A Novel All-trans Retinoid Acid Derivative Induces Apoptosis in MDA-MB-231 Breast Cancer Cells

Wang, Bei; Yan, Yun-Wen; Zhou, Qing; Gui, Shu-Yu; Chen, Fei-Hu; Wang, Yuan

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자료유형: 학술저널

저자정보: Wang, Bei (Department of Pathology and Pathophysiology, medical School, Southeast University) Yan, Yun-Wen (Laboratory of Molecular Biology, Dept of Biochemistry, Anhui Medical University) Zhou, Qing (Laboratory of Molecular Biology, Dept of Biochemistry, Anhui Medical University) Gui, Shu-Yu (Key Laboratory of Gene Resource Utilization for Severe Disease of Anhui Province, Anhui Medical University) Chen, Fei-Hu (School of Pharmacy, Anhui Medical University) Wang, Yuan (Laboratory of Molecular Biology, Dept of Biochemistry, Anhui Medical University)

저널정보: 아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제15권 제24호

발행연도: 2014.1

수록면: 10,819 - 10,824 (6page)

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Aims: To explore the effect and probable mechanism of a synthetic retinoid 4-amino-2-tri-fluoromethylphenyl ester (ATPR) on apoptosis of MDA-MB-231 breast cancer cells. Materials and Methods: MTT assays were performed to measure the proliferation of MDA-MB-231 cells treated with different concentrations of all-trans retinoic acid (ATRA) and ATPR. Morphologic changes were observed by microscopy. The apoptosis rates and cell cycling of MDA-MB-231 cells treated with ATRA or ATPR were assessed using flow cytometry analysis. Expression of retinoic acid receptor and phosphorylation of ERK, JNK, p38 proteins were detected by Western blotting. Results: Treatment of the cells with the addition of $15{\mu}mol/L$ ATPR for 48 h clearly demonstrated reduced cell numbers and deformed cells, whereas no changes in the number and morphology were observed after treatment with ATRA. The apoptosis rate was 33.2% after breast cancer MDA-MB-231 cells were treated by ATPR ($15{\mu}mol/L$) whereas ATRA ($15{\mu}mol/L$) had no apoptotic effect. ATPR inhibited the phosphorylation of ERK, JNK, and p38 while ATRA had no significant effect. ATPR inhibited the expression of BiP and increased the expression of Chop at the protein level compared with control groups, ATRA and ATPR both decreased the protein expression of $RXR{\alpha}$, ATPR reduced the protein expression of $RAR{\beta}$ and $RXR{\beta}$ while ATRA did not decrease $RAR{\beta}$ or $RXR{\beta}$. Conclusions: ATPR could induce apoptosis of breast cancer MDA-MB-231 cells, possible mechanisms being binding to $RAR{\beta}/RXR{\beta}$ heterodimers, then activation of ER stress involving the MAPK pathway.

#Breast cancer #ATPR #ER stress #MAPK pathway #retinoic acid receptor

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Wang, Bei

소속기관 Key Laboratory of Preclinical Study for New Drugs of Gansu Province, School of Basic Medical Science