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Identification of Key Factors Regulating Self-renewal and Differentiation in EML Hematopoietic Precursor Cells by RNA-sequencing Analysis
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LncRNA NR-104098 Inhibits AML Proliferation and Induces Differentiation Through Repressing EZH2 Transcription by

Yubin Feng1,2, Shuang Hu1,2, Lanlan Li1,2

  • 1The Key Laboratory of Major Autoimmune Diseases of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, China.

Frontiers in Cell and Developmental Biology
|April 17, 2020
PubMed

Insights

Long non-coding RNA NR-104098 acts as a tumor suppressor in acute myeloid leukemia (AML). It inhibits cancer cell proliferation and promotes differentiation by targeting EZH2, offering new therapeutic insights.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • Long non-coding RNAs (lncRNAs) are critical regulators in cancer development.
  • While many lncRNAs are implicated in acute myeloid leukemia (AML), their specific roles and mechanisms require further elucidation.

Purpose of the Study:

  • To investigate the function and mechanism of lncRNA NR-104098 in acute myeloid leukemia (AML).
  • To explore the potential of NR-104098 as a therapeutic target in AML.

Main Methods:

  • Microarray analysis in NB4 cells to identify differentially expressed lncRNAs.
  • In vitro studies to assess the effects of NR-104098 on AML cell proliferation and differentiation.
  • Mouse xenograft models to evaluate in vivo efficacy.
  • Molecular mechanism studies involving EZH2, E2F1, and ATPR.

Main Results:

  • lncRNA NR-104098 was found to be significantly upregulated in AML cells and functions as a tumor suppressor.
  • Overexpression of NR-104098 inhibited AML cell proliferation and induced differentiation in vitro and in vivo.
  • NR-104098 inhibits EZH2 transcription by binding to E2F1 and recruiting it to the EZH2 promoter.
  • ATPR treatment increased NR-104098 expression, mediating its anti-leukemic effects.

Conclusions:

  • lncRNA NR-104098 is a crucial tumor suppressor in AML, inhibiting proliferation and promoting differentiation.
  • The mechanism involves the NR-104098/E2F1/EZH2 axis, highlighting a novel regulatory pathway.
  • ATPR exerts its anti-AML effects partly through upregulating NR-104098, suggesting therapeutic potential.
Keywords:
E2F1EZH2NR-104098acute myeloid leukemia (AML)differentiationlong non-coding RNAsproliferation

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