Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster presentation 1

1112 - Role of cytoplasmic Bcl-xl in interplay apoptosis and autophagy in combination of genistein with radiation-induced cell death


19 Dec 2015


Poster presentation 1


Zhimin Zhang


Annals of Oncology (2015) 26 (suppl_9): 1-7. 10.1093/annonc/mdv517


Z.M. Zhang

Author affiliations

  • Medicine Oncology, Daping Hospital of Chongqing, Yuzhong - Chongqing/CN


Abstract 1112


Genistein (GEN) has been previously reported to induce apoptosis through changing bcl-x(l) expression and autophagy on cancer cells, the mechanism of which remains unclear. In this study we investigated the effect of the differentiation of Bcl-xl distribution induced by GEN on cell death by examining the activation of autophagy and apoptosis in A549 cell.


CCK-8 assay indicated the resistance to radiation, the subcellular distribution of bcl-xl was observed by Immunofluorescence, cell DNA damage were analyzed by neutral Comet assays the interaction of Beclin1/Bcl-xl was detected by Co-Immunoprecipitation, western blot measured the expression of cell autophagy and apoptosis related protein, flow cytometry analyzed cell autophagy and apoptosis level, The expression of cytoplasmic Bcl-xl protein was analyzed using immunohistochemistry in NSCLC patient tumor tissue.


We initially showed that the differentiation of cytoplasmic Bcl-xl in GEN A549 cells. By examining both cytoplasmic and nuclear of Bcl-xl in H1975, A549 and 293T cell, we found that the Bcl-xl cytoplasmic expression and cell death caused by radiation were negatively related. Furthermore, the expression of Bcl-xl cytoplasmic immunohistochemistry levels in tumor tissue, scored for intensity as 0, 1 + , 2 + , 3 + , were 26.7, 43.3, 26.7, and 3.3% in human non-small lung cancer, respectively, clearly showing the high expression of Bcl-xl cytoplasmic have a low overall response rate (ORR) of radiotherapy. Interestingly, we found that the treatment of combining GEN with radiation inhibited the cytoplasmic Bcl-xl and increased the Autophagy associated cell death by promoting the dissociation of Bcl-xl/beclin1 complex. In addition, the combinatorial treatment significantly inhibited the DNA damage repair and contributed to oligomerization of Bax and activation of cleaved caspase-3 and PARP.


Our data suggest that the autophagy and apoptosis promote cell death induced by radiation when the distribution of cytoplasmic Bcl-xl is inhibited by GEN. Based on this evidence, we hereby report that crosstalk between apoptosis and autophagy by Inhibition of cytoplasmic Bcl-xl will support the application of using GEN on radiation therapy.

Clinical trial identification


All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings