Long non-coding RNA ncRuPAR regulates gastric cancer cell proliferation and apoptosis via phosphoinositide 3-kinase/protein kinase B signaling
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PROVIDER: PRJNA871030 | ENA |
REPOSITORIES: ENA
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Project description:Objective: To determine the effect and mechanism of the long non-coding RNA (lncRNA) ncRuPAR (non-protein coding RNA, upstream of coagulation factor II thrombin receptor [F2R]/protease-activated receptor-1 [PAR-1]) in human gastric cancer. Methods: HGC-27-ncRuPAR overexpression and MGC-803-ncRuPAR-RNAi knockdown gastric cancer cell lines were established. We assessed the effect of ncRuPAR on cell proliferation, apoptosis, migration, and invasion using Cell Counting Kit 8, flow cytometry, scratch and transwell assays, respectively. Differentially expressed genes in HGC-27-ncRuPAR overexpression and HGC-27-empty vector cell lines were identified using Affymetrix GeneChip microarray analysis. Ingenuity Pathway Analysis (IPA) of the microarray results was subsequently conducted to identify ncRuPAR-enriched pathways, followed by validation using real time-quantitative PCR (RT-qPCR). As one of the top enriched pathways, phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway was further examined by western blotting to determine its role in ncRuPAR-mediated regulation of gastric cancer pathogenesis. Results: ncRuPAR inhibited human gastric cancer cell proliferation and induced G1/S phase arrest and apoptosis, but did not affect migration or invasion in vitro. Overexpression of ncRuPAR in vitro was found to inhibit its known target PAR-1, as well as PI3K/Akt signaling. The downstream targets of PI3K/Akt, cyclin D1 was downregulated, but there was no change in expression level of B-cell lymphoma 2 (Bcl-2). Conclusions: We showed that lncRNA-ncRuPAR could inhibit tumor cell proliferation and promote apoptosis of human gastric cancer cells, potentially by inhibiting PAR-1, PI3K/Akt signaling, and cyclin D1. The results suggest a potential role for lncRNAs as key regulatory hubs in GC progression.
2022-08-19 | GSE211598 | GEO
Project description:Isorhamnetin Inhibits Proliferation and Invasion and Induces Apoptosis Through the Mitochondria‑Dependent Apoptosis in Human Gastric Cancer Cells
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Project description:We used RNA-seq to study the function of FABP5 in gastric cancer cells (AGS and MGC803). Down-regulation of FABP5 suppressed cell proliferation, cell migration and invasion, and induced cell apoptosis. Bioinformatics analysis revealed that Hippo signaling pathway was related to FABP5 in GC cells.Our data suggested that FABP5 might act as a potential target associated with Hippo signaling pathway for GC treatment.
2022-12-31 | GSE171838 | GEO
Project description:Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor that negatively regulates cell survival and proliferation by antagonizing phosphatidylinositol 3-kinase(PI3K)/protein kinase B(PKB/Akt) signaling. Loss of heterozygosity (LOH) of PTEN, reduced expression of PTEN and overexpression of phosphorylated Akt are frequently found in human gastric cancer, and their changes correlate with tumor progression and prognosis. Previous studies have shown that the deregulated miRNAs in human gastric cancer play important roles in gastric cancer cell proliferation, apoptosis and inflammation. However, miRNAs downstream PTEN/Akt signaling is poorly investigated. To clarify whether PTEN is involved in gastric tumorigenesis, we have generated a gastric epithelium specific PTEN knockout mouse which exhibited gastric tumor formation with enhanced cell proliferation.So the objectives of the microarray experiment were to, a) screen miRNAs which might be regulated by PTEN/Akt signaling by comparing the miRNA expression profiles between PTEN deficient and control gastric epithelia. 2) explore the microRNA mechanism involved in gastric cell proliferation and gastric tumorigenesis. miRNA profiling of mouse gastric epithelium,comparing Pten mutant mouse with controls. 4 samples. Experiments in 2 different time point, 20 days and 60 days after birth, 2 Biological replicates. Mutant tissue vs. controls from mixture of 3-4 mouse.
2013-09-02 | E-GEOD-27047 | biostudies-arrayexpress
Project description:Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor that negatively regulates cell survival and proliferation by antagonizing phosphatidylinositol 3-kinase(PI3K)/protein kinase B(PKB/Akt) signaling. Loss of heterozygosity (LOH) of PTEN, reduced expression of PTEN and overexpression of phosphorylated Akt are frequently found in human gastric cancer, and their changes correlate with tumor progression and prognosis. Previous studies have shown that the deregulated miRNAs in human gastric cancer play important roles in gastric cancer cell proliferation, apoptosis and inflammation. However, miRNAs downstream PTEN/Akt signaling is poorly investigated. To clarify whether PTEN is involved in gastric tumorigenesis, we have generated a gastric epithelium specific PTEN knockout mouse which exhibited gastric tumor formation with enhanced cell proliferation.So the objectives of the microarray experiment were to, a) screen miRNAs which might be regulated by PTEN/Akt signaling by comparing the miRNA expression profiles between PTEN deficient and control gastric epithelia. 2) explore the microRNA mechanism involved in gastric cell proliferation and gastric tumorigenesis.
