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Ji Shufeng, Yang Huafeng, Wu Aiguo. Progesterone Receptor Membrane Component-1 Regulates Proliferation and Drug Sensitivity of Breast Cancer Cells[J]. Cancer Research on Prevention and Treatment, 2012, 39(02): 123-126. DOI: 10.3971/j.issn.1000-8578.2012.02.001
Citation: Ji Shufeng, Yang Huafeng, Wu Aiguo. Progesterone Receptor Membrane Component-1 Regulates Proliferation and Drug Sensitivity of Breast Cancer Cells[J]. Cancer Research on Prevention and Treatment, 2012, 39(02): 123-126. DOI: 10.3971/j.issn.1000-8578.2012.02.001

Progesterone Receptor Membrane Component-1 Regulates Proliferation and Drug Sensitivity of Breast Cancer Cells

  • Objective To study on the roles of progesterone receptor membrane component-1(PGRMC1) to inhibit proliferation and improve drug sensitivity in breast cancer cell. MethodssiRNA targeting PGRMC1 was designed and chemically synthesized,and then transfected into high invasive breast cancer cell line MDA-MB-231 and low invasive cell line MCF-7 by lipofectin2000.The mRNA and protein of PGRMC1 were detected by QRT-PCR and Western blot method respectively.The siRNA-GFP was used as positive control, and 0.9% saline as blank control.The drug sensitivity of DTX was detected by CCK8 method before and after transfection siRNA- PGRMC1.Breast cancer cell lines were treated by 50% of IC50 DTX,and detected cell cycle,apoptotic ratio and ROS level after stained by PI,annexin V and DCFH-DA respectively by FCM.After stained by JC-1,the membrane potential of mitochondrion was identified by immunofluorescence method. Results siRNA was able to significantly inhibit more than 70% PGRMC1 expression of mRNA and protein in both high and low invasive breast cell lines.The proliferation of cancer cells was decreased and drug sensitivity was increased through PGRMC1 inhibiting.After inhibition of PGRMC1,the cell was arrested on stage G2.Comparing with control group,the higher apoptosis ratio and ROS level and lower membrane potential were observed in treatment group. Conclusion PGRMC1 played an important role in regulating the viability and drug resistance of breast cancer.
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