Molecular mechanisms of action in TSH-mediated regulation of thyroid cancer cells. Role of PKC

ROSEMBLIT C; DIAZ FLAQUE MARIA MC; DÍAZ ALBUJA JA; BARREIRO ARCOS ML; CAYROL F; STERLE HA; DEBERNARDI MM; KLECHA AJ; CREMASCHI GA

Congreso; Reunión Anual SAIC; 2018

The incidence of thyroid cancer has increased significantly within last decades in Argentina as in the rest of the world. Thyroid stimulating hormone (TSH) controls thyroid function by binding to TSH receptor (TSHR) coupled to G protein. TSH hyperactivation could be involved in thyroid diseases and cancer. PKC, a serine/threonine protein kinase, has been widely implicated in malignant transformation, cell survival, motility and invasion. Classical and novel PKC are activated by PLC activation vía tyrosine kinases and G protein-coupled receptors. Numerous studies established that PKC is overexpressed in human cancer and its expression correlates with tumor aggressiveness in prostate, lung and breast cancer. However, the role of PKC in thyroid cancer remains poorly studied. We here addressed the potential role of PKC in TSHR transduction pathways involved in cellular proliferation and tumorigenesis. Analysis of PKC expression in human thyroid cancer cell lines (2 papilar, 1 follicular and 3 anaplastic) revealed high protein and mRNA levels relative to 2 ?normal? immortalized cell lines. Treatment of thyroid cancer cells with TSH induced an increase in cellular proliferation compared to untreated cells (Ct) (p