Gynura procumbens Prevents Chemoresistance through Inhibition MDR1 Expression on MCF-7 Breast Cancer Cell Line and Sensitizes the Cells to Doxorubicin

• Main Authors: Nunuk Aries Nurulita, Edy Meiyanto, Eishou Matsuda, Masashi Kawaichi
• Format: Article
• Language: English
• Published: Universitas Gadjah Mada, Yogyakarta 2012-06-01
• Series: Indonesian Journal of Biotechnology
• Subjects: Gynura procumbens; Chemoresistance; MDR1; MCF-7; MCF-7/Dox
• Online Access: https://jurnal.ugm.ac.id/ijbiotech/article/view/15998

The long-term exposure of doxorubicin (Dox) causes enhancement in MDR1 expression that leads to breast cancer cell resistance. This protein become a serious problem in cancer treatment and also well-known as negative prognostic factor in breast cancer malignancies. The new approach using natural chemopreventive substance was developed to inhibit this resistance progress. This study was aimed to investigate whether ethyl acetate fraction of Gynura procumnens (FEG) can prevent chemoresistance through suppressing the MDR1 protein expression. MCF-7 cell was used as chemoresistance cell model. The MCF-7 cells were maintained with 100 nM Dox-contained medium for five weeks. The chemoprevention effect of FEG was investigated by treated MCF-7/Dox with sub-toxic concentration of FEG. The cytotoxic properties of MCF-7 cells were determined using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) assay. Immunofluorescence and western blotting analysis was performed to detect the MDR1 expression. MCF-7/Dox cells need higher concentration for inhibiting cell growth, were compared with MCF-7, shown by IC50value. The MDR1 protein level elevated after Dox exposure in time dependent manner. The FEG treatment decreased MDR-1 protein level with dose dependent manner. FEG in combination with DOX potentiates the DOX effect on breast cancer cell growth inhibition. The FEG prevents the chemoresistance development in breast cancer cell line, MCF-7 induced by Dox through inhibiting MDR1 expression. The additional of FEG enhances Dox effect on cell death induction. Thus, FEG could be developed as co-chemotherapy agent for reverse multidrug resistance