scholarly journals The novel mechanism of anticancer effect on gastric cancer through inducing G0/G1 cell cycle arrest and caspase-dependent apoptosis in vitro and in vivo by methionine enkephalin

2018 ◽  
Vol Volume 10 ◽  
pp. 4773-4787 ◽  
Author(s):  
Xiaonan Wang ◽  
Jing Tian ◽  
Xue Jiao ◽  
Jin Geng ◽  
Reizhe Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
The Novel ◽  
Anticancer Effect ◽  
Methionine Enkephalin ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

scholarly journals Menadione reduces CDC25B expression and promotes tumor shrinkage in gastric cancer

2020 ◽  
Vol 13 ◽  
pp. 175628481989543
Author(s):  
Amanda Braga Bona ◽  
Danielle Queiroz Calcagno ◽  
Helem Ferreira Ribeiro ◽  
José Augusto Pereira Carneiro Muniz ◽  
Giovanny Rebouças Pinto ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Specific Inhibitor ◽  
Gastric Carcinogenesis ◽  
In Vivo Experiments ◽  
Cycle Arrest

Background: Gastric cancer is one of the most incident types of cancer worldwide and presents high mortality rates and poor prognosis. MYC oncogene overexpression is a key event in gastric carcinogenesis and it is known that its protein positively regulates CDC25B expression which, in turn, plays an essential role in the cell division cycle progression. Menadione is a synthetic form of vitamin K that acts as a specific inhibitor of the CDC25 family of phosphatases. Methods: To better understand the menadione mechanism of action in gastric cancer, we evaluated its molecular and cellular effects in cell lines and in Sapajus apella, nonhuman primates from the new world which had gastric carcinogenesis induced by N-Methyl-N-nitrosourea. We tested CDC25B expression by western blot and RT-qPCR. In-vitro assays include proliferation, migration, invasion and flow cytometry to analyze cell cycle arrest. In in-vivo experiments, in addition to the expression analyses, we followed the preneoplastic lesions and the tumor progression by ultrasonography, endoscopy, biopsies, histopathology and immunohistochemistry. Results: Our tests demonstrated menadione reducing CDC25B expression in vivo and in vitro. It was able to reduce migration, invasion and proliferation rates, and induce cell cycle arrest in gastric cancer cell lines. Moreover, our in-vivo experiments demonstrated menadione inhibiting tumor development and progression. Conclusions: We suggest this compound may be an important ally of chemotherapeutics in the treatment of gastric cancer. In addition, CDC25B has proven to be an effective target for investigation and development of new therapeutic strategies for this malignancy.

DT-13 synergistically potentiates the sensitivity of gastric cancer cells to topotecan via cell cycle arrest in vitro and in vivo

2018 ◽  
Vol 818 ◽  
pp. 124-131 ◽  
Author(s):  
Hongzhi Du ◽  
Yang Liu ◽  
Xudong Chen ◽  
Xiaowen Yu ◽  
Xiaoying Hou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Cycle Arrest

Induction of G1 Cell Cycle Arrest in Human Glioma Cells by Salinomycin Through Triggering ROS-Mediated DNA Damage In Vitro and In Vivo

2016 ◽  
Vol 42 (4) ◽  
pp. 997-1005 ◽  
Author(s):  
Shi-Jun Zhao ◽  
Xian-Jun Wang ◽  
Qing-Jian Wu ◽  
Chao Liu ◽  
Da-Wei Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

Piperlongumine induces gastric cancer cell apoptosis and G2/M cell cycle arrest both in vitro and in vivo

Tumor Biology ◽  
2016 ◽  
Vol 37 (8) ◽  
pp. 10793-10804 ◽  
Author(s):  
Chaoqin Duan ◽  
Bin Zhang ◽  
Chao Deng ◽  
Yu Cao ◽  
Fan Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Gastric Cancer Cell ◽  
M Cell ◽  
Cycle Arrest

scholarly journals JAZ mediates G1 cell-cycle arrest and apoptosis by positively regulating p53 transcriptional activity

