scholarly journals Promoter histone H3 lysine 9 di-methylation is associated with DNA methylation and aberrant expression of p16 in gastric cancer cells

2009 ◽  
Vol 22 (05) ◽  
Author(s):  
Dai
Keyword(s):  
Gastric Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Histone H3 ◽  
Gastric Cancer Cells ◽  
Aberrant Expression

scholarly journals Apoptotic mechanisms of gastric cancer cells induced by isolated Erinacine S through epigenetic histone H3 methylation of FasL and TRAIL

2021 ◽  
Author(s):  
Hsing-Chun Kuo ◽  
Shui-Yi Tung ◽  
Ko-Chao Lee ◽  
Kam-Fai Lee ◽  
Ya-Ling Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Histone H3 ◽  
Ethanol Extract ◽  
Gastric Cancer Cells ◽  
Hericium Erinaceus ◽  
Histone H3 Methylation ◽  
Health Promoting ◽  
Great Health

Erinacine S, the new bioactive diterpenoid compound isolated from the ethanol extract of the mycelia of Hericium erinaceus, displays great health-promoting properties. However, the effects of erinacine S on inductive...

scholarly journals miR-335-5p Suppresses Gastric Cancer Progression by Targeting MAPK10

2020 ◽  
Author(s):  
Yi Gao ◽  
Yanfeng Wang ◽  
Xiaofei Wang ◽  
Changan Zhao ◽  
Fenghui Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Progression ◽  
Target Gene ◽  
Luciferase Reporter ◽  
Gastric Cancer Cells ◽  
Aberrant Expression ◽  
Related Target

Abstract Background: In recent years, many microRNAs(miRNAs) involved in cancer progression. The aberrant expression of miR-335-5p in tumorigenesis has been demonstrated. The present study aimed to investigate the molecular mechanisms underlying miR-335-5p- regulated MAPK10 expression in human gastric cancer（GC）.Methods: The quantitative real-time PCR was used to study the level of miR-335-5p expression in gastric cancer cell lines and tissues. Subsequently, the MTT and cloning formation assays were used to detect cell proliferation, while transwell and wound-healing assays were used to identify invasion and migration of the gastric cancer cells. The correlation between the miR-335-5p and the cell cycle-related target gene mitogen‑activated protein kinase 10 (MAPK10) in gastric cancer was analyzed based on the website. In addition, the target gene of miR-335-5p was detected by luciferase reporter assay, qRT-PCR, and western blotting.Results: The miR-335-5p level was down-regulated in GC tissues and cell lines. Furthermore, miR-335-5p inhibited proliferation, migration of gastric cancer cells, and induced apoptosis. During the G1/S phase, miR-335-5p arrested the cycle of gastric cancer cells in vitro. The correlation between the miR-335-5p and the cell cycle-related target gene MAPK10 in GC was analyzed, MAPK10 was directly targeted by the miR-335-5p.Conclusion: These data suggested that miR-335-5p acts as a tumor suppressor, and go through the MAPK10 to inhibit the GC progression.

Downregulation of CCKBR Expression Inhibits the Proliferation of Gastric Cancer Cells, Revealing a Potential Target for Immunotoxin Therapy

2022 ◽  
Vol 22 ◽  
Author(s):  
Meng Li ◽  
Jiang Chang ◽  
Honglin Ren ◽  
Defeng Song ◽  
Jian Guo ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
Aberrant Expression ◽  
Promising Target ◽  
The Impact

