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Retracted Article: Long non-coding RNA KCNQ1OT1 regulates cell proliferation, apoptosis and chemo-sensitivity through

Jing Dai1, Kai Wang1, Tao Liu1

  • 1Department of Hematology, Zhoukou Central Hospital No. 26, Renmin East Road, Zhoukou 466000 Zhengzhou China yangzhiming117@163.com +86 394 8521603.

RSC Advances
|May 11, 2022
PubMed

Insights

Long non-coding RNA KCNQ1OT1 promotes acute myeloid leukemia (AML) by downregulating microRNA-186-5p (miR-186-5p), which targets neural cell adhesion molecule 1 (NCAM1). This reveals a novel KCNQ1OT1/miR-186-5p/NCAM1 axis in AML progression.

Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • Long non-coding RNA KCNQ1OT1 and microRNA-186-5p (miR-186-5p) are implicated in human cancers.
  • KCNQ1OT1 expression is elevated in acute myeloid leukemia (AML), but its role is unclear.

Purpose of the Study:

  • To elucidate the functional mechanism of KCNQ1OT1 and miR-186-5p in AML development.
  • To investigate the regulatory relationship between KCNQ1OT1, miR-186-5p, and neural cell adhesion molecule 1 (NCAM1) in AML.

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) for gene expression analysis.
  • Cell proliferation (MTT assay) and apoptosis (flow cytometry) assays.
  • Western blot for protein level assessment and dual-luciferase reporter assay for interaction confirmation.

Main Results:

  • KCNQ1OT1 and NCAM1 were upregulated, while miR-186-5p was downregulated in AML samples.
  • KCNQ1OT1 depletion inhibited proliferation and promoted apoptosis and chemo-sensitivity in AML cells.
  • KCNQ1OT1 directly downregulated miR-186-5p, which in turn decreased NCAM1 expression, mediating AML progression.

Conclusions:

  • KCNQ1OT1 promotes AML progression by regulating the miR-186-5p/NCAM1 axis.
  • This study reveals a novel molecular mechanism involving KCNQ1OT1, miR-186-5p, and NCAM1 in AML pathogenesis.

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