scholarly journals High SLC2A1 expression associated with suppressing CD8 T cells and B cells promoted cancer survival in gastric cancer

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0245075
Author(s):  
Kyueng-Whan Min ◽  
Dong-Hoon Kim ◽  
Byoung Kwan Son ◽  
Kyoung Min Moon ◽  
So Myoung Kim ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
T Cells ◽  
B Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cd8 T Cells ◽  
Immune Cells ◽  
Gastric Cancer Cell ◽  
Glucose Transporter ◽  
Gastric Cancer Cell Lines

High expression of glucose transporter family members, which augment glucose uptake and glycolytic flux, has been shown to play a pivotal role in the proliferation and survival of tumor cells, contributing to the energy supply, biosynthesis and homeostasis of cancer cells. Among the many members, solute carrier family 2 member 1 (SLC2A1) encodes a glucose transporter, GLUT1, that is critical in the metabolism of glucose, which is an energy source for cell growth that contributes to cancer progression and development. The aim of this study was to analyze the survival and genetic changes/immune profiles in patients with gastric cancer with high SLC2A1 expression and to provide treatment for improving prognosis. This study investigated the clinicopathologic parameters, the proportion of immune cells and gene sets affecting SLC2A1 expression in 279 and 415 patients with gastric cancer from the Eulji Hospital cohort and The Cancer Genome Atlas, respectively. We assessed the response to conventional chemotherapy drugs, including fluorouracil, a compound of fluoropyrimidine S-1, oxaliplatin, and all−trans−retinoic acid (ATRA), in gastric cancer cell lines with high SLC2A1 expression. High SLC2A1 expression was associated with poor prognosis, cancer cell proliferation, decreased immune cells, including CD8 T cells and B cells, and a low prognostic nutrition index, representing body nutrition-related status. In pathway network analysis, SLC2A1 was indirectly linked to the retinoic signaling pathway and negatively regulated immune cells/receptors. In the drug response analysis, the drug ATRA inhibited gastric cancer cell lines with high SLC2A1 expression. Treatment involving the use of SLC2A1 could contribute to better clinical management/research for patients with gastric cancer.

Pharmacological Synergism Between Cannabinoids and Paclitaxel in Gastric Cancer Cell Lines

2009 ◽  
Vol 155 (1) ◽  
pp. 40-47 ◽  
Author(s):  
Hideyo Miyato ◽  
Joji Kitayama ◽  
Hiroharu Yamashita ◽  
Daisuke Souma ◽  
Masahiro Asakage ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Lines ◽  
Gastric Cancer Cell Lines

scholarly journals Comprehensive analysis of the gene expression profiles in human gastric cancer cell lines

Oncogene ◽  
2002 ◽  
Vol 21 (42) ◽  
pp. 6549-6556 ◽  
Author(s):  
Jiafu Ji ◽  
Xin Chen ◽  
Suet Yi Leung ◽  
Jen-Tsan A Chi ◽  
Kent Man Chu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Comprehensive Analysis ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cell Lines

Low-Dose Oxaliplatin Enhances the Antitumor Efficacy of Paclitaxel in Human Gastric Cancer Cell Lines

Digestion ◽  
2006 ◽  
Vol 74 (1) ◽  
pp. 19-27 ◽  
Author(s):  
Jinyu Gu ◽  
Hirofumi Yamamoto ◽  
Xueying Lu ◽  
Chew Yee Ngan ◽  
Tadashi Tsujino ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Low Dose ◽  
Cancer Cell Lines ◽  
Antitumor Efficacy ◽  
Human Gastric Cancer ◽  
Human Gastric Cancer Cell ◽  
Gastric Cancer Cell Lines

scholarly journals Gastric Cancer Cell Lines Have DifferentMYC-Regulated Expression Patterns but Share a Common Core of Altered Genes

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Jersey Heitor da S. Maués ◽  
Helem Ferreira Ribeiro ◽  
Giovanny R. Pinto ◽  
Luana de Oliveira Lopes ◽  
Letícia M. Lamarão ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Common Core ◽  
Gastric Cancer Cell ◽  
Histological Subtypes ◽  
Gene Sets ◽  
Regulated Expression ◽  
Gastric Cancer Cell Lines

