Research Papers:
Novel leptin OB3 peptide-induced signaling and progression in thyroid cancers: Comparison with leptin
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Abstract
Yu-Chen SH Yang1,*, Yu-Tang Chin2,*, Meng-Ti Hsieh2,3, Hsuan-Yu Lai2, Chien-Chih Ke4, Dana R. Crawford5, Oscar K. Lee6, Earl Fu7, Shaker A. Mousa8, Patricia Grasso9, Leroy F. Liu2, Heng-Yu Chang10,11, Heng-Yuan Tang8, Hung-Yun Lin2,3, Paul J. Davis8,9
1Joint Biobank, Office of Human Research, Taipei Medical University, Taipei, Taiwan
2Taipei Cancer Center, Taipei Medical University, Taipei, Taiwan
3PhD Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan
4Biomedical Imaging Research Center, National Yang-Ming University, Taipei, Taiwan
5Center for Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA
6Stem Cell Research Center, National Yang-Ming University, Taipei, Taiwan
7Department of Periodontology, School of Dentistry, National Defense Medical College, Taipei, Taiwan
8Pharmaceutical Research Institute, Albany College of Pharmacy and Health Sciences, Albany, New York, USA
9Department of Medicine, Albany Medical College, Albany, New York, USA
10Department of Biochemistry and Molecular Cell Biology, College of Medicine, Taipei Medical University, Taipei, Taiwan
11Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan
*These authors have contributed equally to this work
Correspondence to:
Heng-Yu Chang, e-mail: [email protected]
Hung-Yun Lin, e-mail: [email protected]
Keywords: obesity, leptin, OB3-leptin peptide, cancer cell invasion
Received: September 15, 2015 Accepted: March 18, 2016 Published: March 30, 2016
ABSTRACT
Obesity results in increased secretion of cytokines from adipose tissue and is a risk factor for various cancers. Leptin is largely produced by adipose tissue and cancer cells. It induces cell proliferation and may serve to induce various cancers. OB3-leptin peptide (OB3) is a new class of functional leptin peptide. However, its mitogenic effect has not been determined. In the present study, because of a close link between leptin and the hypothalamic-pituitary-thyroid axis, OB3 was compared with leptin in different thyroid cancer cells for gene expression, proliferation and invasion. Neither agent stimulated cell proliferation. Leptin stimulated cell invasion, but reduced adhesion in anaplastic thyroid cancer cells. Activated ERK1/2 and STAT3 contributed to leptin-induced invasion. In contrast, OB3 did not affect expression of genes involved in proliferation and invasion. In vivo studies in the mouse showed that leptin, but not OB3, significantly increased circulating levels of thyrotropin (TSH), a growth factor for thyroid cancer. In summary, OB3 is a derivative of leptin that importantly lacks the mitogenic effects of leptin on thyroid cancer cells.
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