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Calcitonin targets extracellular signal-regulated kinase signaling pathway in human cancers

Misa Nakamura1, Bo Han, Toshihide Nishishita

  • 1Department of Pathology, Wakayama Medical University, Kimiidera 811-1, Wakayama 641-0012, Japan. nakamuram@kawasakigakuen.ac.jp

Journal of Molecular Endocrinology
|December 7, 2007
PubMed

Insights

Calcitonin (CT) reduces tumor growth by decreasing extracellular signal-regulated kinase (ERK1/2) phosphorylation in certain cancers. This suggests CT as a potential targeted cancer therapy by inhibiting the mitogen-activated protein kinases (MAPKs) pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • The mitogen-activated protein kinases (MAPKs) pathway, particularly extracellular signal-regulated kinase (ERK1/2), is frequently dysregulated in various cancers.
  • Constitutive ERK1/2 phosphorylation is a hallmark of certain tumor types, making it a potential therapeutic target.
  • Calcitonin (CT), a thyroid hormone, is known for treating osteoporosis and hypercalcemia of malignancy.

Purpose of the Study:

  • To investigate the effect of Calcitonin (CT) on ERK1/2 phosphorylation in cancer cells.
  • To determine if CT-mediated inhibition of ERK1/2 phosphorylation impacts tumor growth.
  • To explore the potential of CT as a targeted cancer therapy.

Main Methods:

  • Utilized MDA-MB-231 (breast cancer) and MCF-7 (breast cancer) cell lines with differing ERK1/2 phosphorylation statuses.
  • Administered CT and analyzed its effect on c-Raf phosphorylation at Ser(259) via the protein kinase A pathway.
  • Assessed CT's impact on ERK1/2 phosphorylation levels.
  • Measured tumor volume in vivo following CT treatment in a xenograft model.

Main Results:

  • CT significantly decreased ERK1/2 phosphorylation in MDA-MB-231 cells with constitutive phosphorylated ERK1/2.
  • CT treatment led to the phosphorylation of c-Raf at Ser(259) through the protein kinase A pathway, suppressing ERK1/2 activity.
  • CT administration markedly reduced tumor volume in MDA-MB-231 xenografts.
  • CT did not significantly affect the proliferation of MCF-7 cells, which lack constitutive ERK1/2 phosphorylation.

Conclusions:

  • Calcitonin (CT) effectively inhibits the ERK1/2 signaling pathway in specific cancer types characterized by constitutive ERK1/2 phosphorylation.
  • CT demonstrates anti-tumor efficacy by reducing tumor volume, likely through the suppression of the MAPK pathway.
  • These findings highlight CT as a promising therapeutic agent for targeting ERK in cancer treatment.

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