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H22954, a novel long non-coding RNA down-regulated in AML, inhibits cancer growth in a BCL-2-dependent mechanism

Xiaofei Qi1, Yang Jiao2, Chao Cheng3

  • 1Cyrus Tang Hematology Center, Jiangsu Institute of Hematology, Collaborative Innovation Center of Hematology, Suzhou, 215000, China; Departments of Urology, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China; Departments of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.

Cancer Letters
|April 9, 2019
PubMed

Insights

A novel long non-coding RNA, H22954, is downregulated in acute myeloid leukemia (AML). Its restoration inhibits AML cell proliferation and tumor growth by targeting BCL2, suggesting therapeutic potential.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) play crucial roles in cancer biology.
  • Identifying novel molecular players in acute myeloid leukemia (AML) is essential for understanding pathogenesis and developing treatments.

Purpose of the Study:

  • To identify and characterize novel lncRNAs involved in AML.
  • To investigate the functional role of the identified lncRNA, H22954, in AML progression.
  • To elucidate the molecular mechanism by which H22954 affects AML cells.

Main Methods:

  • Differential gene expression analysis in CD34+ hematopoietic cells.
  • In vitro studies using cultured AML cells and in vivo mouse xenograft models.
  • Bioinformatic analysis, RNA antisense purification, and luciferase assays to determine molecular targets and mechanisms.
  • Correlation analysis of H22954 expression with clinical parameters in AML patients.

Main Results:

  • A novel lncRNA, H22954, was identified and found to be downregulated in AML patients.
  • H22954 expression inhibited AML cell proliferation and tumor growth in preclinical models.
  • H22954 was shown to target the 3' untranslated region of the BCL2 gene, inhibiting BCL2 expression.
  • Overexpression of H22954 reduced BCL-2 protein levels, promoted cell death, and correlated inversely with disease severity and poor prognosis in AML patients.

Conclusions:

  • H22954 acts as a novel regulator of BCL-2 in acute myeloid leukemia.
  • Reduced H22954 expression is implicated in the pathogenesis of AML.
  • H22954 represents a potential therapeutic target for AML treatment.
Keywords:
AMLApoptosisBCL-2H22954Long non-coding RNA

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