Investigating the effect of visfatin on ERalpha phosphorylation (Ser118 and Ser167) and ERE-dependent transcriptional activity
| Autor: | Zangooei, Mohammad, Nourbakhsh, Mitra, Ghahremani, Mohammad Hossein, Meshkani, Reza, Khedri, Azam, Shadboorestan, Amir, Shokri Afra, Hajar, Shahmohamadnejad, Shiva, Mirmiranpour, Hossein, Khaghani, Shahnaz |
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| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Serine 167 phosphorylation Visfatin 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Breast cancer Serine 118 phosphorylation 030220 oncology & carcinogenesis Estrogen receptor Original Article hormones hormone substitutes and hormone antagonists |
| Zdroj: | EXCLI Journal |
| ISSN: | 1611-2156 |
| Popis: | Obesity is associated with higher postmenopausal breast cancer incidence. Visfatin level alteration is one of the mechanisms by which obesity promotes cancer. Ligand-independent activation of estrogen receptor alpha (ERα) is also associated with carcinogenesis. The activity of ERα is modulated through phosphorylation on multiple sites by a number of protein kinases. Here we investigated the effect of visfatin as a novel adipocytokine on the phosphorylation and activity of ERα in MCF-7 breast cancer cells. We showed that exogenous administration of visfatin significantly increased the phosphorylation of ERα at serine 118 (Ser118) and 167 (Ser167) residues. Visfatin-induced Ser118 phosphorylation was diminished after treatment of cells with U0126 (MEK1/2 inhibitor). Furthermore, our results showed that visfatin-induced Ser167 phosphorylation is mediated through both MAPK and PI3K/Akt signaling pathways. Inhibition of the enzymatic activity of visfatin by FK866 had no effect on phosphorylation of ERα. We also showed that visfatin enhanced the estrogen response element (ERE)-dependent activity of ER in the presence of 17-β estradiol (E2). Additional study on T47D cells showed that visfatin also increased Ser118 and Ser167 phosphorylation of ERα and enhanced ERE-dependent activity in the presence of E2 in these cells. EXCLI Journal; 17:Doc516; ISSN 1611-2156 |
| Databáze: | OpenAIRE |
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