on chromosome 6p21.1, is implicated in tumor progression, but its role in acute myeloid leukemia (AML) remains unclear. BYSL expression was analyzed using public databases and AML clinical samples. A prognostic model incorporating BYSL was constructed and validated. Functional assays were performed by knocking down BYSL in AML cell lines to evaluate proliferation, apoptosis, and cell cycle regulation. To investigate the underlying mechanism, Gene set enrichment analysis (GSEA), Western blotting and chromatin immunoprecipitation-quantitative polymerase chain reaction (ChIP-qPCR) assays were performed. BYSL was significantly overexpressed in AML, with high expression correlating with severe anemia and poor overall survival. A risk model incorporating BYSL along with clinical factors (age, cytogenetic risk, transplantation, gene mutations) demonstrated strong predictive accuracy (c-index = 0.754). Functional assays showed that BYSL knockdown significantly inhibited cell proliferation, reduced colony-forming ability, and induced cell cycle arrest at the G0/G1 phase. Mechanistically, BYSL suppression notably decreased PI3K and AKT phosphorylation, implicating this signaling pathway. Additionally, ChIP-qPCR experiments confirmed that BYSL is transcriptionally regulated by c-MYC through direct promoter binding. Our findings support a role for BYSL in AML pathogenesis, potentially through modulation of the PI3K/AKT signaling pathway. Transcriptionally regulated by c-MYC, BYSL may serve as a prognostic biomarker and warrants further investigation as a potential therapeutic target.