The small heat shock protein B8 (HSPB8) modulates proliferation and migration of breast cancer cells
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Margherita Piccolella1, Valeria Crippa1,2, Riccardo Cristofani1, Paola Rusmini1, Mariarita Galbiati1, Maria Elena Cicardi1, Marco Meroni1, Nicola Ferri3, Federica F. Morelli4, Serena Carra4, Elio Messi1,*, Angelo Poletti1,*
1Dipartimento di Scienze Farmacologiche e Biomolecolari (DiSFeB), Centro di Eccellenza sulle Malattie Neurodegenerative, Università degli Studi di Milano, Milano, Italy
2C. Mondino National Neurological Institute, Pavia, Italy
3Dipartimento di Scienze del Farmaco, Università degli Studi di Padova, Padova, Italy
4Dipartimento di Scienze Biomediche, Metaboliche e Neuroscienze, Università di Modena e Reggio Emilia, Modena, Italy
*These authors have contributed equally to this work
Angelo Poletti, email: email@example.com
Keywords: breast cancer, HSPB8, proliferation, migration, MCF-7 cells
Received: June 30, 2016 Accepted: December 12, 2016 Published: January 02, 2017
Breast cancer (BC) is one of the major causes of cancer death in women and is closely related to hormonal dysregulation. Estrogen receptor (ER)-positive BCs are generally treated with anti hormone therapy using antiestrogens or aromatase inhibitors. However, BC cells may become resistant to endocrine therapy, a process facilitated by autophagy, which may either promote or suppress tumor expansion. The autophagy facilitator HSPB8 has been found overexpressed in some BC. Here we found that HSPB8 is highly expressed and differentially modulated by natural or synthetic selective ER modulators (SERMs), in the triple-positive hormone-sensitive BC (MCF-7) cells, but not in triple-negative MDA-MB-231 BC cells. Specific SERMs induced MCF-7 cells proliferation in a HSPB8 dependent manner whereas, did not modify MDA-MB-231 cell growth. ER expression was unaffected in HSPB8-depleted MCF-7 cells. HSPB8 over-expression did not alter the distribution of MCF-7 cells in the various phases of the cell cycle. Conversely and intriguingly, HSPB8 downregulation resulted in an increased number of cells resting in the G0/G1 phase, thus possibly reducing the ability of the cells to pass through the restriction point. In addition, HSPB8 downregulation reduced the migratory ability of MCF-7 cells. None of these modifications were observed, when another small HSP (HSPB1), also expressed in MCF-7 cells, was downregulated. In conclusion, our data suggest that HSPB8 is involved in the mechanisms that regulate cell cycle and cell migration in MCF-7 cells.
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