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1. Inhibition of Akt phosphorylation attenuates resistance to TNF-α cytotoxic effects in MCF-7 cells, but not in their doxorubicin resistant derivatives

Author

Morteza Ghandadi, Atieh Mohammadi, Javad Behravan, Khalil Abnous, Negin Haj-Ali, Melika Ehtesham Gharaee, and Fatemeh Mosaffa

Subjects
Akt, Breast carcinoma, Multidrug resistance, Protein kinase B, Tumor necrosis factor-alpha, Medicine
Abstract

Objective(s): Acquisition of TNF-α resistance plays role in the onset and growth of malignant tumors. Previous studies have demonstrated that MCF-7 cell line and its doxorubicin resistant variant MCF-7/Adr are resistant against the cytotoxic effects of TNF-α. In this study, we investigated the role of Akt activation in resistance of MCF-7 and MCF-7/Adr against TNF-α cytotoxicity. Materials and Methods: The role of Akt activation in TNF-α cytotoxicity was investigated by MTT cell viability assay following treatment of the cells with the chemical inhibitor of Akt activation with or without TNF-α treatment. Phosphorylation of Akt at Ser473 before and after 72 hr TNF-α treatment was also determined by western blot. Results: TNF-α treatment led to enhancement of Akt Ser473 phosphorylation. Treatment of MCF-7 cells with TNF-α along with Akt-inhibitor agent, tricribine, attenuated Akt Ser473 phosphorylation and sensitized these cells to the cytotoxic effects of TNF-α in a dose and time dependent manner while tricribine treatment did not cause any significant cytotoxicity in MCF-7/Adr cells alone or in combination with TNF-α. Conclusion: These results demonstrate that Akt phosphorylation plays pivotal role in the resistance of MCF-7 cells against TNF-α-induced cytotoxicity while it might play no significant role in the resistance of MCF-7/Adr cells against TNF-α.

Published
2016
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2. TNF-α exerts higher cytotoxic effect on MCF-7 multidrug resistant derivative, role of Akt activation

Author

Morteza Ghandadi, Javad Behravan, Negin Haj-Ali, Khalil Abnous, Fatemeh Mosaffa, Melika Ehtesham Gharaee, and Atieh Mohammadi

Subjects
Cancer Research, Cell Survival, medicine.medical_treatment, Antineoplastic Agents, Biology, medicine, Cytotoxic T cell, Humans, Phosphorylation, skin and connective tissue diseases, Cytotoxicity, Protein kinase B, PI3K/AKT/mTOR pathway, Tumor Necrosis Factor-alpha, General Medicine, Molecular biology, Drug Resistance, Multiple, Cytokine, Oncology, MCF-7, Drug Resistance, Neoplasm, MCF-7 Cells, Tumor necrosis factor alpha, Ribonucleosides, Mitoxantrone, Phosphatidylinositol 3-Kinase, Proto-Oncogene Proteins c-akt, Signal Transduction
Abstract

Background TNF-α is a pleiotropic cytokine which activates different downstream signaling pathways leading cells to death or survival. In some in vitro examinations, TNF-α treatment demonstrated higher cytotoxic effects on MDR cancer cell lines compared to their parental counterparts. Objective This study investigated effects of TNF-α in MCF-7 and its mitoxantrone (MX) resistant variant of breast cancer cell line, MCF-7/MX. Moreover, the role of Akt phosphorylation in TNF-α effect was also investigated. Methods Akt phosphorylation was evaluated using Western blotting and TNF-α effect was examined using cytotoxicity assay following treatment of the cells with TNF-α . Results TNF-α treatment exerted higher cytotoxic effects on MCF-7/MX compared to MCF-7 cells. Akt phosphorylation was enhanced following TNF-α treatment in MCF-7 cells while it did not change in MCF-7/MX cells. TNF-α treatment along with inhibition of Akt phosphorylation by a chemical inhibitor triciribine, sensitized MCF-7 cells to cytotoxic effects of TNF-α. Moreover, activation of PI3K/Akt pathway by activator peptide 740 Y-P in MCF-7/MX cells enhanced resistance against TNF-α cytotoxicity. Conclusion Alteration in Akt phosphorylation is involved in the resistance of MCF-7 cells and sensitivity of MCF-7/MX cells to TNF-α -induced cytotoxicity, respectively.

Published
2015

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