Background Increased CCKBR expression density or frequency has been reported in many neoplasms. Objective We aimed to investigate whether CCKBR drives the growth of gastric cancer (GC) and its potential as a therapeutic target of immunotoxins. Methods A lentiviral interference system was used to generate CCKBR-knockdown gastric cancer cells. Cell Counting Kit-8 and clonogenic assays were used to evaluate cell proliferation. Wound-healing and cell invasion assays were performed to evaluate cell mobility. Cell cycle was analyzed by flow cytometry. Tumor growth in vivo was investigated using a heterologous tumor transplantation model in nude mice. In addition, we generated the immunotoxin FQ17P and evaluated the combining capacity and tumor cytotoxicity of FQ17P in vitro. Results Stable downregulation of CCKBR expression resulted in reduced proliferation, migration and invasion of BGC-823 and SGC-7901 cells. The impact of CCKBR on gastric cancer cells was further verified through CCKBR overexpression studies. Downregulation of CCKBR expression also inhibited the growth of gastric tumors in vivo. Furthermore, FQ17P killed CCKBR-overexpressing GC cells by specifically binding to CCKBR on the tumor cell surface. Conclusion The CCKBR protein drives the growth, migration, and invasion of gastric cancer cells, and it might be a promising target for immunotoxin therapy based on its aberrant expression, functional binding interactions with gastrin, and subsequent internalization.

scholarly journals The relationship between DNA methylation and Reprimo gene expression in gastric cancer cells

Oncotarget ◽  
2017 ◽  
Vol 8 (65) ◽  
pp. 108610-108623 ◽  
Author(s):  
Junzhong Lai ◽  
Hanze Wang ◽  
Qianping Luo ◽  
Shanlu Huang ◽  
Shujin Lin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
The Relationship

scholarly journals The effect of two nucleoside antitumor drugs on the proliferation and DNA methylation of human gastric cancer cells

2015 ◽  
Vol 10 (3) ◽  
pp. 1919-1923 ◽  
Author(s):  
XIU-LI CHEN ◽  
FENG-MEI WANG ◽  
JIA-JIA LI ◽  
XIAO-YING HE ◽  
XI-YU LIU ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Antitumor Drugs ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

scholarly journals DNA Methylation in the Exon 1 Region and Complex Regulation of Twist1 Expression in Gastric Cancer Cells

PLoS ONE ◽  
2015 ◽  
Vol 10 (12) ◽  
pp. e0145630 ◽  
Author(s):  
Ayuna Sakamoto ◽  
Yoshimitsu Akiyama ◽  
Shu Shimada ◽  
Wei-Guo Zhu ◽  
Yasuhito Yuasa ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Twist1 Expression ◽  
Exon 1 ◽  
Complex Regulation

scholarly journals Comparative Proteomic Profiling of Tumor-Associated Proteins in Human Gastric Cancer Cells Treated with Pectolinarigenin

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1596 ◽  
Author(s):  
Ho Jeong Lee ◽  
Venu Venkatarame Gowda Saralamma ◽  
Seong Min Kim ◽  
Sang Eun Ha ◽  
Preethi Vetrivel ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Cell Lines ◽  
Proteomic Analysis ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Antitumor Effects ◽  
Aberrant Expression ◽  
Target Proteins

Pectolinarigenin (PEC), a natural flavonoid that is present in citrus fruits, has been reported to exhibit antitumor effects in several cancers. Though the mechanism of PEC-induced cytotoxicity effects has been documented, the proteomic changes that are associated with the cellular response to this flavonoid are poorly understood in gastric cancer cells. In this study, a comparative proteomic analysis was performed to identify proteins associated with PEC-induced cell death in two human gastric cancer cell lines: AGS and MKN-28. Two-dimensional gel electrophoresis (2-DE) revealed a total of 29 and 56 protein spots with significant alteration were screened in AGS and MKN-28 cells respectively. In total, 13 (AGS) and 39 (MKN28) proteins were successfully identified by mass spectrometry from the differential spots and they are known to be involved in signal transduction, apoptosis, transcription and translation, cell structural organization, and metabolism, as is consistent with multiple effects of PEC on tumor cells. Notably, novel target proteins like Probable ATP-dependent RNA helicase DDX4 (DDX4) and E3 ubiquitin-protein ligase LRSAM1 (LRSAM1) along with the commonly differential expressed proteins on both the cell lines that are treated with PEC were confirmed by immunoblotting. The DDX4 accelerates cell cycle progression by abrogating the G2 checkpoint when overexpressed in cancer cells, while the aberrant expression of LRSAM1 may be involved in the cancer pathology. Thus, proteomic analysis provides vital information about target proteins that are important for PEC-induced cell death in gastric cancer cells.

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