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Modified Annexin V/Propidium Iodide Apoptosis Assay For Accurate Assessment of Cell Death
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Analysis of naproxen activation of cell death pathways in Colo320 cells

Andrew Chen1,2, Wei Zhu2,3, Rian Goding2,4

  • 1College of Arts and Sciences at The State University of New York at Stony Brook, Stony Brook, NY 11794, USA.

Molecular and Clinical Oncology
|July 29, 2024
PubMed

Insights

Naproxen sodium (NS) shows promise in fighting colorectal cancer by significantly reducing cancer cell survival and migration. This non-steroidal anti-inflammatory drug also downregulates key genes involved in cancer proliferation and drug resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Colorectal cancer (CRC) is a leading cause of cancer-related mortality.
  • Current CRC treatments often involve severe side effects, necessitating the exploration of alternative therapies.
  • Non-steroidal anti-inflammatory drugs (NSAIDs) exhibit potential chemopreventive properties.

Purpose of the Study:

  • To investigate the chemopreventive potential of naproxen sodium (NS) against colorectal cancer.
  • To elucidate the molecular pathways and mechanisms underlying the anti-cancer effects of NS.
  • To assess the impact of NS on colorectal cancer cell viability, migration, and specific gene expression.

Main Methods:

  • Treatment of cancerous Colo320 and healthy CCD-18 cells with varying concentrations of naproxen sodium (NS).
  • Caspase-3 activity assay to measure apoptosis.
  • Cell survival and migration assays.
  • RNA sequencing to identify gene expression changes.
  • Enzyme-linked immunosorbent assays (ELISAs) for validation.

Main Results:

  • NS significantly increased caspase-3 activity (300%) and decreased cell survival (-72.888%) in Colo320 cells, with no significant effect on CCD-18 cells.
  • NS markedly reduced Colo320 cell migration (86.58%).
  • RNA sequencing revealed significant downregulation of MUC5B, S100A9, and MUC5AC genes in NS-treated Colo320 cells, which are associated with CRC proliferation, stemness, and drug resistance.

Conclusions:

  • Naproxen sodium (NS) demonstrates significant anti-colorectal cancer activity.
  • NS exerts its effects by inducing apoptosis, inhibiting cell migration, and downregulating key cancer-associated genes.
  • This study identifies a novel molecular mechanism for the anti-colorectal cancer efficacy of NS, highlighting its therapeutic potential.
Keywords:
apoptosisccd-18colo320colorectal cancernaproxennonsteroidal anti-inflammatory drugs

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