The aim of the present study is to investigate the effect of genistein on human neuroblastoma SK-N-MC cells. MTT proliferation assay, LDH cytotoxicity assay, flow cytometric analysis, real-time quantitative RT-PCR and western blotting were used to investigate the effect of genistein on cell survival, cellular toxicity, cell cycle progression, and mRNA and protein alterations of selected DNA damage-, cell cycle- and apoptosis-related genes in SK-N-MC cells. Genistein suppressed cell proliferation, increased LDH release and modulated cell cycle distribution through accumulation of cells at G2/M- and S-phase and sub-G0 (cell death) with a concurrent decrease of cells at G0/G1 phase. Genistein increased the MDC1 (Mediator of DNA damage Checkpoint protein 1), p53, p21(waf1/cip1), Cdc2 and Bax mRNA levels in a dose-dependent manner. However, PLK1 (Polo-Like Kinase 1) and Cyclin B1 mRNAs were down-regulated after genistein treatment. Furthermore, Genistein did not alter Chk2 (Checkpoint Kinase 2), Bcl-2 and Cdc25C mRNA levels. On western blotting analyses; genistein increased the protein level of MDC1, p53, p21(waf1/cip1), and Bax in a dose-dependent manner. Genistein also increased the phosphorylation of Chk2 and Cdc25C at Thr-68 and Ser-216, respectively. In addition, consistently with PLK1 down-regulation, the phosphorylation of Cdc25C at Ser-198 was markedly decreased after genistein treatment. Additionally, Chk2, Cdc25C, Cyclin B1, p-Cyclin B1 (Ser-147), and Cdc2 as well as Bcl-2 proteins were down-regulated after genistein treatment. Altogether, these results suggest for the first time the involvement of MDC1 up-regulation after genistein treatment in DNA damage-induced Chk2 activation- and PLK1 down-regulation-mediated apoptosis and cell cycle checkpoint pathways.

2’-Benzoyloxycinnamaldehyde (BCA) is a promising anticancer candidate against several types of cancers, including breast cancer. DJ-1 has been found to act as an oncogene, protecting cells against oxidative stress. A previous study showed that BCA-inducing antiproliferation was associated with continuous decrease in DJ-1 expression in MDA-MB-435 breast cancer cells. In this study, we found that this DJ-1 decrease after BCA treatment is associated with increased reactive oxygen species (ROS) release, and depletion of glutathione (GSH), and γ-glutamylcysteine synthetase (γ-GCS). The tumor suppressor Pten protein is known to be a downstream target for DJ-1. Therefore, Pten expression was investigated after BCA treatment and DJ-1 siRNA transfection. DJ-1 knockdown with DJ-1 siRNA transfection markedly increased Pten expression. However, unexpectedly BCA-inducing DJ-1 downregulation is associated with decreased Pten protein expression. Altogether, these data suggest that BCA downregulates Pten protein expression in MDA-MB-435 cells independent of DJ-1.

Hesperidin, a flavonoid found mainly in citrus, was reported to inhibit growth and proliferation of several cancers, including colon cancer cells. However, the question does p53 tumor suppressor protein is required for the effect of hesperidin is not yet clarified. In the present study, the effect of hesperidin on p53-expressing (HCT116 p53+/+) and p53-knockout (HCT116 p53-/-) human colon cancer cells was investigated. Hesperidin inhibits cell growth of both HCT116 p53+/+ and HCT116 p53-/- cells, however, it was more effective in p53-expressing cells. Hesperidin induced G1 cell cycle arrest in only HCT116 p53+/+ cells however induction of reactive oxygen species (ROS) and apoptosis was induced in both cells. Furthermore, hesperidin activates the proapoptotic (Bax) and cyclin dependent kinase inhibitor (p21) in only HCT116 p53+/+ cells. Interestingly, using p53 transcriptional inhibitor (pifithrin-a), hesperidin-inducing Bax and p21 upregulation in only HCT116 p53+/+ cells was reduced by cotreatment with pifithrin-a without inducing any changes in HCT116 p53-/- cells. Altogether; these results showed that hesperidin induced apoptosis and G1 cell cycle arrest in colon cancer cells in a p53/Bax -- dependent and -- independent, and p53/p21 - dependent manners; respectively.

Angular distributions of 16O + 16O elastic scattering at energies that range from 124 to 1120 MeV have
been analyzed in the framework of the double folding (DF) optical model. Based upon the α-cluster structure
of the 16O nucleus, two different versions of the real DF optical potential have been generated by using three
effective α-α, α-nucleon (N) and nucleon-nucleon (NN) interactions. A microscopic optical potential built upon
the M3Y effective NN interaction and the matter density distribution of the 16O nucleus has also been extracted.
The obtained real potentials, in conjunction with phenomenological squaredWoods-Saxon imaginary parts, have
successfully reproduced seven sets of elastic-scattering data. No renormalization of the real folded α-cluster
potentials is required to fit the data. The energy dependence of the extracted real and imaginary volume integrals
and total reaction cross section has also been investigated.

Angular distributions of 16O + 16O elastic scattering at energies that range from 124 to 1120 MeV have
been analyzed in the framework of the double folding (DF) optical model. Based upon the α-cluster structure
of the 16O nucleus, two different versions of the real DF optical potential have been generated by using three
effective α-α, α-nucleon (N) and nucleon-nucleon (NN) interactions. A microscopic optical potential built upon
the M3Y effective NN interaction and the matter density distribution of the 16O nucleus has also been extracted.
The obtained real potentials, in conjunction with phenomenological squaredWoods-Saxon imaginary parts, have
successfully reproduced seven sets of elastic-scattering data. No renormalization of the real folded α-cluster
potentials is required to fit the data. The energy dependence of the extracted real and imaginary volume integrals
and total reaction cross section has also been investigated.

Angular distributions of 16O + 16O elastic scattering at energies that range from 124 to 1120 MeV have
been analyzed in the framework of the double folding (DF) optical model. Based upon the α-cluster structure
of the 16O nucleus, two different versions of the real DF optical potential have been generated by using three
effective α-α, α-nucleon (N) and nucleon-nucleon (NN) interactions. A microscopic optical potential built upon
the M3Y effective NN interaction and the matter density distribution of the 16O nucleus has also been extracted.
The obtained real potentials, in conjunction with phenomenological squaredWoods-Saxon imaginary parts, have
successfully reproduced seven sets of elastic-scattering data. No renormalization of the real folded α-cluster
potentials is required to fit the data. The energy dependence of the extracted real and imaginary volume integrals
and total reaction cross section has also been investigated.

Angular distributions of 16O + 16O elastic scattering at energies that range from 124 to 1120 MeV have
been analyzed in the framework of the double folding (DF) optical model. Based upon the α-cluster structure
of the 16O nucleus, two different versions of the real DF optical potential have been generated by using three
effective α-α, α-nucleon (N) and nucleon-nucleon (NN) interactions. A microscopic optical potential built upon
the M3Y effective NN interaction and the matter density distribution of the 16O nucleus has also been extracted.
The obtained real potentials, in conjunction with phenomenological squaredWoods-Saxon imaginary parts, have
successfully reproduced seven sets of elastic-scattering data. No renormalization of the real folded α-cluster
potentials is required to fit the data. The energy dependence of the extracted real and imaginary volume integrals
and total reaction cross section has also been investigated.