scholarly journals 4-Methylthio-3-butenyl isothiocyanate (MTBITC) induced apoptotic cell death and G2/M cell cycle arrest via ROS production in human esophageal epithelial cancer cells

2019 ◽  
Vol 44 (2) ◽  
pp. 73-81 ◽  
Author(s):  
Tadashi Hirata ◽  
Young-Man Cho ◽  
Isamu Suzuki ◽  
Takeshi Toyoda ◽  
Jun-ichi Akagi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Ros Production ◽  
Epithelial Cancer ◽  
M Cell ◽  
Cycle Arrest

Synthetic polysulfane derivatives induce cell cycle arrest and apoptotic cell death in human hematopoietic cancer cells

2014 ◽  
Vol 64 ◽  
pp. 249-257 ◽  
Author(s):  
Brigitte Czepukojc ◽  
Anne-Kathrin Baltes ◽  
Claudia Cerella ◽  
Mareike Kelkel ◽  
Uma M. Viswanathan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Induce Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Hematopoietic Cancer

scholarly journals RUNX Family Participates in the Regulation of p53-Dependent DNA Damage Response

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Toshinori Ozaki ◽  
Akira Nakagawara ◽  
Hiroki Nagase
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Dna Damage Response ◽  
Apoptotic Cell ◽  
Genetic Alterations ◽  
Apoptotic Cell Death ◽  
Cycle Arrest ◽  
Damage Response

A proper DNA damage response (DDR), which monitors and maintains the genomic integrity, has been considered to be a critical barrier against genetic alterations to prevent tumor initiation and progression. The representative tumor suppressor p53 plays an important role in the regulation of DNA damage response. When cells receive DNA damage, p53 is quickly activated and induces cell cycle arrest and/or apoptotic cell death through transactivating its target genes implicated in the promotion of cell cycle arrest and/or apoptotic cell death such asp21WAF1,BAX, andPUMA. Accumulating evidence strongly suggests that DNA damage-mediated activation as well as induction of p53 is regulated by posttranslational modifications and also by protein-protein interaction. Loss of p53 activity confers growth advantage and ensures survival in cancer cells by inhibiting apoptotic response required for tumor suppression. RUNX family, which is composed of RUNX1, RUNX2, and RUNX3, is a sequence-specific transcription factor and is closely involved in a variety of cellular processes including development, differentiation, and/or tumorigenesis. In this review, we describe a background of p53 and a functional collaboration between p53 and RUNX family in response to DNA damage.

Propylparaben induces apoptotic cell death in human placental BeWo cells via cell cycle arrest and enhanced caspase-3 activity

2019 ◽  
Vol 16 (1) ◽  
pp. 83-92 ◽  
Author(s):  
Mi Jin Kim ◽  
Chul-Hong Kim ◽  
Mi-Jin An ◽  
Ju-Hyun Lee ◽  
Geun-Seup Shin ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Bewo Cells ◽  
Cycle Arrest

scholarly journals p53: The Attractive Tumor Suppressor in the Cancer Research Field

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Toshinori Ozaki ◽  
Akira Nakagawara
Keyword(s):  
Cell Cycle ◽  
Cancer Research ◽  
Cell Death ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Apoptotic Cell ◽  
Genetic Alterations ◽  
Research Field ◽  
Apoptotic Cell Death ◽  
Cycle Arrest

p53 is one of the most studied tumor suppressors in the cancer research field. Of note, over 50% of human tumors carry loss of function mutations, and thus p53 has been considered to be a classical Knudson-type tumor suppressor. From the functional point of view, p53 is a nuclear transcription factor to transactivate a variety of its target genes implicated in the induction of cell cycle arrest, DNA repair, and apoptotic cell death. In response to cellular stresses such as DNA damage, p53 is activated and promotes cell cycle arrest followed by the replacement of DNA lesions and/or apoptotic cell death. Therefore, p53 is able to maintain the genomic integrity to prevent the accumulation of genetic alterations, and thus stands at a crossroad between cell survival and cell death. In this paper, we describe a variety of molecular mechanisms behind the regulation of p53.

scholarly journals Nomad Jellyfish Rhopilema nomadica Venom Induces Apoptotic Cell Death and Cell Cycle Arrest in Human Hepatocellular Carcinoma HepG2 Cells

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5185
Author(s):  
Mohamed M. Tawfik ◽  
Nourhan Eissa ◽  
Fayez Althobaiti ◽  
Eman Fayad ◽  
Ali H. Abu Almaaty
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Dna Fragmentation ◽  
Hepg2 Cells ◽  
Apoptotic Cell ◽  
Cycle Arrest ◽  
Jellyfish Venom

Jellyfish venom is a rich source of bioactive proteins and peptides with various biological activities including antioxidant, antimicrobial and antitumor effects. However, the anti-proliferative activity of the crude extract of Rhopilema nomadica jellyfish venom has not been examined yet. The present study aimed at the investigation of the in vitro effect of R. nomadica venom on liver cancer cells (HepG2), breast cancer cells (MDA-MB231), human normal fibroblast (HFB4), and human normal lung cells (WI-38) proliferation by using MTT assay. The apoptotic cell death in HepG2 cells was investigated using Annexin V-FITC/PI double staining-based flow cytometry analysis, western blot analysis, and DNA fragmentation assays. R. nomadica venom displayed significant dose-dependent cytotoxicity on HepG2 cells after 48 h of treatment with IC50 value of 50 μg/mL and higher toxicity (3:5-fold change) against MDA-MB231, HFB4, and WI-38 cells. R. nomadica venom showed a prominent increase of apoptosis as revealed by cell cycle arrest at G2/M phase, upregulation of p53, BAX, and caspase-3 proteins, and the down-regulation of anti-apoptotic Bcl-2 protein and DNA fragmentation. These findings suggest that R. nomadica venom induces apoptosis in hepatocellular carcinoma cells. To the best of the authors’ knowledge, this is the first scientific evidence demonstrating the induction of apoptosis and cell cycle arrest of R. nomadica jellyfish venom.

scholarly journals p73-Binding Partners and Their Functional Significance

2010 ◽  
Vol 2010 ◽  
pp. 1-12 ◽  
Author(s):  
Toshinori Ozaki ◽  
Natsumi Kubo ◽  
Akira Nakagawara
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Protein Interactions ◽  
Functional Significance ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Protein Protein Interactions ◽  
Dna Damages ◽  
Cycle Arrest

p73 is one of the tumor-suppressor p53 family of nuclear transcription factor. As expected from the structural similarity between p53 and p73, p73 has a tumor-suppressive function. However, p73 was rarely mutated in human primary tumors. Under normal physiological conditions, p73 is kept at an extremely low level to allow cells normal growth. In response to a certain subset of DNA damages, p73 is induced dramatically and transactivates an overlapping set of p53-target genes implicated in the promotion of cell cycle arrest and/or apoptotic cell death. Cells undergo cell cycle arrest and/or apoptotic cell death depending on the type and strength of DNA damages. p73 is regulated largely through the posttranslational modifications such as phosphorylation and acetylation. These chemical modifications are tightly linked to direct protein-protein interactions. In the present paper, the authors describe the functional significance of the protein-protein interactions in the regulation of proapoptotic p73.

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