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LQFM030 reduced Ehrlich ascites tumor cell proliferation and VEGF levels

Mariana Flavia da Mota1, Flávio Silva de Carvalho2, Renato Ivan de Ávila1

  • 1Laboratório de Farmacologia e Toxicologia Celular, Faculdade de Farmácia, Universidade Federal de Goiás, Goiânia, GO, Brazil.

Life Sciences
|December 27, 2017
PubMed
Abstract

Insights

LQFM030, a simplified nutlin-1 compound, effectively reduced tumor growth and increased survival in mice by inducing apoptosis and inhibiting angiogenesis. It demonstrated low oral toxicity, suggesting potential as an anticancer agent.

Area of Science:

  • Pharmacology
  • Oncology
  • Molecular Biology

Background:

  • Nutlin-1 is a known compound with biological properties.
  • LQFM030 is a molecular simplification of nutlin-1.
  • Understanding the in vivo biological properties of LQFM030 is crucial for its potential therapeutic applications.

Purpose of the Study:

  • To investigate the in vivo biological properties of LQFM030.
  • To evaluate the antitumor effects of LQFM030 in Ehrlich ascites tumor (EAT)-bearing mice.
  • To assess the toxicity profile of LQFM030.

Main Methods:

  • EAT-bearing mice were treated with LQFM030 (50, 75, or 150mg/kg) intraperitoneally for 10 days.
  • Tumor volume, body weight, cytotoxicity, and angiogenesis were measured.
  • Flow cytometry was used to analyze p53, p21, and caspase activation in EAT cells.
  • Acute oral toxicity was assessed using an alternative method.

Main Results:

  • LQFM030 treatment significantly reduced tumor cell proliferation and vascular endothelial growth factor (VEGF) levels.
  • Enhanced survival and apoptotic tumor cell death were observed, indicated by p53 and p21 modulation and increased caspase activity.
  • LQFM030 was well-tolerated orally, with LD50 >2000-5000mg/Kg (UN GHS category 5).

Conclusions:

  • LQFM030 shows promise as an antitumor candidate, potentially for combination therapy to enhance efficacy and reduce toxicity.
  • LQFM030 exhibits antiangiogenic properties, suggesting its utility in treating diseases with VEGF overexpression.
  • Further research into LQFM030 could lead to novel therapeutic strategies in cancer treatment.
Keywords:
Ehrlich ascites tumorMDM2 inhibitorsNutlinsVEGFp21p53

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