Effect of Chrysanthemum flavonoids on growth and cell cycle regulators of gastric cancer cell

2010 ◽  
Vol 34 (8) ◽  
pp. S50-S50
Author(s):  
Xiaoyan Pan ◽  
Xinmei Zhou ◽  
Guangtao Xu ◽  
Lingfen Miao ◽  
Shuoru Zhu
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cell Cycle Regulators

scholarly journals ZHX1 Inhibits Gastric Cancer Cell Growth through Inducing Cell-Cycle Arrest and Apoptosis

2016 ◽  
Vol 7 (1) ◽  
pp. 60-68 ◽  
Author(s):  
Xingjie Ma ◽  
Minlu Huang ◽  
Zhenqiang Wang ◽  
Bingya Liu ◽  
Zhenggang Zhu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Growth ◽  
Cycle Arrest

miR-3613 Regulates Gastric Cancer Cells Proliferation, Invasion, Migration and Apoptosis by Targeting Suppressor of Cytokine Signaling 4

2019 ◽  
Vol 9 (12) ◽  
pp. 1699-1705
Author(s):  
Yuming Luo ◽  
Wei Cao
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Western Blot ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Target Genes ◽  
Luciferase Reporter ◽  
Gastric Cancer Cells ◽  
And Migration

The present study aimed to investigate the effect of miR-3613 on the biological functions of gastric cancer cell lines. The expression of miR-3613 and SOCS4 in gastric cancer cells were detected by RT-qPCR and western blot. The target genes of miR-3613 were verified with the luciferase reporter system and western blot. The SOCS4 overexpression plasmid was constructed and transfected into gastric cancer cells. To further investigate the function of miR-3613, shRNA targeting miR-3613 and SOCS4 overexpression were transfected into SGC-7901. The growth of cells was detected by CCK-8, then the cell invasion and migration ability were detected by wound healing and transwell. Furthermore, the level of cell cycle was detected by flow cytometry. The expression of cell proliferation, cyclin and migration-related proteins were detected by western blot. The results revealed that the expression of miR-3613 is significantly increased in gastric cancer cells. SOCS4 is one of the target genes of miR-3613. Additionally, interference with miR-3613 promotes cell cycle arrest in gastric cancer cells and reversed the inhibitory effect of miR-3613 on biological function of gastric cells. Collectively, the data demonstrated that miR-3613 regulates gastric cancer cell by targeting SOCS4, which is expected to be an attractive target for the development of new drugs for the treatment of gastric cancer.

The cell cycle regulation of anti-cancer bioactive peptide (ACBP) on gastric cancer cell lines

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 15087-15087
Author(s):  
X. Su ◽  
X. Ouyang ◽  
G. Xu ◽  
J. Shen ◽  
M. Yan
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cyclin D1 ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Lines ◽  
Human Gastric Cancer ◽  
Human Gastric Cancer Cell ◽  
Gastric Cancer Cell Lines

15087 Background: Anti-cancer bioactive peptide (ACBP) was extracted from the spleen of the goat suffered immune inducement by immunoreaction, supercentrifuge and ultra-filtration. Our previous studies have identified ACBP had significantly inhibited the growth of the human gastric cancer cell lines BGC-823 and MGC-803, the human rhinopharyngocele cell line CNE and the leukemic cell line. The in vivo experiments showed ACBP could dramatically repress the growth of tumor, and had few side-effects in the long-term toxic experiments. In clinical trials, ACBP could enhance the survival and life quality of the patients with advanced gastric cancer. In this study, we will explore the influence and mechanism of the effect of ACBP on cell cycle using human gastric cancer cell lines BGC-823 and MGC-803. Methods: Human gastric cancer cell lines BGC-823 and MGC-803 were cultured with different concentrations (10–25 ug/ml) of ACBP. The MTT method was employed to measure the growth inhibition rates of the cells with different concentrations of ACBP; the morphological changes were observed under the light microscope; the semi-quantitative RT-PCR was used to assay the changes of mRNA for p16,p21,p27,c-myc,cyclin D1,bax,bcl-2 gene. Results: Different concentrations of ACBP in the range of 10.0–25.0 μg/ml could inhibit the growth of BGC-823 and MGC-803 cell and such effect was both concentration and time dependent. 25.0 μg/ml ACBP had an inhibition rate (IR) of 84.4%, 72.3% and a median concentration (IC50) of 17.86 μg/ml, 13.16 ug/ml. After ACBP treatment, the cells showed typical apoptotic changes under the light microscope. On RT-PCR, the expressions of p16,p21,p27,bax mRNA in the two cell lines were markedly increased after ACBP treatment. On the contrary, the expression of c-myc,cyclin D1,bcl-2 mRNA in the two cell lines were obviously decreased after ACBP treatment. Conclusion: ACBP had markedly repressed the growth of BGC-823 and MGC-803 cell lines through inducing the cellular apoptosis. The possible mechanism is ACBP affects the cell cycle molecules expression including p16,p21,p27,cyclin D1 and regulate c-myc,bcl-2 and bax to induce apoptosis. No significant financial relationships to disclose.

miR-218 suppresses gastric cancer cell cycle progression through the CDK6/Cyclin D1/E2F1 axis in a feedback loop

2017 ◽  
Vol 403 ◽  
pp. 175-185 ◽  
Author(s):  
Min Deng ◽  
Chao Zeng ◽  
Xihong Lu ◽  
Xiusheng He ◽  
Ruixin Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cyclin D1 ◽  
Cancer Cell ◽  
Feedback Loop ◽  
Cell Cycle Progression ◽  
Gastric Cancer Cell ◽  
Cycle Progression

scholarly journals PAFAH1B3 Expression Is Correlated With Gastric Cancer Cell Proliferation and Immune Infiltration

2021 ◽  
Vol 11 ◽  
Author(s):  
Tianyu Xie ◽  
Xin Guo ◽  
Di Wu ◽  
Shuo Li ◽  
Yixun Lu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cell Infiltration ◽  
Gastric Cancer Cells ◽  
Cancer Data ◽  
M1 Macrophage ◽  
The Impact

BackgroundPlatelet activating factor acetylhydrolase 1b catalytic subunit 3 (PAFAH1B3) is associated with a variety of human diseases. However, its function in gastric cancer remains uncertain.MethodsPAFAH1B3 expression was analyzed in The Cancer Genome Atlas (TCGA) and genotype-tissue expression pan-cancer data. The association between PAFAH1B3 expression and patient prognosis was evaluated using TCGA clinical survival data. Enrichment analysis of PAFAH1B3 was performed using the clusterProfiler R software package. Moreover, the correlation between PAFAH1B3 expression and immune cell infiltration were evaluated by analyzing TCGA database. CCK8 assay and colony-formation assay were performed to assess the effect of PAFAH1B3 on the proliferation of gastric cancer cells. Transwell assay was used to evaluate the impact of PAFAH1B3 on gastric cancer cell migration. Western blot was performed to evaluate the role of PAFAH1B3 on signaling pathways in gastric cancer cells.ResultsPAFAH1B3 was highly expressed in many types of tumors including gastric cancer. High PAFAH1B3 expression was significantly correlated with proliferation-related gene sets involved in DNA replication, the cell cycle, and cell cycle checkpoints. Further analysis showed that high PAFAH1B3 expression was associated with high M1 macrophage and CD8-positive T cell infiltration scores. PAFAH1B3 knockdown inhibited the proliferation, migration, and the activation of oncogenic signaling in gastric cancer cells.ConclusionsOur findings suggest that PAFAH1B3 may be an oncogene in gastric cancer.

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