TY - JOUR
T1 - Adiponectin and leptin exert antagonizing effects on proliferation and motility of papillary thyroid cancer cell lines
AU - Nigro, Ersilia
AU - Orlandella, Francesca Maria
AU - Polito, Rita
AU - Mariniello, Raffaela Mariarosaria
AU - Monaco, Maria Ludovica
AU - Mallardo, Marta
AU - De Stefano, Anna Elisa
AU - Iervolino, Paola Lucia Chiara
AU - Salvatore, Giuliana
AU - Daniele, Aurora
N1 - Funding Information:
Open Access funding provided by Università degli Studi della Campania Luigi Vanvitelli. This study was partially supported by “Bando di Ateneo per il sostegno alla partecipazione ai bandi di ricerca individuale (quota A) per l’anno 2017” (code DSMB187) from University of Naples “Parthenope” and by “Ricerca Corrente” from the Italian Ministry of Health.
Publisher Copyright:
© 2021, The Author(s).
PY - 2021/5
Y1 - 2021/5
N2 - 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.
AB - 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.
KW - Adiponectin
KW - Leptin
KW - Motility
KW - Proliferation
KW - Thyroid cancer
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U2 - 10.1007/s13105-021-00789-x
DO - 10.1007/s13105-021-00789-x
M3 - Article
C2 - 33587254
AN - SCOPUS:85101448588
SN - 1138-7548
VL - 77
SP - 237
EP - 248
JO - Journal of Physiology and Biochemistry
JF - Journal of Physiology and Biochemistry
IS - 2
ER -