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<p>Progression and chemoresistance is the main cause of acute lymphoblastic leukemia(ALL) treatment failure. However, its mechanism has not been fully understood. Herein, Annexin A1 (ANXA1) overexpression was found by bioinformatic analysis in B-ALL cells. Clinical specimens were collected to preliminarily explore the role of ANXA1 in B-ALL. It showed that ANXA1 was obviously upregulated in bone marrow samples from B-ALL patients with chemoresistance and correlated with relapse or resistance. Then, we performed cell proliferation and apoptosis assays in CCRF-SB and Nalm6 cells lines in vitro. Overexpression of ANXA1 protected the B-ALL cells from apoptosis induced by dexamethasone and promoted cell cycle progression in vitro. We also found that ANXA1 promoted B-ALL cell proliferation, which correlated with the activated fatty acid metabolism in vitro. Moreover, the content of neutral lipids and the protein expression levels of fatty acid metabolism related ACC1 and FASN proteins were significantly decreased following downregulation of ANXA1. Additionally, high expression of ANXA1 promoted leukemia cell progression by regulating fatty acid metabolism through activating PI3K/AKT signaling pathway. Then in vivo results indicated that downregulation of ANXA1 in B-ALL cells could significantly reduce leukemic cell burden and increase dexamethasone sensitivity. Therefore, ANXA1 was identified as an oncogene in the development and progression of B-ALL and might be a promising biomarker for treating B-ALL.</p>

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ANXA1 overexpression promotes B cell acute lymphoblastic leukemia progression and resistance by regulating fatty acid metabolism through PI3K/Akt signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月12日

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  • Ping Liu,
  • Dan Ma,
  • Chengyun Pan,
  • Qian Kang,
  • Yan Wang,
  • Min Zhang,
  • Jishi Wang

摘要

Progression and chemoresistance is the main cause of acute lymphoblastic leukemia(ALL) treatment failure. However, its mechanism has not been fully understood. Herein, Annexin A1 (ANXA1) overexpression was found by bioinformatic analysis in B-ALL cells. Clinical specimens were collected to preliminarily explore the role of ANXA1 in B-ALL. It showed that ANXA1 was obviously upregulated in bone marrow samples from B-ALL patients with chemoresistance and correlated with relapse or resistance. Then, we performed cell proliferation and apoptosis assays in CCRF-SB and Nalm6 cells lines in vitro. Overexpression of ANXA1 protected the B-ALL cells from apoptosis induced by dexamethasone and promoted cell cycle progression in vitro. We also found that ANXA1 promoted B-ALL cell proliferation, which correlated with the activated fatty acid metabolism in vitro. Moreover, the content of neutral lipids and the protein expression levels of fatty acid metabolism related ACC1 and FASN proteins were significantly decreased following downregulation of ANXA1. Additionally, high expression of ANXA1 promoted leukemia cell progression by regulating fatty acid metabolism through activating PI3K/AKT signaling pathway. Then in vivo results indicated that downregulation of ANXA1 in B-ALL cells could significantly reduce leukemic cell burden and increase dexamethasone sensitivity. Therefore, ANXA1 was identified as an oncogene in the development and progression of B-ALL and might be a promising biomarker for treating B-ALL.