Silencing of the hPOT1 gene by RNA inference promotes apoptosis and inhibits proliferation and aggressive phenotype of gastric cancer cells, likely through up-regulating PinX1 expression

2011 ◽  
Vol 64 (12) ◽  
pp. 1051-1057 ◽  
Author(s):  
Shun-Mei Wan ◽  
Jun Tie ◽  
Ya-Fei Zhang ◽  
Jun Guo ◽  
Liu-Qin Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Intestinal Metaplasia ◽  
Cancer Cells ◽  
Protein A ◽  
Normal Mucosa ◽  
Gastric Cancer Cells ◽  
Down Regulation ◽  
Proliferation And Invasion

BackgroundThe human protection of telomeres 1 (hPOT1) protein, a single-strand telomeric DNA binding protein, plays an important role in telomere protection and telomere length regulation. However, its effect on invasion of gastric cancer remains unclear.AimsTo explore the role of hPOT1 in the proliferation and invasion of gastric cancer cells.MethodsThe gastric expression of hPOT1 was examined in normal gastric mucosa (n=25), intestinal metaplasia (n=20), gastric dysplasia (n=20) and gastric cancer (n=150) by immunohistochemistry. The mean optical density (MOD) of the immunostaining was determined by semi-quantitative image analysis. The role of hPOT1 in the cell proliferation, apoptosis and invasion of gastric cancer 7901 cells was determined by means of the RNA interference (RNAi) of hPOT1 mRNA. The effects of hPOT1 RNAi on the expression of hPinX1 and hTERT were detected with western blotting.ResultsThe hPOT1 MOD was progressively increased from the normal mucosa to intestinal metaplasia, dysplasia, and gastric cancer. An increased hPOT1 expression significantly correlated with tumour serosal invasion, node metastasis and advanced stage. Transfection of hPOT1 siRNA into SGC-7901 cells led to a decrease in cell proliferation, colony formation and invasion, and also an increase of apoptosis. An up-regulation of hPinX1 and down-regulation of hTERT were found in gastric cancer cells with hPOT1 siRNA.ConclusionsIncreased hPOT1 expression is associated with an advanced tumour stage. hPOT1 RNAi inhibits proliferation and invasion, and induces apoptosis of gastric cancer cells. The effects of hPOT1 RNAi seem to be functionally linked to up-regulation of PinX1 and down-regulation of hTERT.

scholarly journals Chrysophanol Inhibits the Progression of Gastric Cancer by Activating NLRP3

2021 ◽  
Author(s):  
Hou Binfen ◽  
Li Zhao ◽  
Min Deng
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Gastric Cancer Cells ◽  
Antitumor Effects ◽  
Ags Cells ◽  
Anti Cancer ◽  
Colony Forming Assay

Abstract AimGastric cancer is one of the most common malignant tumors.Chrysophanol has been reported to have antitumor effects on a variety of cancers, but the role of chrysophanol in gastric cancer remains unclear. The aim of this study was to investigate the effects of chrysophanol on proliferation, pyroptosis, migration and invasion of gastric cancer cells.MethodsMKN 28 and AGS cells were treatde with different concentrations of chrysophanol, then cell proliferation, migration,invasion and pyroptosis were decteed by CCK-8, Colony-forming assay, Wound Healing assay, Transwell and flow cytometry, respectively.Subsequently, NLRP3 siRNA was transfected into MKN 28 cells, cell proliferation pyroptosis, migration and invasion were reassessed in these transfected cells. The expression of caspase-1 and IL-1β in the downstream of NLRP3 was detected by qRT PCR and Western blot.ResultsChrysophanol significantly inhibited the proliferation of GC cells, promoted pyroptosis, inhibited cell migration and invasion, and up-regulated the expression level of NLRP3 inflammasome in GC cells. Silencing NLRP3 inhibited the effects of chrysophanol on proliferation, pyroptosis, migration and invasion of MKN 28 cells. Chrysophanol plays an anti-cancer role through high expression of NLRP3.CoclusionsChrysophanol can inhibit the proliferation, migration and invasion of gastric cancer cells by regulating NLRP3, promote the death of gastric cancer cells, and play an anti-tumor role,which is a clinical strategy with great potential for the treatment of gastric cancer.

miRNA423-5p regulates cell proliferation and invasion by targeting trefoil factor 1 in gastric cancer cells

2014 ◽  
Vol 347 (1) ◽  
pp. 98-104 ◽  
Author(s):  
Jingjing Liu ◽  
Xu Wang ◽  
Xiaoning Yang ◽  
Yunpeng Liu ◽  
Ying Shi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Trefoil Factor ◽  
Gastric Cancer Cells ◽  
Proliferation And Invasion ◽  
Trefoil Factor 1

scholarly journals Knockdown of NCOA2 Inhibits the Growth and Progression of Gastric Cancer by Affecting the Wnt Signaling Pathway–Related Protein Expression

2020 ◽  
Vol 19 ◽  
pp. 153303382092807
Author(s):  
Zhenlv Lin ◽  
Fan Yang ◽  
Dong Lu ◽  
Wenjie Sun ◽  
Guangwei Zhu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Nuclear Receptor ◽  
Wnt Signaling Pathway ◽  
Related Protein ◽  
Gastric Cancer Cells ◽  
Nuclear Receptor Coactivator ◽  
Proliferation And Invasion

