Copper oxide nanoparticles inhibit pancreatic tumor growth primarily by targeting tumor initiating cells

Madeleine Benguigui1, Iris S Weitz2, Michael Timaner1

  • 1Cell Biology and Cancer Science, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, 31096, Israel.

Scientific Reports
|September 1, 2019
PubMed

Insights

Copper oxide nanoparticles (CuO-NPs) show promise in treating pancreatic cancer by targeting cancer stem cells (CSCs). These nanoparticles effectively reduce CSC viability and induce apoptosis, inhibiting tumor growth in preclinical models.

Area of Science:

  • Nanotechnology
  • Oncology
  • Cell Biology

Background:

  • Cancer stem cells (CSCs), or tumor-initiating cells (TICs), drive tumor growth and metastasis.
  • CSCs exhibit intrinsic resistance, leading to tumor re-growth after therapy, particularly in pancreatic cancer.

Purpose of the Study:

  • To investigate the cytotoxic effects of copper oxide nanoparticles (CuO-NPs) on CSC-enriched pancreatic cancer cells.
  • To evaluate the therapeutic potential of CuO-NPs against pancreatic cancer stem cells in vitro and in vivo.

Main Methods:

  • Treatment of TIC-enriched PANC1 human pancreatic cancer cell cultures with CuO-NPs.
  • Assessment of cell viability, apoptosis, reactive oxygen species (ROS) levels, and mitochondrial membrane potential.
  • Evaluation of CuO-NP efficacy in a mouse model of pancreatic cancer.

Main Results:

  • CuO-NPs demonstrated significant cytotoxicity against TIC-enriched PANC1 cells, decreasing viability and increasing apoptosis.
  • Treatment with CuO-NPs led to elevated ROS levels and reduced mitochondrial membrane potential in cancer cells.
  • CuO-NPs inhibited tumor growth in vivo and increased apoptosis in tumor-initiating cells within the tumors.

Conclusions:

  • Copper oxide nanoparticles exhibit potent anti-cancer effects by targeting pancreatic cancer stem cells.
  • CuO-NPs represent a potential novel therapeutic strategy for pancreatic cancer, addressing therapeutic resistance mediated by CSCs.

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