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Effects of Nicotinamide on Cervical Cancer-Derived Fibroblasts: Evidence for Therapeutic Potential

Reem N Hassan1, Hualei Luo1, Weiying Jiang1

  • 1Department of Medical Genetics, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, Guangdong 510080, People's Republic of China.

Cancer Management and Research
|February 28, 2020
PubMed
Abstract

Insights

Nicotinamide (NAM) reduces cervical cancer-associated fibroblast (CAF) viability by increasing reactive oxygen species (ROS) and inducing apoptosis. This suggests NAM has therapeutic potential for cervical cancer treatment.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Cervical cancer-associated fibroblasts (CAFs) play a crucial role in tumor progression.
  • Understanding the mechanisms that inhibit CAF growth is essential for developing novel cancer therapies.

Purpose of the Study:

  • To investigate the in vitro efficacy of nicotinamide (NAM) on cervical cancer-associated fibroblasts (CAFs).
  • To elucidate the mechanism by which NAM inhibits CAF proliferation and induces apoptosis.

Main Methods:

  • Cell viability was assessed using the CCK-8 assay.
  • Reactive oxygen species (ROS) production was measured using 2',7'-Dichlorofluorescin diacetate.
  • Apoptosis, mitochondrial membrane potential, and cell cycle arrest were analyzed by flow cytometry (Annexin-V, JC-1 assay) and qRT-PCR.

Main Results:

  • Nicotinamide significantly reduced fibroblast viability.
  • NAM treatment led to increased intracellular ROS and decreased glutathione (GSH) levels, indicating oxidative stress.
  • Apoptosis was induced in fibroblasts via the mitochondrial pathway, with observed changes in apoptotic gene expression and cell cycle arrest.

Conclusions:

  • Nicotinamide demonstrates therapeutic potential against cervical cancer-associated fibroblasts in vitro.
  • The findings highlight NAM's ability to induce oxidative stress, apoptosis, and cell cycle arrest in CAFs.
  • Further research is warranted to explore NAM's clinical application in cervical cancer treatment.
Keywords:
apoptosiscervical cancerfibroblastsmitochondrial pathwaynicotinamidetherapeutic potential

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