scholarly journals Core 1–derived mucin-type O-glycosylation protects against spontaneous gastritis and gastric cancer

2019 ◽  
Vol 217 (1) ◽  
Author(s):  
Fei Liu ◽  
Jianxin Fu ◽  
Kirk Bergstrom ◽  
Xindi Shan ◽  
J. Michael McDaniel ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Critical Role ◽  
Gastric Epithelium ◽  
Tn Antigen ◽  
Gastric Mucus ◽  
Truncated Form ◽  
Gastric Cancer Patients ◽  
Gastric Cancer Progression

Core 1–derived mucin-type O-glycans (O-glycans) are a major component of gastric mucus with an unclear role. To address this, we generated mice lacking gastric epithelial O-glycans (GEC C1galt1−/−). GEC C1galt1−/− mice exhibited spontaneous gastritis that progressed to adenocarcinoma with ∼80% penetrance by 1 yr. GEC C1galt1−/− gastric epithelium exhibited defective expression of a major mucus forming O-glycoprotein Muc5AC relative to WT controls, which was associated with impaired gastric acid homeostasis. Inflammation and tumorigenesis in GEC C1galt1−/− stomach were concurrent with activation of caspases 1 and 11 (Casp1/11)–dependent inflammasome. GEC C1galt1−/− mice genetically lacking Casp1/11 had reduced gastritis and gastric cancer progression. Notably, expression of Tn antigen, a truncated form of O-glycan, and CASP1 activation was associated with tumor progression in gastric cancer patients. These results reveal a critical role of O-glycosylation in gastric homeostasis and the protection of the gastric mucosa from Casp1-mediated gastric inflammation and cancer.

scholarly journals The Emerging Role of GC-MSCs in the Gastric Cancer Microenvironment: From Tumor to Tumor Immunity

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Zhaoji Pan ◽  
Yiqing Tian ◽  
Guoping Niu ◽  
Chengsong Cao
Keyword(s):  
Gastric Cancer ◽  
Tumor Microenvironment ◽  
Cancer Progression ◽  
Wound Repair ◽  
Critical Role ◽  
The Novel ◽  
Potential Biomarker ◽  
Underlying Mechanisms ◽  
Gastric Cancer Progression

Mesenchymal stem cells (MSCs) have been declared to not only participate in wound repair but also affect tumor progression. Tumor-associated MSCs, directly existing in the tumor microenvironment, play a critical role in tumor initiation, progression, and development. And different tumor-derived MSCs have their own unique characteristics. In this review, we mainly describe and discuss recent advances in our understanding of the emerging role of gastric cancer-derived MSC-like cells (GC-MSCs) in regulating gastric cancer progression and development, as well as the bidirectional influence between GC-MSCs and immune cells of the tumor microenvironment. Moreover, we also discuss the potential biomarker and therapeutic role of GC-MSCs. It is anticipated that new and deep insights into the functionality of GC-MSCs and the underlying mechanisms will promote the novel and promising therapeutic strategies against gastric cancer.

scholarly journals NUSAP1 Promotes Gastric Cancer Progression Through Regulation of Yap Stability

2020 ◽  
Author(s):  
Hui Guo ◽  
Jianping Zou ◽  
Ling Zhou ◽  
Yan He ◽  
Miao Feng ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Target Genes ◽  
Hippo Pathway ◽  
Critical Role ◽  
Xenograft Model ◽  
Migration And Invasion

Abstract Background:Nucleolar and spindle associated protein (NUSAP1) is involved in tumor initiation, progression and metastasis. However, there are limited studies regarding the role of NUSAP1 in gastric cancer (GC). Methods: The expression profile and clinical significance of NUSAP1 in GC were analysed in online database using GEPIA, Oncomine and KM plotter, which was further confirmed in clinical specimens.The functional role of NUSAP1 were detected utilizing in vitro and in vivo assays. Western blotting, qRT-PCR, the cycloheximide-chase, immunofluorescence staining and Co-immunoprecipitaion (Co-IP) assays were performed to explore the possible molecular mechanism by which NUSAP1 stabilizes YAP protein. Results:In this study, we found that the expression of NUSAP1 was upregulated in GC tissues and correlates closely with progression and prognosis. Additionally, abnormal NUSAP1 expression promoted malignant behaviors of GC cells in vitro and in a xenograft model. Mechanistically, we discovered that NUSAP1 physically interacts with YAP and furthermore stabilizes YAP protein expression, which induces the transcription of Hippo pathway downstream target genes. Furthermore, the effects of NUSAP1 on GC cell growth, migration and invasion were mainly mediated by YAP. Conclusions:Our data demonstrates that the novel NUSAP1-YAP axis exerts an critical role in GC tumorigenesis and progression, and therefore could provide a novel therapeutic target for GC treatment.

scholarly journals Microbiome signatures in a fast and slow progressing gastric cancer murine model and their contribution to gastric carcinogenesis

2020 ◽  
Author(s):  
Prerna Bali ◽  
Joanna Coker ◽  
Ivonne Lozano-Pope ◽  
Karsten Zengler ◽  
Marygorret Obonyo
Keyword(s):  
Gastric Cancer ◽  
Microbial Diversity ◽  
Cancer Progression ◽  
Double Knockout ◽  
Histological Data ◽  
H Pylori ◽  
Faster Development ◽  
Gastric Cancer Progression ◽  
Development Of Gastric Cancer

