Abstract

s, 5th AOS and 9th Annual Conference of OOTR, 2013 / European Journal of Cancer 49S1 (2013) S1−S22 S15 Discussion. Polz expression can be used as the predictor for poor prognosis, which might be caused by the potential chemoradiation resistance of the cervical cancer patients. The mechanism deserves further exploration. Funding. This study was supported by Science Foundation for Young Scholars of Fudan University. The authors declared no conflicts of interest. AOSP25 EXPRESSION OF SURVIVIN, FAS, CYCLIN E, AND CASPASE-3 IN APOPTOTIC BREAST CANCER CELLS INDUCED BY ELECTROCHEMICAL THERAPY B. Zhoua, C. Weib, Z. Zhangb, T. Yangb, S. Yua, J. Yua, W. Looc *, L. Chowc, A. Yipc. aNingxia People’s Hospital, Yinchuan, China, bNingxia Medical University, Yinchuan, China, cOrganisation for Oncology and Translational Research and UNIMED Medical Institute, Hong Kong Introduction. Electrochemical therapy (EChT) in malignant tumours had been identified as a possible adjunctive treatment for cancers. However, the mechanism of action remains largely unknown. In this study, we explored further the mechanisms of EChT on breast cancer cell line in vitro by detecting cell growth, cell cycle changes, cell apoptosis, and protein expression of survivin, Fas, cyclin E, and caspase-3. Methods.Humanbreast cancer cellswere treated by EChTwith different levels of electricity at 0C (control), 3C, 5C, 10C, and 20C. Cell inhibition, cell cycle distribution, and cell apoptosis were analysed by MMT and flow cytometry analysis. The expression of survivin, Fas, cyclin E, and caspase-3 in breast cancer cells was analysed with western blot. Results.The cell inhibitory rate and necrosis were significantly increased in breast cancer cells after EChT treatment compared with control (p<0.05). The apoptosis ratio within 3C, 5C, and 10C was increased obviously in order. The proportion of G0/G1 phase was higher than that in control group (p<0.05). The expression levels of survivin, cyclin E, and caspase-3 protein in the treatment group were decreased, but the expression of Fas protein was increased with higher power of EChT treatment. Discussion. The study showed that EChT could inhibit breast cancer cell growth by regulating apoptotic pathway proteins such as survivin, Fas, and cyclin E, and arresting the cell cycle at G0/G1 phase. Considering the change in expression of the regulatory proteins and strong apoptotic effect of EChT in breast cancer cells, further investigation is warranted to explore its possible treatment strategy in breast cancer. Funding. This study was supported by Natural Science grant of Ningxia, China (NZ009164). The authors declared no conflicts of interest. AOSP26 EFFECT OF RAT HYPERPLASIA SUPPRESSOR GENE ON GLIOMA IN VIVO AND IN VITRO P. Gaoa, Y. Zoua, Z. Wangc, W. Haod, H. Guoa, B. Zhanga, W. Zhaob, B. Shena *. aThe General Hospital of Ningxia Medical University, Yinchuan, China, bNingxia Medical University, Yinchuan, China, cThe Zhengzhou No. 7 People’s Hospital, Zhengzhou, China, dThe Affiliated Hospital of Yanan University,

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