Objective: The aim of the study is to determine the role of nuclear receptor coactivator 2 in cell proliferation and invasion ability of gastric cancer cells and to explore its possible mechanisms. Methods: Immunohistochemical staining was used to determine NCOA2 gene expression in gastric cancer. Western blotting was used to detect Wnt signal pathways–related protein expression. Colony formation assays, Cell Counting Kit-8 assays, and transwell assays were used to determine cell proliferation, metastasis, and invasion ability of gastric cancer cells. A flow cytometric apoptosis tests determine gastric cancer cell apoptosis ability after inhibition of the expression of nuclear receptor coactivator 2. Subcutaneous mouse models were used to determine the gastric cancer growth and peritoneal metastasis differences after inhibition the expression of nuclear receptor coactivator 2. Results: The expression of nuclear receptor coactivator 2 in gastric cancer cells is high ( P < .01), including lymph node metastasis, TNM staging, and gender differences in nuclear receptor coactivator 2 expression were statistically significant ( P < .01). Short interfering nuclear receptor coactivator 2 could inhibit the proliferation and invasion ability of gastric cancer cells. Short interfering nuclear receptor coactivator 2 promotes the apoptosis of gastric cancer cells. Animal experiments showed that short interfering nuclear receptor coactivator 2 could inhibit the growth and invasion of gastric cancer-transplantable tumors. Knockdown of the expression of nuclear receptor coactivator 2 inhibited the Wnt/β-catenin signaling pathway in the gastric cancer cells. Conclusions: Knockdown of the expression of nuclear receptor coactivator 2 can inhibit the proliferation and invasion of human gastric cancer in vitro and in vivo. The underlying mechanism of NOCA2 affects the Wnt signaling pathway.

scholarly journals The Role of Tumoral FOXP3 on Cell Proliferation, Migration, and Invasion in Gastric Cancer

2017 ◽  
Vol 42 (5) ◽  
pp. 1739-1754 ◽  
Author(s):  
Lu Zhang ◽  
Jianghao Xu ◽  
Xuan Zhang ◽  
Yi Zhang ◽  
Lu Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Foxp3 Expression ◽  
Migration And Invasion ◽  
Published Data ◽  
Rt Pcr ◽  
Gastric Cancer Cells ◽  
Cancer Tissues

Background/Aims: There is little published data on the role of FOXP3 in gastric cancer. Methods: FOXP3 expression and localization in gastric cancer tissues and cells were examined by immunohistochemistry, RT-PCR, flow cytometry, western blot, and laser confocal microscopy. CCK8, plate clone, wound healing, and transwell insert assays were performed for gastric cancer cells. Potential molecules and signaling pathways were screened using high-throughput transcriptome sequencing. Results: FOXP3 expression in gastric cancer tissues was higher than that in para-carcinoma tissues. It was restricted to the cytoplasm of para-carcinoma tissues, but was observed in the cytoplasm or/and nuclei of gastric cancer tissues. FOXP3 expression was positively correlated with pathological grading, and was detected in gastric cancer and GES-1 cells, where it was expressed in the cytoplasm alone, or in both the cytoplasm and the nucleus. FOXP3 overexpression promoted cell proliferation, migration, and invasion, while FOXP3 knockdown suppressed these effects. Furthermore, RT-PCR and ELISA confirmed that FOXP3 upregulation resulted in increased TGF-β expression and secretion in gastric cancer cells. Conclusion: FOXP3 expression was associated with degree of gastric cancer differentiation. In addition, upregulated and ectopic tumoral FOXP3 can promote gastric cancer proliferation, migration, and invasion, partly through the TGF-β pathway.

scholarly journals miR-1290 stimulates proliferation of gastric cancer by targeting SP1 with overexpression of fucosyltransferase IV and α1, 3-fucosylated glycans

2020 ◽  
Author(s):  
Faisal Aziz ◽  
Li Yulin ◽  
Qiu Yan
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Specific Protein ◽  
Dependent Manner ◽  
Gastric Cancer Cells ◽  
H Pylori ◽  
Dose Dependent ◽  
Development Of Gastric Cancer

AbstractFucosylation plays an important role in the development of carcinogenesis. miRNA-1290 emerged as crucial molecule to regulate cancer cell proliferation. This study evaluated the role of miRNA-1290 to development of gastric cancer by regulation of fucosyltransferase-IV, specific protein-1 (SP1) and α1,3-fucosylated glycans.We analyzed the role of H. pylori and miR-1290 in gastric cancer cells in induce fucosylation and cell proliferation, as well as SP1 and ubiquitin protein interaction. We found miR-1290 induced proliferation in H. pylori CagA treated gastric cancer cells by stimulating FUT4/LeY fucosylation, as evidence by high expression of miR-1290 and phosphorylation of EGFR and MAPKs pathway in dose–dependent manner. In addition, miR-1290 inhibited SP1 protein with the regulation of ubiquitin-proteasomal system and leads to stimulate FUT4 and α1,3-fucosylated glycans level. We report the role of miRNA-1290 to stimulate FUT4 fucosylation and LeY through EGFR/MAPKs pathway by targeting SP1 in the development of gastric cancer.

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