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RanBP3 Regulates Proliferation, Apoptosis and Chemosensitivity of Chronic Myeloid Leukemia Cells via Mediating

Qian Li1, Zhenglan Huang1, Yuhang Peng1

  • 1Key Laboratory of Laboratory Medical Diagnostics Designated by the Ministry of Education, Department of Clinical Hematology, Chongqing Medical University, Chongqing, China.

Frontiers in Oncology
|September 10, 2021
PubMed

Insights

Ran Binding Protein 3 (RanBP3) is elevated in chronic myeloid leukemia (CML). Silencing RanBP3 inhibits CML cell growth and restores imatinib sensitivity, offering a new therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Abnormal protein localization drives cancer and drug resistance.
  • CRM1 is a known target, but its cofactor RanBP3's role in CML is unknown.
  • RanBP3 is a CRM1 cofactor involved in nuclear export.

Purpose of the Study:

  • To investigate the role of RanBP3 in chronic myeloid leukemia (CML).
  • To determine if RanBP3 is a potential therapeutic target in CML.

Main Methods:

  • Measured RanBP3 levels in CML patient samples.
  • Utilized shRNA lentivirus to down-regulate RanBP3 in K562 and K562/G01 cells.
  • Assessed cell proliferation, apoptosis, and drug sensitivity in vitro and in vivo (NOD/SCID mice).

Main Results:

  • RanBP3 expression is elevated in CML.
  • RanBP3 silencing inhibited proliferation, induced apoptosis, and enhanced imatinib sensitivity in CML cells.
  • RanBP3 knockdown restored imatinib sensitivity in vivo.

Conclusions:

  • RanBP3 plays a significant role in CML pathogenesis.
  • Targeting RanBP3, alone or with TKIs, may improve CML treatment outcomes.
  • RanBP3 silencing impacts the TGF-β-SMAD2/3-p21 and ERK1/2-BAD pathways.
Keywords:
CMLERK1/2RanBP3imatinibnuclear export

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