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Modulation of NDEA activated ras expression and protein kinase C activity by nicotinamide

S Choudhury1, M Krishna, R K Bhattacharya

  • 1Radiation Biology Division, Bhabha Atomic Research Centre, Mumbai, India.

Cancer Letters
|February 5, 2000
PubMed

Insights

Nicotinamide, a vitamin B3 derivative, inhibits key molecules like ras expression and protein kinase C (PKC) activity in rats exposed to a carcinogen. This modulation suggests its potential role in cancer prevention and radiosensitization.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Carcinogenesis involves complex molecular pathways.
  • Nicotinamide (vitamin B3) is being investigated for therapeutic potential.
  • Ras expression, protein kinase C (PKC), and diacylglycerol (DAG) are implicated in cancer development.

Purpose of the Study:

  • To investigate the effects of nicotinamide on specific molecular markers during N-nitrosodiethylamine (NDEA)-induced carcinogenesis in rats.
  • To determine if nicotinamide can modulate key signaling pathways involved in cancer initiation.

Main Methods:

  • Rats were treated with N-nitrosodiethylamine (NDEA) to induce carcinogenesis.
  • Nicotinamide was administered to assess its impact on ras expression, PKC activity, and DAG levels.
  • PKC activity was measured in cytosolic, particulate, and nuclear fractions.

Main Results:

  • Nicotinamide significantly inhibited the NDEA-induced increase in ras expression, PKC activity, and DAG levels.
  • It modulated PKC activity in cytosolic and particulate fractions but not in the nuclear fraction.
  • Nicotinamide effectively modulated endobiotic DAG levels.

Conclusions:

  • Nicotinamide demonstrates potential as a modulator of carcinogenesis by inhibiting key molecular events.
  • Its ability to interfere with these pathways may contribute to its efficacy as a radiosensitizer.
  • Further research into nicotinamide's role in cancer prevention and therapy is warranted.

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