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MiR-140 Targets lncRNA DNAJC3-AS1 to Suppress Cell Proliferation in Acute Myeloid Leukemia

Hong Li1, Kehong Bi1, Saran Feng1

  • 1Department of Hematology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, No. 16766 Jingshi Road, Jinan 250014, Shandong Province, P.R. China.

Mediterranean Journal of Hematology and Infectious Diseases
|January 24, 2022
PubMed
Abstract

Insights

MicroRNA-140 (miR-140) targets DNAJC3-AS1 to suppress cell proliferation in acute myeloid leukemia (AML). This study found that increased DNAJC3-AS1 and decreased miR-140 expression are linked to AML progression.

Area of Science:

  • Molecular biology
  • Cancer research
  • Hematology

Background:

  • MicroRNA-140 (miR-140) and DNAJC3-AS1 are implicated in cancer biology.
  • Their specific roles in acute myeloid leukemia (AML) remain largely uncharacterized.
  • Understanding these roles is crucial for developing novel AML therapies.

Purpose of the Study:

  • To investigate the expression patterns of miR-140 and DNAJC3-AS1 in AML.
  • To elucidate the regulatory relationship between miR-140 and DNAJC3-AS1.
  • To determine the impact of miR-140 and DNAJC3-AS1 on AML cell proliferation.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) for expression analysis.
  • Overexpression assays to study regulatory interactions.
  • RNA pull-down assays to confirm direct binding.
  • Cellular fractionation and BrdU assays for proliferation analysis.

Main Results:

  • AML patients exhibited elevated DNAJC3-AS1 and reduced miR-140 expression.
  • DNAJC3-AS1 was localized in both nuclear and cytoplasmic compartments.
  • A direct interaction between DNAJC3-AS1 and miR-140 was confirmed.
  • Overexpression of miR-140 led to decreased DNAJC3-AS1 levels in AML cells.

Conclusions:

  • DNAJC3-AS1 promotes cell proliferation and antagonizes miR-140's suppressive effects in AML.
  • MiR-140 may exert its anti-proliferative function in AML by targeting DNAJC3-AS1.
  • These findings highlight a potential therapeutic target for AML treatment.
Keywords:
Acute myeloid leukemiaDNAJC3-AS1ProliferationmiR-140

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