AbstractGastric cancer is the third most common cancer in the world and Helicobacter spp. being one of the main factors responsible for development of cancer. Alongside Helicobacter the microbiota of the stomach mucosa may also play an important role in gastric cancer progression. Previously we had established that MyD88 deficient mice rapidly progressed to neoplasia when infected with H. felis. Thus, in order to assess the role of microbiota in gastric cancer progression we measured the changes in microbial diversity of the stomach in mice with different genotypic backgrounds (Wild type (WT), MyD88 deficient (MyD88−/−), mice deficient in the Toll/IL-1R (TIR) domain-containing adaptor-inducing interferon-β (TRIF, Triflps2), and MyD88 and Trif deficient (MyD88−/− and Trif−/−)double knockout (DKO) mice), both in uninfected and Helicobacter infected mice and its correlation of these changes with gastric cancer progression. We observed that there was an overall reduction in microbial diversity post infection with H. felis across all genotypes. Campylobacterales were observed in all infected mice, with marked reduction in abundance at 3 and 6 months in MyD88−/− mice. This low abundance of H. pylori could facilitate dominance of other organisms of microbiome like Lactobacilliales. A sharp increase in Lactobacilliales in infected MyD88−/− and DKO mice at 3 and 6 months was observed as compared to Trif−/− and WT mice suggesting its possible role in gastric cancer progression. This was further reinforced upon comparison of Lactobacillus ratio with histological data suggesting that Lactobacillales is closely associated with Helicobacter infection and gastric cancer progression. Thus, this study firstly suggests that difference in genotypes could define the stomach microbiome and make it more susceptible to development of gastric cancer upon Helicobacter infections. Secondly the increase in Lactobacillales could contribute to faster development of gastric cancer and serve as a probable bio marker for fast progressing form of gastric cancer.

The role of caveolin-1 in gastric cancer progression

2007 ◽  
Vol 45 (08) ◽  
Author(s):  
E Burgermeister ◽  
X Xing ◽  
M Hiber ◽  
C Röcken ◽  
R Schmid ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Caveolin 1 ◽  
Gastric Cancer Progression

Role of hMLH1 and E-Cadherin Promoter Methylation in Gastric Cancer Progression

2013 ◽  
Vol 45 (1) ◽  
pp. 40-47 ◽  
Author(s):  
Meysam Moghbeli ◽  
Omeed Moaven ◽  
Bahram Memar ◽  
Hamid Reza Raziei ◽  
Azadeh Aarabi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Promoter Methylation ◽  
Gastric Cancer Progression ◽  
E Cadherin

scholarly journals Increased prevalence of precancerous changes in relatives of gastric cancer patients: Critical role of H. pylori

2000 ◽  
Vol 118 (1) ◽  
pp. 22-30 ◽  
Author(s):  
Emad M. El–Omar ◽  
Karin Oien ◽  
Lilian S. Murray ◽  
Adil El–Nujumi ◽  
Angela Wirz ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Patients ◽  
Critical Role ◽  
H Pylori ◽  
Gastric Cancer Patients

scholarly journals The different role of intratumoral and peritumoral lymphangiogenesis in gastric cancer progression and prognosis

BMC Cancer ◽  
2015 ◽  
Vol 15 (1) ◽  
Author(s):  
Kyung Ho Pak ◽  
Ara Jo ◽  
Hye Ji Choi ◽  
Younghee Choi ◽  
Hyunki Kim ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Gastric Cancer Progression

scholarly journals Sialosyl-Tn, antigen as a marker of gastric cancer progression: An international study

1996 ◽  
Vol 69 (3) ◽  
pp. 193-199 ◽  
Author(s):  
J. Lawrence Werther ◽  
Masac Tatematsu ◽  
Roger Klein ◽  
Minoru Kurihara ◽  
Kazulade Kumagat ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
International Study ◽  
Tn Antigen ◽  
Gastric Cancer Progression

scholarly journals ELK4-mediated lncRNA SNHG22 promotes gastric cancer progression through interacting with EZH2 and regulating miR-200c-3p/Notch1 axis

2021 ◽  
Author(s):  
Xiaqiong Mao ◽  
Tao Ji ◽  
Aiguo Liu ◽  
Yunqi Weng
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Tumor Suppressor Genes ◽  
Luciferase Reporter ◽  
Diagnosis And Prognosis ◽  
Reporter Assays ◽  
Non Coding Rnas ◽  
Gastric Cancer Progression ◽  
Proliferation And Invasion

Abstract Background Long non-coding RNAs (lncRNAs) play important regulatory roles in the initiation and progression of various cancers. However, the biological roles and the potential mechanisms of lncRNAs in gastric cancers remain unclear. Methods The expression of SNHG22 in gastric cancer was analyzed in public databases (TCGA) and validated via qRT-PCR. SNHG22 knockdown cell lines were construced, and cell proliferation and invasion were analyzed. CHIP and luciferase reporter assays were performed to clarify the transcriptional role of ELK4. RNA pull-down followed MS and RIP assays were employed to identify the interaction between SNHG22 and EZH2. Luciferase reporter assays and RIP assays were used to confirm the regulation of SNHG22 on Notch1 by sponging miR-2003-3p. Results Knockdown of SNHG22 inhibited the proliferation and invasion ability of GC cells. Moreover, we identified that the transcriptional factor, ELK4, could promote SNHG22 expression in GC cells. In addition, using RNA pull-down followed MS assay, we found that SNHG22 directly bound to EZH2 to suppress the expression of tumor suppressor genes. At the same time, SNHG22 sponged miR-200c-3p to increase Notch1 expression. Conclusions Taken together, our findings demonstrated the role of SNHG22 on promoting proliferation and invasion of GC cells. And we revealed a new regulatory mechanism of SNHG22 in GC cells. SNHG22 is a promising lncRNA biomarker for diagnosis and prognosis and a potential target for GC treatment.

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