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An Orthotopic Murine Model of Human Prostate Cancer Metastasis
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Nuclear MET requires ARF and is inhibited by carbon nanodots through binding to phospho-tyrosine in prostate cancer

Yingqiu Xie1, Haiyan Fan2, Wenfu Lu3

  • 1Department of Biology, Nazarbayev University School of Science and Technology, Astana, 010000, Kazakhstan. xieautumnus@yahoo.com.

Oncogene
|December 21, 2018
PubMed

Insights

Androgen deprivation therapy (ADT) can increase nMET in prostate cancer. Carbon nanodots overcome resistance to MET inhibitors by inducing DNA damage, offering a new strategy for cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Nuclear receptor tyrosine kinases (nRTKs) are frequently upregulated in various cancers, yet their regulatory mechanisms remain largely unknown.
  • Androgen deprivation therapy (ADT) has been observed to induce nMET in castration-resistant prostate cancer (CRPC) specimens.
  • The precise role and regulation of nMET in cancer progression, particularly in prostate cancer, require further elucidation.

Purpose of the Study:

  • To investigate the regulatory mechanisms of nMET in castration-resistant prostate cancer (CRPC).
  • To explore the potential of carbon nanodots in overcoming resistance to MET inhibitors.
  • To identify novel therapeutic strategies targeting the nMET axis for improved cancer treatment.

Main Methods:

  • Reanalysis of gene expression microarray profiles from a Pten/Trp53 conditional knockout mouse model.
  • Correlation analysis of MET/nMET and ARF expression in human prostate cancer (PCa) specimens.
  • Biochemical assays and computational calculations to determine the mechanism of carbon nanodot action on MET phosphorylation.

Main Results:

  • nMET signaling was identified as essential for CRPC growth, requiring ARF.
  • Aberrant MET/nMET elevation was found to correlate with ARF in human PCa specimens.
  • Carbon nanodots resensitize cancer cells to MET inhibitors by inducing DNA damage response and inhibiting phosphorylation.

Conclusions:

  • ARF stabilizes MET, thereby elevating nMET and promoting CRPC growth.
  • Targeting the nMET axis with carbon nanodots represents a novel strategy for overcoming drug resistance in cancers, particularly prostate cancer.
  • Carbon nanodots offer a promising approach to enhance the efficacy of MET inhibitors in precision therapy.

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