PI3K/AKT INHIBITION AND DOWN-REGULATION OF BCRP RE-SENSITIZE MCF7 BREAST CANCER CELL LINE TO MITOXANTRONE CHEMOTHERAPY

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KOMEILI MOVAHHED TAHEREH; FOULADDEL SHAMILEH; BARZEGAR ELMIRA; ATASHPOUR SHEKOUFEH; GHAHREMANI MOHAMMAD HOSEIN; OSTAD SEYED NASSER; MADJD ZAHRA; AZIZI EBRAHIM

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Journal: Iranian Journal of Basic Medical Sciences Year:2015 | Volume:18 | Issue:5 Page(s): 472-477

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Title

PI3K/AKT INHIBITION AND DOWN-REGULATION OF BCRP RE-SENSITIZE MCF7 BREAST CANCER CELL LINE TO MITOXANTRONE CHEMOTHERAPY

Author(s)

Keywords

BREAST CANCER

BCRP

COMBINATION THERAPY

MITOXANTRONE

PI3K/AKT

SIRNA

Abstract

Objective(s): Multidrug resistance (MDR) of cancer cells is a major obstacle to successful chemotherapy. Overexpression of BREAST CANCER resistance protein (BCRP) is one of the major causes of MDR. In addition, it has been shown that PI3K/AKT signaling pathway involves in drug resistance. Therefore, we evaluated the effects of novel approaches including SIRNA directed against BCRP and targeted therapy against PI3K/AKT signaling pathway using LY294002 (LY) to re-sensitize BREAST CANCER MCF7 cell line to MITOXANTRONE (MTX) chemotherapy.Materials and Methods: Anticancer effects of MTX, SIRNA, and LY alone and in combination were evaluated in MCF7 cells using MTT cytotoxicity assay and flow cytometry analysis of cell cycle distribution and apoptosis induction.Results: MTT and apoptosis assays showed that both MTX and LY inhibited cell proliferation and induced apoptosis in MCF7 cells. Results indicated that inhibition of BCRP by SIRNA or PI3K/AKT signaling pathway by LY significantly increased sensitivity of MCF7 cells to antiproliferation and apoptosis induction of MTX. Furthermore, MTX showed G2/M arrest, whereas LY induced G0/G1 arrest in cell cycle distribution of MCF7 cells. Combination of SIRNA or LY with MTX chemotherapy significantly increased accumulation of MCF7 cells in the G2/M phase of cell cycle.Conclusion: Combination of MTX chemotherapy with BCRP SIRNA and PI3K/AKT inhibition can overcome MDR in BREAST CANCER cells. This study furthermore suggests that novel therapeutic approaches are needed to enhance anticancer effects of available drugs in BREAST CANCER.

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APA: Copy

KOMEILI MOVAHHED, TAHEREH, FOULADDEL, SHAMILEH, BARZEGAR, ELMIRA, ATASHPOUR, SHEKOUFEH, GHAHREMANI, MOHAMMAD HOSEIN, OSTAD, SEYED NASSER, MADJD, ZAHRA, & AZIZI, EBRAHIM. (2015). PI3K/AKT INHIBITION AND DOWN-REGULATION OF BCRP RE-SENSITIZE MCF7 BREAST CANCER CELL LINE TO MITOXANTRONE CHEMOTHERAPY. IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES, 18(5), 472-477. SID. https://sid.ir/paper/677863/en

Vancouver: Copy

KOMEILI MOVAHHED TAHEREH, FOULADDEL SHAMILEH, BARZEGAR ELMIRA, ATASHPOUR SHEKOUFEH, GHAHREMANI MOHAMMAD HOSEIN, OSTAD SEYED NASSER, MADJD ZAHRA, AZIZI EBRAHIM. PI3K/AKT INHIBITION AND DOWN-REGULATION OF BCRP RE-SENSITIZE MCF7 BREAST CANCER CELL LINE TO MITOXANTRONE CHEMOTHERAPY. IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES[Internet]. 2015;18(5):472-477. Available from: https://sid.ir/paper/677863/en

IEEE: Copy

TAHEREH KOMEILI MOVAHHED, SHAMILEH FOULADDEL, ELMIRA BARZEGAR, SHEKOUFEH ATASHPOUR, MOHAMMAD HOSEIN GHAHREMANI, SEYED NASSER OSTAD, ZAHRA MADJD, and EBRAHIM AZIZI, “PI3K/AKT INHIBITION AND DOWN-REGULATION OF BCRP RE-SENSITIZE MCF7 BREAST CANCER CELL LINE TO MITOXANTRONE CHEMOTHERAPY,” IRANIAN JOURNAL OF BASIC MEDICAL SCIENCES, vol. 18, no. 5, pp. 472–477, 2015, [Online]. Available: https://sid.ir/paper/677863/en

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