Abstract
Adiponectin (Acrp30) and leptin, adipokines produced and secreted mainly by the adipose tissue, are involved in human carcinogenesis. Thyroid carcinomas are frequent endocrine cancers, and several evidences suggest that they are correlated with obesity. In this study, we first analyzed the expression levels and prognostic values of Acrp30, leptin, and their receptors in thyroid cancer cells. Then, we investigated the role of Acrp30 and leptin in proliferation, migration, and invasion. We found that Acrp30 treatment alone inhibits cell proliferation and cell viability in a time and dose-dependent manner; leptin alone does not influence thyroid cancer cells (BCPAP and K1) proliferation, but the combined treatment reverts Acrp30-induced effects on cell proliferation. Additionally, through wound healing and Matrigel Matrix invasion assays, we unveiled that Acrp30 inhibits thyroid cancer cell motility, while leptin induces the opposite effect. Importantly, in the combined treatment, Acrp30 and leptin exert antagonizing effects on papillary thyroid cancer cells’ migration and invasion in both BCPAP and K1 cell lines. Highlights of these studies suggest that Acrp30 and leptin could represent therapeutic targets and biomarkers for the management of thyroid cancer.
Highlights
The increasing prevalence of obesity is associated with the rising incidence, progression, and worse prognosis of various human cancers including the breast, colon, and prostate [3, 4].obesity is responsible of the more complicated management of patients with cancer [31]
Since leptin is known to exhibit opposite Acrp30 actions, we evaluated the combined effect of these adipokines on malignant hallmarks of papillary thyroid cancer (PTC) transformation, and we found that Acrp30 and leptin have antagonizing effects on thyroid cancer cell proliferation and motility
BCPAP and K1 (1 × 103) cells were seeded in 96-well plates, incubated overnight in DMEM 5% fetal bovine serum (FBS) treated with different doses of Acrp30 (0.15, 1.5, 15 or 50 μg/ml) (Biovendor, Heidelberg, Germany), or treated with leptin (125 ng/ml)
Summary
The increasing prevalence of obesity is associated with the rising incidence, progression, and worse prognosis of various human cancers including the breast, colon, and prostate [3, 4]. Obesity is responsible of the more complicated management of patients with cancer [31]. The molecular basis linking obesity to carcinogenesis is not yet completely elucidated, but several mechanisms cooperate to create a functional relationship between these two pathologic. Ersilia Nigro and Francesca Maria Orlandella contributed to this work
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
