DNA methyltransferase 3 beta regulates ras related domain family 1 methylation leading to enhanced proliferation and migration in gastric cancer cells

Silencing expression of RASSF1A, which is induced by DNA hypermethylation, contributes to proliferation and migration in gastric cancer. However, the molecular mechanisms of this process remain unclear. In order to investigate the effect and mechanisms of RASSF1A methylation on proliferation and migration of gastric cancer, DNA methyltransferase inhibitors (5-AZA-CdR) were used to interfere with expression of DNMT3B and RASSF1A in gastric cancer AGS cells. Fe3O4–SiO2 nanoparticles were used to extract mRNA for RT-qPCR, and RT-qPCR and western blotting were used to measure the effect of RASSF1A expression on the expression of Caspase 3, Bcl-2, and Bax in AGS cells. MTT and cell scratch assays were used to assess the proliferation and migration of AGS cells. Our findings show that DNA methyltransferase inhibitors inhibit expression of DNMT3B, which leads to an increase in the expression of RASSF1A, Caspase3, and Bax at both the mRNA and protein levels, and inhibits the expression of Bcl-2. Thus, inhibiting the expression of DNMT3B and altering levels of DNA methylation can promote the expression of RASSF1A, regulate the expression of apoptosis-related genes, and inhibit proliferation and migration of gastric cancer cells. It is helpful to explore the pathological mechanism of endometrial cancer and provide theoretical basis for RASSF1A as a potential therapeutic target of gastric cancer.

Download Full-text

Effects and Mechanisms of Anlotinib and Dihydroartemisinin Combination Therapy in Ameliorating Malignant Biological Behavior of Gastric Cancer Cells

Current Pharmaceutical Biotechnology ◽

10.2174/1389201021666200623132803 ◽

2020 ◽

Vol 21 ◽

Author(s):

Qiong Luo ◽

Suyun Zhang ◽

Donghuan Zhang ◽

Rui Feng ◽

Nan Li ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Molecular Mechanisms ◽

Chorioallantoic Membrane ◽

Cell Counting ◽

Biological Behavior ◽

Gastric Cancer Cells ◽

Invasion And Migration ◽

Apoptosis Related Protein ◽

And Migration

Background: Gastric cancer(GC) is currently one of the major malignancies that threatens human lives and health. Anlotinib is a novel small-molecule that inhibits angiogenesis to exert anti-tumor effects. However, the function in gastric cancer is incompletely understood. Objective: The aim of the present study was to investigate the anti-tumor effects and molecular mechanisms of anlotinib combined with dihydroartemisinin (DHA) in SGC7901 gastric cancer cells. Method: Different concentrations of anlotinib and DHA were used to treat SGC7901 gastric cancer cells, after which cell proliferation was measured. Drug interactions of anlotinib and DHA were analyzed by the Chou-Talalay method with CompuSyn software. proliferation, apoptosis, invasion, migration, and angiogenesis were measured using the cell counting kit-8 (CCK8) assay, flow cytometry, Transwell invasion assays, scratch assays, and chicken chorioallantoic membrane (CAM) assays. proliferation-associated protein (Ki67), apoptosis-related protein (Bcl-2), and vascular endothelial growth factor A (VEGF-A) were quantified by Western bloting. Results: The combination of 2.5 μmol/L of anlotinib and 5 of μmol/L DHA was highly synergistic in inhibiting cell growth, significantly increased the apoptosis rate and suppressed obviously the invasion and migration capability and angiogenesis of gastric cancer cells. In addition, the expression levels of Ki67, Bcl-2, and VEGF-A, as well as angiogenesis, were significantly decreased in the Combination of drugs compared with in control and either drug alone. Conclusion: The combination of anlotinib and DHA showed synergistic antitumor activity, suggesting their potential in treating patients with gastric cancer.

Download Full-text

Overexpression of PIP5KL1 suppresses cell proliferation and migration in human gastric cancer cells

Molecular Biology Reports ◽

10.1007/s11033-009-9701-5 ◽

2009 ◽

Vol 37 (5) ◽

pp. 2189-2198 ◽

Cited By ~ 12

Author(s):

Lan Shi ◽

Mei Zhao ◽

Qing Luo ◽

Yi-Ming Ma ◽

Jia-Ling Zhong ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Proliferation ◽

Cancer Cells ◽

Human Gastric Cancer ◽

Gastric Cancer Cells ◽

Cell Proliferation And Migration ◽

And Migration ◽

Proliferation And Migration

Download Full-text

Overexpression of stathmin1 in the diffuse type of gastric cancer and its roles in proliferation and migration of gastric cancer cells

British Journal of Cancer ◽

10.1038/sj.bjc.6605537 ◽

2010 ◽

Vol 102 (4) ◽

pp. 710-718 ◽

Cited By ~ 76

Author(s):

T-Y Jeon ◽

M-E Han ◽

Y-W Lee ◽

Y-S Lee ◽

G-H Kim ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Diffuse Type ◽

Gastric Cancer Cells ◽

And Migration ◽

Proliferation And Migration

Download Full-text

Exosomal miR-155-5p promotes proliferation and migration of gastric cancer cells by inhibiting TP53INP1 expression

Pathology - Research and Practice ◽

10.1016/j.prp.2020.152986 ◽

2020 ◽

Vol 216 (6) ◽

pp. 152986

Author(s):

Shuai-Shuai Shi ◽

Hui-Peng Zhang ◽

Chang-Qing Yang ◽

Li-Na Li ◽

Yu Shen ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Gastric Cancer Cells ◽

And Migration ◽

Proliferation And Migration

Download Full-text

TRAF6 Promotes Gastric Cancer Cell Self-Renewal, Proliferation, and Migration

Stem Cells International ◽

10.1155/2020/3296192 ◽

2020 ◽

Vol 2020 ◽

pp. 1-11

Author(s):

Mengting Yang ◽

Meng Jin ◽

Kailong Li ◽

Haifeng Liu ◽

Xiaxia Yang ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Tumor Necrosis Factor Receptor ◽

Gastric Cancer Cells ◽

Mesenchymal Transition ◽

In The Wild ◽

And Migration ◽

Exact Effect ◽

Proliferation And Migration

Gastric cancer is the third most common type of tumor associated with death. TRAF6 belongs to the tumor necrosis factor receptor-associated factor family and has been demonstrated to be involved in tumor progression in various cancers. However, the exact effect of TRAF6 on gastric cancer stem cells has not been extensively studied. In this study, abnormal expression of TRAF6 was found in gastric cancer tissues. Overexpression of TRAF6 enhanced proliferation and migration, and TRAF6 knockdown reversed this phenomenon in gastric cancer cells. Moreover, TRAF6 may inhibit differentiation and promote stemness and epithelial-mesenchymal transition (EMT). Transcriptome profiles revealed 701 differentially expressed genes in the wild-type group and the TRAF6 knockout group. Potential molecules associated with cell proliferation and migration were identified, including MAPK, FOXO, and IL-17. In conclusion, TRAF6 is a significant factor promoting proliferation and migration in gastric cancer cells and may provide a new target for the accurate treatment of gastric cancer.

Download Full-text