2013-09-02 | GSE27047 | GEO
Project description:The major treatment strategies for gastric cancer (GC) including surgery, chemotherapy, and molecular-targeted therapy are limited by tumor recurrence and chemoresistance. Isorhamnetin (ISO) derives from the total flavones of Hippophae rhamnoides L. and has been used as potential antitumor medicine in several types of cancer. However, the antitumor effect of ISO on GC cells remains unclear. Here, we investigated the effects of ISO on two types of GC cells and explored its apoptotic mechanisms underlying such effects. The transcriptomic analysis of ISO-treated GC cells enriched multiple targets on cell growth and apoptosis. The CCK-8, colony formation and morphology observation assays demonstrated that ISO treatment significantly inhibited the growth and proliferation of GC cells in time- and dose-dependent manners. In addition, we also found that ISO treatment inhibited cell migration and invasion. Furthermore, ISO increased TUNEL positive apoptotic bodies as well as severe cell apoptosis. Intriguingly, ISO treatment significantly increased the expression of mitochondria-associated Bax/Bcl-2, cytosolic Cytochrome c and activated the cleavage of Caspase-3 and PARP, followed by severe reduction of mitochondrial potential. Moreover, the apoptosis of ISO-treated GC cells was blocked by the specific inhibitor of Caspase-3. Therefore, we demonstrated that ISO could induce apoptosis of GC cells through mitochondria-dependent apoptotic pathway. In summary, we reported for the first time the antitumor function of ISO in GC via intervening apoptosis, indicating a potential application in GC therapy.
2022-05-30 | GSE204967 | GEO
Project description:Fucoidan is a high-molecular polysaccharide whose main constituent is sulfated fucose. Extensive studies have demonstrated numerous interesting biological activities for fucoidan. We specifically focused on the anti-proliferation activity of fucoidan and examined the underlying mechanism in MKN45 gastric cancer cells. BrdU assay revealed that fucoidan impeded the MKN45 cell cycle by approximately 50%, and clonogenic assay also showed that fucoidan inhibited cell proliferation. Preliminary examinations of fucoidan using LDH assay showed no immediate cytotoxic effects at 24-h exposure. However, longer time courses revealed inhibition of cell growth at 4 days in a dose-dependent manner. Microarray analysis in MKN45 cells treated with fucoidan identified genes that were upregulated and downregulated in response to fucoidan, including MAP3K5, or ASK1 (apoptosis signal-regulating kinase), which was upregulated by 1.38-fold. Western blot confirmed that fucoidan increased ASK1 protein levels, while reducing the levels of phosphorylated ASK1. Reduction of ASK1 by siRNA decreased proliferation of MKN45 cells. Our findings show that fucoidan may suppress cellular proliferation and DNA synthesis in MKN45 cells by suppressing the ASK1-p38 signaling pathway through reduction of phosphorylated ASK1 levels.
2017-02-09 | GSE58774 | GEO
Project description:GFI1 promotes gastric cancer cell HS746T proliferation
| PRJNA475274 | ENA
Project description:Objective: To determine the effect and mechanism of the long non-coding RNA (lncRNA) ncRuPAR (non-protein coding RNA, upstream of coagulation factor II thrombin receptor [F2R]/protease-activated receptor-1 [PAR-1]) in human gastric cancer. Methods: HGC-27-ncRuPAR overexpression and MGC-803-ncRuPAR-RNAi knockdown gastric cancer cell lines were established. We assessed the effect of ncRuPAR on cell proliferation, apoptosis, migration, and invasion using Cell Counting Kit 8, flow cytometry, scratch and transwell assays, respectively. Differentially expressed genes in HGC-27-ncRuPAR overexpression and HGC-27-empty vector cell lines were identified using Affymetrix GeneChip microarray analysis. Ingenuity Pathway Analysis (IPA) of the microarray results was subsequently conducted to identify ncRuPAR-enriched pathways, followed by validation using real time-quantitative PCR (RT-qPCR). As one of the top enriched pathways, phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway was further examined by western blotting to determine its role in ncRuPAR-mediated regulation of gastric cancer pathogenesis. Results: ncRuPAR inhibited human gastric cancer cell proliferation and induced G1/S phase arrest and apoptosis, but did not affect migration or invasion in vitro. Overexpression of ncRuPAR in vitro was found to inhibit its known target PAR-1, as well as PI3K/Akt signaling. The downstream targets of PI3K/Akt, cyclin D1 was downregulated, but there was no change in expression level of B-cell lymphoma 2 (Bcl-2). Conclusions: We showed that lncRNA-ncRuPAR could inhibit tumor cell proliferation and promote apoptosis of human gastric cancer cells, potentially by inhibiting PAR-1, PI3K/Akt signaling, and cyclin D1. The results suggest a potential role for lncRNAs as key regulatory hubs in GC progression.
| S-EPMC9682512 | biostudies-literature
Project description:As a monocyclic sesquiterpene, Germacrone has remarkable anti-tumor effect in a variety of cancers such as hepatocellular carcinoma, gastric cancer, and breast cancer. However, the mechanism of Germacrone on gastric cancer was still unclear. In our study, Germacrone inhibited gastric cancer cells proliferation in a dose-dependent manner. As shown, Germacrone induced G0 / G1 phase arrest and apoptosis in gastric cancer. Germacrone increased the expression of LC3ii/LC3i, p62. Then combined with CQ, the expression of LC3ii/LC3i, p62 continued to increase. As a result, Germacrone partially blocked the autophagy process. Through proteomic technology, a total of 596 proteins were screened and the top hits were Hepatitis B X-interacting protein (HBXIP). Overexpression of HBXIP delayed the cycle arrest, induction of apoptosis, and autophagy inhibition induced by Germacrone. Germacrone inhibits proliferation in gastric cancer cells by inhibiting HBXIP, and this process is related to G0 / G1 phase arrest, induction apoptosis, and autophagy inhibition.
2020-10-14 | PXD021980 |