br accelerated tumor growth induced by Bach However lower
accelerated tumor growth induced by Bach1. However, lower levels of Bach1 expression were associated with increases in HO-1 levels and cell viability after exposure to an anticancer drug in acute myeloid leukemia Cell Counting Kit  and with increased cell proliferation in human umbilical vein endothelial cells , demonstrating that the eﬀect of Bach1 on cell proliferation can diﬀer profoundly among cell types. The contrasting roles of Bach1 in cell proliferation are most likely related to its role as a transcriptional repressor or as a transcriptional activator in diﬀerent cells or under diﬀerent experimental conditions.
In summary, we identified Bach1 as a key regulator that controls multiple factors essential for EOC metastasis and growth. Bach1
promotes EMT gene expression by recruiting HMGA2 in EOC cells, and HMGA2 plays a role in Bach1-induced EMT of epithelial ovarian tumor cells. On the other hand, it was demonstrated that the enhancement of ovarian tumor cell proliferation and CXCR4 expression by Bach1 does not seem to be mediated by HMGA2, suggesting diﬀerent mechanisms by which Bach1 acts on ovarian tumor progression. Thus, Bach1 may be a novel candidate target for metastatic ovarian cancer therapy.
M.D. and L.Y. conceived and designed the project. W.H. performed
Fig. 7. Bach1 enhances EOC cell growth in vivo. A. Comparison of the gross morphology of the EOC tumors developed in nude mice injected subcutaneously with stably transfected A2780 cells (WT, KO, LV-Con and LV-Bach1). BeC. Comparison of tumor volumes by serial measurement (B) and tumor weights at the time of sacrifice (C) of the tumors derived from mice implanted with stably transfected A2780 cells. n = 6. ##P < 0.01 vs LV-con, **P < 0.01 vs WT. ANOVA with post hoc test. D. IHC staining for Bach1 and Ki67. Higher expression of Bach1 in xenograft tumors was associated with an increased number of Ki67-positive cells. Scale bar, 50 μm t-test. E-F. Comparison by western blotting of the levels of p-AKT and Cyclin D1 in xenograft tumors. Tumors from Bach1-overexpressing cells exhibited an increase in p-AKT and Cyclin D1 (E), whereas tumors from Bach1-KO cells showed a reduction in the expression of these proteins (F). ##P < 0.01 vs LV-con, **P < 0.01 vs WT. t-test.
most experiments and analyzed the results. Y.Z. performed the IHC experiments and data analysis. Y.Z. and C.N. assisted with and repeated some of the experiments. J.G., N.C., and Y.W. performed the western blot experiments. W.X., J.L. and M.J. performed the ChIP-qPCR ex-periments. M.D. and X.Z. supervised the whole study and wrote the manuscript.
Declarations of interest
Conflict of interest disclosure
The authors declare no potential conflicts of interest.
We thank Dr. Mo Chen and Dr. Chen Chen (Obstetrics & Gynecology Hospital, Fudan University) for the histological analysis.
Appendix A. Supplementary data
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Buforin IIb induces androgen-independent prostate cancer cells apoptosis though p53 pathway in vitro
Yangyang Han, Ming Lu, Jinsong Zhou∗
Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, 710061, PR China
Prostate cancer cells
Prostate cancer (PCa) is one of the most common male cancer types, androgen-independent prostate cancer possesses poor prognosis. Buforin IIb, an attractive antibacterial peptide derived from histone H2A, showed selective cytotoxicity against most cancer cell lines. However, the molecular mechanism of buforin IIb on prostate cancer cell has still not been determined. In this study, we found buforin IIb significantly inhibited the prostate cancer cells proliferation, Furthermore, buforin IIb–induced cell apoptosis through downregulation of pro-caspase 3/8/9, poly (ADP-ribose) polymerase PARP and anti-apoptotic Bcl-2 and upregulation of pro-apoptotic Bax. In addition, buforin IIb increased the expression of tumor suppressor p53 and its target genes - p21, fas, noxa and puma. The cytotoxicity of buforin IIb on PC-3 and Du-145 cells is decreased by p53 knock-down. In conclusion, our results indicated that buforin IIb induced PC-3 and Du-145 cell apoptosis and could be considered as a potential drug for prostate cancer.