Blood ◽  
2006 ◽  
Vol 108 (13) ◽  
pp. 4136-4145 ◽  
Author(s):  
Mingli Yang ◽  
Song Wu ◽  
Xuekun Su ◽  
W. Stratford May
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Arrest ◽  
Transcriptional Activity ◽  
Myeloid Cell ◽  
Negative Regulator ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest

Abstract We previously identified JAZ as a novel zinc finger (ZF) protein by screening a murine interleukin-3 (IL-3)–dependent NFS/N1.H7 myeloid cell cDNA library. JAZ is a member of a new class of ZFPs that is evolutionarily conserved and preferentially binds to dsRNA, but its function was unknown. Now, we report that the stress of IL-3 growth factor withdrawal up-regulates JAZ expression in hematopoietic cells in association with p53 activation and induction of cell death. Biochemical analysis reveals that JAZ associates with p53 to stimulate its transcriptional activity in p53-expressing cells, but not in p53-null cells unless complemented with p53. JAZ functions to mediate G1 cell-cycle arrest followed by apoptosis in a p53-dependent mechanism that is associated with up-regulation of p21 and BAX, dephosphorylation of Rb, and repression of cyclin A. Of importance, siRNA “knockdown” of endogenous JAZ inhibits p53 transcriptional activity, decreases the G1/G0 population, and attenuates stress-induced cell death. While JAZ directly binds p53 in vitro in a mechanism requiring p53's C-terminal regulatory domain but independent of dsRNA, the dsRNA-binding ZF domains are required for JAZ's stimulatory role of p53 in vivo by dictating its nuclear localization. Thus, JAZ is a novel negative regulator of cell growth by positively regulating p53.

Bound polyphenol extracted from jujube pulp triggers mitochondria-mediated apoptosis and cell cycle arrest of HepG2 cell in vitro and in vivo

2019 ◽  
Vol 53 ◽  
pp. 187-196 ◽  
Author(s):  
Shuhua Shan ◽  
Yue Xie ◽  
Huiling Zhao ◽  
Jinping Niu ◽  
Sheng Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Hepg2 Cell ◽  
Cycle Arrest

scholarly journals Growth Suppression by Acute PromyelocyticLeukemia-Associated Protein PLZF Is Mediated by Repression ofc-mycExpression

2003 ◽  
Vol 23 (24) ◽  
pp. 9375-9388 ◽  
Author(s):  
Melanie J. McConnell ◽  
Nathalie Chevallier ◽  
Windy Berkofsky-Fessler ◽  
Jena M. Giltnane ◽  
Rupal B. Malani ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Cell Cycle Arrest ◽  
Target Genes ◽  
Ectopic Expression ◽  
Growth Suppression ◽  
Quiescent State ◽  
Cycle Arrest

ABSTRACT The transcriptional repressor PLZF was identified by its translocation with retinoic acid receptor alpha in t(11;17) acute promyelocytic leukemia (APL). Ectopic expression of PLZF leads to cell cycle arrest and growth suppression, while disruption of normal PLZF function is implicated in the development of APL. To clarify the function of PLZF in cell growth and survival, we used an inducible PLZF cell line in a microarray analysis to identify the target genes repressed by PLZF. One prominent gene identified was c-myc. The array analysis demonstrated that repression of c-myc by PLZF led to a reduction in c-myc-activated transcripts and an increase in c-myc-repressed transcripts. Regulation of c-myc by PLZF was shown to be both direct and reversible. An interaction between PLZF and the c-myc promoter could be detected both in vitro and in vivo. PLZF repressed the wild-type c-myc promoter in a reporter assay, dependent on the integrity of the binding site identified in vitro. PLZF binding in vivo was coincident with a decrease in RNA polymerase occupation of the c-myc promoter, indicating that repression occurred via a reduction in the initiation of transcription. Finally, expression of c-myc reversed the cell cycle arrest induced by PLZF. These data suggest that PLZF expression maintains a cell in a quiescent state by repressing c-myc expression and preventing cell cycle progression. Loss of this repression through the translocation that occurs in t(11;17) would have serious consequences for cell growth control.

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