The relationship between gastric cancer cells circulating in the blood and microsatellite instability positive gastric carcinomas

Background: We aimed to investigate the relationship between miR-596, BCL-2, and apoptosis of gastric cancer cells, and to explore the mechanism of miR-596 in gastric cancer. Besides, this study aimed to find the target of miR-596 and explore the mechanism of action of miR-596 in gastric cancer. Methods: Eighteen samples of gastric cancer tissues and 18 samples of corresponding tumor-adjacent tissues were collected from 18 gastric cancer patients (aged from 40 to 55 yr) admitted to Zhuji People's Hospital, Zhuji, China from March 2017 to May 2018. The expression levels of miR-596 and BCL-2 were detected to verify the regulation of miR-596 on the apoptosis and proliferation of gastric cancer cell lines MKN-45 and HGC-27 and its effect on BCL-2 expression. Results: The expression level of miR-596 was notably lower in gastric cancer tissues than in adjacent tissues, and BCL-2 level was notably higher in gastric cancer tissues than in adjacent tissues. After the up-regulation of miR-596 expression, the proliferation of MKN-45 and HGC-27 cells was significantly decreased, the level of apoptosis was significantly increased (P<0.05), and the expression of BCL-2 was decreased. The dual-luciferase report showed that miR-596 had a targeting inhibition of BCL-2. Gastric cancer cells with up-regulated miR596 and BCL-2 had significantly higher proliferation and lower apoptosis than cells with up-regulated miR-596. Conclusions: miR-596 can inhibit the proliferation of gastric cancer cells and promote the apoptosis through its targeting inhibition of BCL-2 expression.

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

Oncotarget ◽

10.18632/oncotarget.21296 ◽

2017 ◽

Vol 8 (65) ◽

pp. 108610-108623 ◽

Cited By ~ 9

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

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Inhibiting PP2Acα Promotes the Malignant Phenotype of Gastric Cancer Cells through the ATM/METTL3 Axis

BioMed Research International ◽

10.1155/2021/1015293 ◽

2021 ◽

Vol 2021 ◽

pp. 1-16

Author(s):

Zhaoxiang Cheng ◽

Shan Gao ◽

Xiaojie Liang ◽

Chao Lian ◽

Jianquan Chen ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Catalytic Subunit ◽

Malignant Progression ◽

Malignant Phenotype ◽

Gastric Cancer Cells ◽

Internal Connection ◽

Phosphatase 2A ◽

The Relationship

This article is aimed at exploring the relationship between the phosphatase 2A catalytic subunit Cα (PP2Acα, encoded by PPP2CA) and methyltransferase-like 3 (METTL3) in the malignant progression of gastric cancer (GC). Through analyzing the bioinformatics database and clinical tissue immunohistochemistry results, we found that abnormal PP2Acα and METTL3 levels were closely related to the malignant progression of GC. To explore the internal connection between PP2Acα and METTL3 in the progression of GC, we carried out cellular and molecular experiments and finally proved that PP2Acα inhibition can upregulate METTL3 levels by activating ATM activity, thereby promoting the malignant progression of GC.

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Knockdown of KREMEN2 inhibits tumor proliferation and metastasis in gastric cancer.

Journal of Clinical Oncology ◽

10.1200/jco.2020.38.15_suppl.e16555 ◽

2020 ◽

Vol 38 (15_suppl) ◽

pp. e16555-e16555

Author(s):

Beibei Chen ◽

Saiqi Wang ◽

Jinxi Huang ◽

Jitian Li ◽

Jianying Zhang ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Cycle ◽

Cancer Cells ◽

Gastric Cancer Cell ◽

Akt Pathway ◽

Gastric Cancer Cells ◽

The Relationship

e16555 Background: KREMEN2 is an important regulator of classical Wnt/β-catenin signaling pathway. However, the relationship between KREMEN2 and gastric cancer is not clear. The aim of this study was to explore the regulatory role of KREMEN2 in the tumorigenesis and metastasis of gastric cancer. Methods: We measured the protein level of KREMEN2 in 156 gastric adenocarcinoma, 40 metastatic gastric adenocarcinoma, 8 marginal and 4 normal tissues using tissue microarray. The differences in KREMEN2 expression were tested with Mann-Whitney U test. The relationship between KREMEN2 expression and pathologic data was determined with Pearson’s correlation analysis. The mRNA and protein level in cultured cell lines were detected by qRT-PCR and western blotting, respectively. Lentivirus was transfected by repressing KREMEN2. Cell viability was determined by the MTT assay. Apoptosis and cell cycle distribution were detected using flow cytometry. The cell migration was investigated by wound healing and transwell assay. Antibody array was performed to explore the underlying molecule mechanism. In vivo, Xenograft assay was established using nude mice to explore the role of KREMEN2 in gastric cancer cell and bioluminescence was observed via an in vivo imaging system. Results: It was demonstrated that, compared to para-cancerous tissues, KREMEN2 was significantly up-regulated in gastric cancer tissues, and was positively correlated with the pathological grade of gastric cancer patients. Given that KREMEN2 is abundantly expressed in most tested gastric cancer cell lines, KREMEN2 knockdown cell models were established and further used to construct mice xenograft model. After knocking down KREMEN2, the proliferation of gastric cancer cells was inhibited both in vivo and in vitro. At the same time, knockdown of KREMEN2 induced apoptosis, cell cycle arrest at G2/M phase and inhibition of migration in gastric cancer cells in vitro. Mechanistically, we found that knockdown of KREMEN2 suppressed PI3K/Akt pathway. Conclusions: Therefore, we revealed that the overexpression of KREMEN2 in gastric cancer may promote the carcinogenesis and metastasis of gastric cancer by activating the PI3K/Akt pathway.

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