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Targeting uPAR by CRISPR/Cas9 System Attenuates Cancer Malignancy and Multidrug Resistance

Kun Wang1, Zi-Hao Xing1, Qi-Wei Jiang1

  • 1Guangdong Provincial Key Laboratory of Bioengineering Medicine, Department of Cell Biology and Institute of Biomedicine, College of Life Science and Technology, Jinan University, National Engineering Research Center of Genetic Medicine, Guangzhou, China.

Frontiers in Oncology
|March 16, 2019
PubMed

Insights

Targeting urokinase plasminogen activator receptor (uPAR) with CRISPR/Cas9 inhibited cancer cell growth and invasion. This knockout also reduced cancer cell resistance to common chemotherapy drugs, highlighting uPAR

Area of Science:

  • Molecular biology
  • Cancer research
  • Gene editing

Background:

  • Urokinase plasminogen activator receptor (uPAR) is overexpressed in various cancers.
  • uPAR is implicated in tumor progression and development.

Purpose of the Study:

  • To investigate the role of uPAR in cancer malignancy and drug resistance.
  • To target uPAR using the CRISPR/Cas9 gene editing system in human cancer cell lines.

Main Methods:

  • CRISPR/Cas9 system was employed to knock out uPAR in two human cancer cell lines.
  • Two distinct single guide RNAs (sgRNAs) were utilized for uPAR targeting.
  • Cell proliferation, migration, invasion, and drug resistance were assessed post-uPAR knockout.

Main Results:

  • uPAR knockout significantly inhibited cancer cell proliferation, migration, and invasion.
  • Knockout of uPAR decreased the resistance of cancer cells to 5-FU, cisplatin, docetaxel, and doxorubicin.
  • The study provides evidence for uPAR's role in cancer malignancy and chemoresistance.

Conclusions:

  • Targeting uPAR via CRISPR/Cas9 is a viable strategy to combat cancer progression.
  • uPAR is a key factor in cancer cell drug resistance.
  • Further research into CRISPR/Cas9 applications for cancer therapy is warranted, despite current limitations.
Keywords:
CRISPR/Cas9cancerdrug resistancemalignancyuPAR

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