scholarly journals Penicillin‑binding protein 1A mutation‑positive Helicobacter�pylori promotes epithelial‑mesenchymal transition in gastric cancer via the suppression of microRNA‑134

2018 ◽  
Author(s):  
Lu Huang ◽  
Zhi‑Yong Wang ◽  
Dao‑Dong Pan
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Epithelial Mesenchymal Transition ◽  
Binding Protein ◽  
Penicillin Binding Protein ◽  
Mesenchymal Transition

Roles of Helicobacter pylori in the Epithelial-Mesenchymal Transition of Gastric Cancer

2020 ◽  
Vol 04 (04) ◽  
Author(s):  
Shuai Ruan ◽  
Wenjie Huang ◽  
Fang Wen ◽  
Xiaona Lu ◽  
Su Ping Gu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals Mechanisms of the Epithelial–Mesenchymal Transition and Tumor Microenvironment in Helicobacter pylori-Induced Gastric Cancer

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 1055 ◽  
Author(s):  
Jacek Baj ◽  
Izabela Korona-Głowniak ◽  
Alicja Forma ◽  
Amr Maani ◽  
Elżbieta Sitarz ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Epithelial Mesenchymal Transition ◽  
Treatment Strategies ◽  
Gastric Ulcers ◽  
Heparin Binding ◽  
Human Pathogens ◽  
Mesenchymal Transition ◽  
Cytotoxin Associated Gene A ◽  
H Pylori

Helicobacter pylori (H. pylori) is one of the most common human pathogens, affecting half of the world’s population. Approximately 20% of the infected patients develop gastric ulcers or neoplastic changes in the gastric stroma. An infection also leads to the progression of epithelial–mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial–mesenchymal transition associated with malignant transformation within the gastric stroma. The reviewed factors included: CagA (cytotoxin-associated gene A) along with induction of cancer stem-cell properties and interaction with YAP (Yes-associated protein pathway), tumor necrosis factor α-inducing protein, Lpp20 lipoprotein, Afadin protein, penicillin-binding protein 1A, microRNA-29a-3p, programmed cell death protein 4, lysosomal-associated protein transmembrane 4β, cancer-associated fibroblasts, heparin-binding epidermal growth factor (HB-EGF), matrix metalloproteinase-7 (MMP-7), and cancer stem cells (CSCs). The review summarizes the most recent findings, providing insight into potential molecular targets and new treatment strategies for gastric cancer.

scholarly journals Calcium Binding Protein S100A16 Expedites Proliferation, Invasion and Epithelial-Mesenchymal Transition Process in Gastric Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Xiaoying You ◽  
Min Li ◽  
Hongwei Cai ◽  
Wenwen Zhang ◽  
Ye Hong ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Calcium Binding ◽  
Epithelial Mesenchymal Transition ◽  
Malignant Tumors ◽  
Binding Protein ◽  
Transition Process ◽  
Calcium Binding Protein ◽  
Mesenchymal Transition

Gastric cancer (GC) is one of the most common malignant tumors of the digestive system, listed as the second cause of cancer-related deaths worldwide. S100 Calcium Binding Protein A16 (S100A16) is an acidic calcium-binding protein associated with several types of tumor progression. However, the function of S100A16 in GC is still not very clear. In this study, we analyzed S100A16 expression with the GEPIA database and the UALCAN cancer database. Meanwhile, 100 clinical GC samples were used for the evaluation of its role in the prognostic analysis. We found that S100A16 is significantly upregulated in GC tissues and closely correlated with poor prognosis in GC patients. Functional studies reveal that S100A16 overexpression triggers GC cell proliferation and migration both in vivo and in vitro; by contrast, S100A16 knockdown restricts the speed of GC cell growth and mobility. Proteomic analysis results reveal a large S100A16 interactome, which includes ZO-2 (Zonula Occludens-2), a master regulator of cell-to-cell tight junctions. Mechanistic assay results indicate that excessive S100A16 instigates GC cell invasion, migration, and epithelial-mesenchymal transition (EMT) via ZO-2 inhibition, which arose from S100A16-mediated ZO-2 ubiquitination and degradation. Our results not only reveal that S100A16 is a promising candidate biomarker in GC early diagnosis and prediction of metastasis, but also establish the therapeutic importance of targeting S100A16 to prevent ZO-2 loss and suppress GC metastasis and progression.

scholarly journals TAZ Controls Helicobacter pylori-Induced Epithelial–Mesenchymal Transition and Cancer Stem Cell-Like Invasive and Tumorigenic Properties

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1462 ◽  
Author(s):  
Camille Tiffon ◽  
Julie Giraud ◽  
Silvia Elena Molina-Castro ◽  
Sara Peru ◽  
Lornella Seeneevassen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Epithelial Mesenchymal Transition ◽  
Gastric Carcinogenesis ◽  
Gastric Epithelium ◽  
Binding Motif ◽  
Mesenchymal Transition ◽  
H Pylori

Helicobacter pylori infection, the main risk factor for gastric cancer (GC), leads to an epithelial–mesenchymal transition (EMT) of gastric epithelium contributing to gastric cancer stem cell (CSC) emergence. The Hippo pathway effectors yes-associated protein (YAP) and transcriptional co-activator with PDZ binding motif (TAZ) control cancer initiation and progression in many cancers including GC. Here, we investigated the role of TAZ in the early steps of H. pylori-mediated gastric carcinogenesis. TAZ implication in EMT, invasion, and CSC-related tumorigenic properties were evaluated in three gastric epithelial cell lines infected by H. pylori. We showed that H. pylori infection increased TAZ nuclear expression and transcriptional enhancer TEA domain (TEAD) transcription factors transcriptional activity. Nuclear TAZ and zinc finger E-box-binding homeobox 1 (ZEB1) were co-overexpressed in cells harboring a mesenchymal phenotype in vitro, and in areas of regenerative hyperplasia in gastric mucosa of H. pylori-infected patients and experimentally infected mice, as well as at the invasive front of gastric carcinoma. TAZ silencing reduced ZEB1 expression and EMT phenotype, and strongly inhibited invasion and tumorsphere formation induced by H. pylori. In conclusion, TAZ activation in response to H. pylori infection contributes to H. pylori-induced EMT, invasion, and CSC-like tumorigenic properties. TAZ overexpression in H. pylori-induced pre-neoplastic lesions and in GC could therefore constitute a biomarker of early transformation in gastric carcinogenesis.

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