Leptin enhances migration of human papillary thyroid cancer cells through the PI3K/AKT and MEK/ERK signaling pathways

Shih Ping Cheng, Pen Hui Yin, Yi Chiung Hsu, Yuan Ching Chang, Shih Yuan Huang, Jie Jen Lee, Chen Wen Chi

Research output: Contribution to journalArticlepeer-review

65 Scopus citations

Abstract

The incidence of thyroid cancer has remarkably increased in recent years. Epidemiologic data suggest that obesity is associated with an increased incidence of several types of malignancies, including thyroid cancer. Leptin, an adipocyte-derived cytokine, has been shown to be involved in cancer development and progression. We previously demonstrated that papillary thyroid cancer expressing leptin receptor and/or leptin has a higher incidence of lymph node metastasis. In this study, we investigated the effects of leptin on cell migration in K1 and B-CPAP papillary thyroid cancer cells. Expression of leptin receptor was observed in both cell lines. Leptin enhanced the migratory activity significantly in a dose-dependent manner. We showed that leptin induced AKT and extracellular signal-regulated kinase (ERK) phosphorylation. Inhibition of phosphatidylinositol 3-kinase and ERK activation using pharmacological inhibitors effectively blocked leptin-induced migration of K1 and B-CPAP cells. Taken together, this study provides new mechanistic evidence for a role of leptin in the regulation of papillary thyroid cancer progression by stimulating tumor cell migration.

Original languageEnglish
Pages (from-to)1265-1271
Number of pages7
JournalOncology Reports
Volume26
Issue number5
DOIs
StatePublished - Nov 2011

Keywords

  • Cell migration
  • Leptin
  • MAPK
  • PI3K/AKT
  • Thyroid cancer

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