MYCis an oncogene responsible for excessive cell growth in cancer, enabling transcriptional activation of genes involved in cell cycle regulation, metabolism, and apoptosis, and is usually overexpressed in gastric cancer (GC). By using siRNA and Next-Generation Sequencing (NGS), we identifiedMYC-regulated differentially expressed Genes (DEGs) in three Brazilian gastric cancer cell lines representing the histological subtypes of GC (diffuse, intestinal, and metastasis). The DEGs were picked usingSailfishsoftware, followed by Gene Set Enrichment Analysis (GSEA) and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway analysis using KEGG. We found 11 significantly enriched gene sets by using enrichment score (ES), False Discovery Rate (FDR), and nominal P-values. We identified a total of 5.471 DEGs with correlation over (80%). In diffuse-type and in metastatic GC cell lines,MYC-silencing caused DEGs downregulation, while the intestinal-type GC cells presented overall DEGs upregulation afterMYCsiRNA depletion. We were able to detect 11 significant gene sets when comparing our samples to the hallmark collection of gene expression, enriched mostly for the following hallmarks: proliferation, pathway, signaling, metabolic, and DNA damage response. When we analyzed our DEGs considering KEGG metabolic pathways, we found 12 common branches covering a wide range of biological functions, and three of them were common to all three cell lines: ubiquitin-mediated proteolysis, ribosomes, and system and epithelial cell signaling inHelicobacter pyloriinfection. The GC cell lines used in this study share 14MYC-regulated genes, but their gene expression profile is different for each histological subtype of GC. Our results present a computational analysis ofMYC-related signatures in GC, and we present evidence that GC cell lines representing distinct histological subtypes of this disease have differentMYC-regulated expression profiles but share a common core of altered genes. This is an important step towards the understanding ofMYC’s role in gastric carcinogenesis and an indication of probable new drug targets in stomach cancer.

scholarly journals IFT80 Improves Invasion Ability in Gastric Cancer Cell Line via ift80/p75NGFR/MMP9 Signaling

2018 ◽  
Vol 19 (11) ◽  
pp. 3616 ◽  
Author(s):  
Rui Wang ◽  
Xiaoyan Deng ◽  
Chengfu Yuan ◽  
Hongmei Xin ◽  
Geli Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Reverse Transcription ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Quantitative Reverse Transcription Pcr ◽  
Reverse Transcription Pcr ◽  
Gastric Cancer Cell Lines

The assembly and maintenance of cilia depend on intraflagellar transport (IFT) proteins, which play an important role in development and homeostasis. IFT80 is a newly defined IFT protein and partial mutation of IFT80 in humans causes diseases such as Jeune asphyxiating thoracic dystrophy (JATD) and short rib polydactyly (SRP) type III, both characterized by abnormal skeletal development. However, the role and mechanism of IFT80 in the invasion of gastric cancer is unknown. We established SGC-7901 and MKN-45 gastric cancer cell lines that stably overexpressed IFT80, as verified by quantitative reverse transcription-PCR, Western blot, and immunofluorescence. Matrix metalloproteinase-9 (MMP9) plays an important role in tumor invasion, and its expression was assessed by quantitative reverse transcription-PCR, Western blotting, and immunofluorescence. The invasion ability of IFT80 on SGC-7901 and MKN-45 cells was examined by the Matrigel invasion assay. The relationship between p75NGFR, and the p75NGFR antagonists, PD90780 and IFT80, were detected by quantitative reverse transcription-PCR and Western blotting. We first detected an IFT80 expression pattern, and found that IFT80 was highly expressed in gastric cancer clinical samples. Overexpression of IFT80 in the gastric cancer cell lines, SGC-7901 and MKN-45, led to lengthening cilia. Additionally, overexpression of IFT80 significantly improved proliferation and invasion, but inhibited apoptosis, in gastric cancer cells. We further found that overexpression of IFT80 increased p75NGFR and MMP9 mRNA and protein expression. Treatment with the p75NGFR antagonist PD90780 inhibited the increased invasion ability resulting from overexpression of IFT80 in SGC-7901 and MKN-45 gastric cancer cells. Thus, these results suggest that IFT80 plays an important role in invasion of gastric cancer through regulating the ift80/p75NGFR/MMP9 signal pathways.

scholarly journals Inhibition of cell proliferation in gastric cancer cell lines on exposure to rubriflordilactone A

2015 ◽  
Vol 11 (1) ◽  
pp. 63
Author(s):  
Shang-Jin Peng ◽  
Jue-Wei Chen
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Underlying Mechanism ◽  
Cancer Cell Lines ◽  
Epithelial Cell Line ◽  
Similar Reduction ◽  
Gastric Cancer Cell Lines

<p class="Abstract">The present study investigates the effect of rubriflordilactone A on the viability and its underlying mechanism in gastric cancer cell lines (SNU-1 and SNU-5) and normal gastric epithelial cell line (GES‑1). Incubation of the gastric cancer and non cancer cell lines in acidic media led to reduction in the viability of the non cancer cells without any effect on cancer cells. Apoptosis in SNU-1 and SNU-5 cells was induced on exposure to rubriflordilactone A after 48 hours compared to the control cells (p&lt;0.01). The percentage of apoptosis in SNU-1 and SNU-5 cells on exposure to rubriflordilactone A was 79.3 ± 4.7 and 74.0 ± 5.1, respectively after 48 hours. Exposure of SNU-1 and SNU-5 cancer cell lines to rubriflordilactone A at a concentration of 10 μM in media with acidic pH decreased phosphorylation of ERK ½. The similar reduction was caused by ERK 1/2 phosphorylation inhibition, PD98059. Thus rubriflordilactone A reduces viability of gastric cancer cell lines by inducing apoptosis through the reduction of ERK 1/2 phosphorylation.</p><p> </p>

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