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Valproic acid, targets papillary thyroid cancer through inhibition of c-Met signalling pathway

Yan-Tao Fu1, Hai-Bo Zheng2, Le Zhou1

  • 1Department of Thyroid Surgery, China-Japan Union Hospital of Jilin UniversityChangchun 130033, China.

American Journal of Translational Research
|July 4, 2017
PubMed

Insights

Valproic acid (VPA) effectively inhibits c-Met activity and cancer cell proliferation in thyroid carcinoma models. This histone deacetylase inhibitor demonstrates dose-dependent anti-cancer effects, suggesting a new therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Tyrosine kinase receptors like c-Met are implicated in cancer progression.
  • Valproic acid (VPA), a histone deacetylase inhibitor, exhibits anti-cancer properties.

Purpose of the Study:

  • To evaluate the c-Met inhibitory activity of VPA in thyroid carcinoma.
  • To investigate the anti-cancer mechanisms of VPA targeting c-Met.

Main Methods:

  • In vitro assays using human thyroid cancer cell lines (SW1736, WRO).
  • In vivo study using a xenograft mouse model with SW1736-induced tumors.
  • Dose-response evaluation of VPA (5, 15, 30 mg/kg/day).
  • Assessment of c-Met phosphorylation, cell proliferation, downstream signaling, and angiogenesis.

Main Results:

  • VPA demonstrated potent c-Met phosphorylation inhibition (IC50, 5-26 nmol/l) and suppressed cell proliferation.
  • VPA inhibited downstream signaling pathways and exhibited anti-angiogenic activity.
  • Significant dose-dependent reduction in tumor size was observed in the xenograft model (P = 0.023).

Conclusions:

  • VPA exhibits significant anti-cancer activity in thyroid carcinoma by inhibiting c-Met signaling.
  • The anti-cancer effects of VPA are dose-dependent and correlate with c-Met expression.
  • VPA represents a potential therapeutic agent for thyroid cancer, warranting further clinical investigation.
Keywords:
RTK inhibitorThyroid cancerc-Met signallingpapillary thyroid carcinomavalproic acid

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