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<p>Acute T lymphocytic leukemia (T-ALL) is a hematological cancer with high mortality. The literature suggests an association between T-ALL and Long non-coding RNAs (lncRNAs). Nevertheless, the mechanism of lncRNA HOXA11-AS in T-ALL remains undetermined. The lncRNA HOXA11-AS expression level were assessed in T-ALL patients and normal controls by qRT-PCR. Furthermore, The proliferation, apoptosis, and autophagy of T-ALL cell (Molt4 and Jurkat cells) were investigated in <i>vitro via</i> EdU incorporation experiment, flow cytometry, immunofluorescence, and Western blotting. Moreover, the relationship between HOXA11-AS and miR-214-3p and between miR-214-3p, and <i>ATG12</i> was verified <i>via</i> dual-luciferase reporter assays. Our investigation demonstrated that compared to normal controls, the HOXA11-AS expression level were increased in T-ALL patients. Furthermore, in T-ALL cells, inhibition of HOXA11-AS or overexpression of miR-214-3p reduced autophagy and proliferation, while stimulating apoptosis. However, miR-214-3p inhibition counteracted HOXA11-AS-mediated suppression of T-ALL cell proliferation, autophagy, and apoptosis. In addition, HOXA11-AS modulated <i>ATG12 via</i> sponging miR-214-3p. Overall, this research indicated that lncRNA HOXA11-AS not only stimulates cell proliferation and autophagy but also inhibits apoptosis <i>via</i> the miR-214-3p/ATG12 axis, thereby suggesting that lncRNA HOXA11-AS might be a new candidate for T-ALL diagnosis and therapy.</p>

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Long non-coding RNA HOXA11-AS inhibits apoptosis, induces proliferation, and promotes autophagy via the miR-214-3p/ATG12 axis in acute T lymphoblastic leukemia

  • 期刊论文

  • 发表日期：

    2025年5月26日

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  • Rui Zhang,
  • YuanYuan Zhang,
  • XiaoFei Li,
  • ShaoHua Wang,
  • Jiao Li,
  • ShuoChun Shao,
  • Bin Liu,
  • WeiWei Guo,
  • Min Shi

摘要

Acute T lymphocytic leukemia (T-ALL) is a hematological cancer with high mortality. The literature suggests an association between T-ALL and Long non-coding RNAs (lncRNAs). Nevertheless, the mechanism of lncRNA HOXA11-AS in T-ALL remains undetermined. The lncRNA HOXA11-AS expression level were assessed in T-ALL patients and normal controls by qRT-PCR. Furthermore, The proliferation, apoptosis, and autophagy of T-ALL cell (Molt4 and Jurkat cells) were investigated in vitro via EdU incorporation experiment, flow cytometry, immunofluorescence, and Western blotting. Moreover, the relationship between HOXA11-AS and miR-214-3p and between miR-214-3p, and ATG12 was verified via dual-luciferase reporter assays. Our investigation demonstrated that compared to normal controls, the HOXA11-AS expression level were increased in T-ALL patients. Furthermore, in T-ALL cells, inhibition of HOXA11-AS or overexpression of miR-214-3p reduced autophagy and proliferation, while stimulating apoptosis. However, miR-214-3p inhibition counteracted HOXA11-AS-mediated suppression of T-ALL cell proliferation, autophagy, and apoptosis. In addition, HOXA11-AS modulated ATG12 via sponging miR-214-3p. Overall, this research indicated that lncRNA HOXA11-AS not only stimulates cell proliferation and autophagy but also inhibits apoptosis via the miR-214-3p/ATG12 axis, thereby suggesting that lncRNA HOXA11-AS might be a new candidate for T-ALL diagnosis and therapy.