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PRKD2 Promotes Progression and Chemoresistance of AML via Regulating Notch1 Pathway

Qian Liu1,2, Wei Li1, Ying Zhou1

  • 1Department of Hematology, Qilu Hospital, Shandong University, Jinan 250012, People's Republic of China.

Oncotargets and Therapy
|December 19, 2019
PubMed
Abstract

Insights

Protein kinase D2 (PRKD2) promotes acute myeloid leukemia (AML) progression and chemoresistance by regulating the Notch1 pathway. This finding offers a new prognostic marker and potential therapeutic target for AML treatment.

Area of Science:

  • Hematology
  • Molecular Biology
  • Oncology

Background:

  • Acute myeloid leukemia (AML) progression and chemoresistance are major causes of treatment failure.
  • The Notch signaling pathway is implicated in various biological processes, including AML pathogenesis.

Purpose of the Study:

  • To investigate genes associated with the Notch1 pathway in AML.
  • To determine the role of these genes in AML progression and chemoresistance.

Main Methods:

  • Utilized TCGA database to identify Notch1-associated genes.
  • Performed survival analysis, qRT-PCR, and Western blot to assess gene expression.
  • Manipulated PRKD2 expression in AML cell lines and analyzed proliferation and chemoresistance using CCK-8 and flow cytometry.

Main Results:

  • PRKD2 expression positively correlated with Notch1, poorer prognosis, and chemoresistance in AML.
  • PRKD2 knockdown induced apoptosis and increased chemosensitivity.
  • PRKD2 overexpression promoted proliferation and chemoresistance, regulating the Notch1 pathway.
  • High PRKD2 expression is an independent prognostic marker for AML risk stratification.

Conclusions:

  • PRKD2 promotes AML cell proliferation and chemoresistance via Notch1 pathway regulation.
  • This study provides insights into AML chemoresistance mechanisms.
  • PRKD2 represents a potential prognostic marker and therapeutic target for AML.
Keywords:
AMLNotch1PRDK2chemoresistanceprogression

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