scholarly journals Evaluation of Epithelial-Mesenchymal Transition Genes Involved in Iranian Gastric Cancer Patients via Transcriptome Analysis

2019 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Shima Abed ◽  
Kaveh Baghaei ◽  
Parviz Pakzad ◽  
Mehrdad Hashemi ◽  
Mohammad Reza Zali
Keyword(s):  
Gastric Cancer ◽  
Cancer Patients ◽  
Transcriptome Analysis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Gastric Cancer Patients

scholarly journals Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Jun Wang ◽  
Zhigang He ◽  
Bo Sun ◽  
Wenhai Huang ◽  
Jianbin Xiang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Patients ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
In Vivo Studies ◽  
Vimentin Expression ◽  
Mesenchymal Transition ◽  
Gastric Cancer Patients

Pleckstrin-2 (PLEK2) is a crucial mediator of cytoskeletal reorganization. However, the potential roles of PLEK2 in gastric cancer are still unknown. PLEK2 expression in gastric cancer was examined by western blotting and real-time PCR. Survival analysis was utilized to test the clinical impacts of the levels of PLEK2 in gastric cancer patients. In vitro and in vivo studies were used to estimate the potential roles played by PLEK2 in modulating gastric cancer proliferation, self-renewal, and tumourigenicity. Bioinformatics approaches were used to monitor the effect of PLEK2 on epithelial-mesenchymal transition (EMT) signalling pathways. PLEK2 expression was significantly upregulated in gastric cancer as compared with nontumour samples. Kaplan-Meier plotter analysis revealed that gastric cancer patients with higher PLEK2 levels had substantially poorer overall survival compared with gastric cancer patients with lower PLEK2 levels. The upregulation or downregulation of PLEK2 in gastric cancer cell lines effectively enhanced or inhibited cell proliferation and proinvasive behaviour, respectively. Additionally, we also found that PLEK2 enhanced EMT through downregulating E-cadherin expression and upregulating Vimentin expression. Our findings demonstrated that PLEK2 plays a potential role in gastric cancer and may be a novel therapeutic target for gastric cancer.

scholarly journals Inhibition or Reversal of the Epithelial-Mesenchymal Transition in Gastric Cancer: Pharmacological Approaches

2020 ◽  
Vol 22 (1) ◽  
pp. 277
Author(s):  
Joanna Kozak ◽  
Alicja Forma ◽  
Marcin Czeczelewski ◽  
Paweł Kozyra ◽  
Elżbieta Sitarz ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Patients ◽  
Epithelial Mesenchymal Transition ◽  
Inorganic Compounds ◽  
Treatment Modalities ◽  
Pharmacological Agents ◽  
Mesenchymal Transition ◽  
Gastric Cancer Treatment ◽  
Induction Of Resistance ◽  
Gastric Cancer Patients

Epithelial-mesenchymal transition (EMT) constitutes one of the hallmarks of carcinogenesis consisting in the re-differentiation of the epithelial cells into mesenchymal ones changing the cellular phenotype into a malignant one. EMT has been shown to play a role in the malignant transformation and while occurring in the tumor microenvironment, it significantly affects the aggressiveness of gastric cancer, among others. Importantly, after EMT occurs, gastric cancer patients are more susceptible to the induction of resistance to various therapeutic agents, worsening the clinical outcome of patients. Therefore, there is an urgent need to search for the newest pharmacological agents targeting EMT to prevent further progression of gastric carcinogenesis and potential metastases. Therapies targeted at EMT might be combined with other currently available treatment modalities, which seems to be an effective strategy to treat gastric cancer patients. In this review, we have summarized recent advances in gastric cancer treatment in terms of targeting EMT specifically, such as the administration of polyphenols, resveratrol, tangeretin, luteolin, genistein, proton pump inhibitors, terpenes, other plant extracts, or inorganic compounds.

scholarly journals Entrectinib Induces Apoptosis and Inhibits the Epithelial–Mesenchymal Transition in Gastric Cancer with NTRK Overexpression

2021 ◽  
Vol 23 (1) ◽  
pp. 395
Author(s):  
Sung-Hwa Sohn ◽  
Hee Jung Sul ◽  
Bum Jun Kim ◽  
Hyeong Su Kim ◽  
Dae Young Zang
Keyword(s):  
Gastric Cancer ◽  
Epithelial Mesenchymal Transition ◽  
High Expression ◽  
Mechanistic Study ◽  
Sequencing Analysis ◽  
Receptor Kinase ◽  
Ags Cells ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
Gastric Cancer Patients

Tropomyosin receptor kinase (TRK) and receptor tyrosine kinase (RTK class VII) expression are important in many human diseases, especially cancers, including colorectal, lung, and gastric cancer. Using RNA sequencing analysis, we evaluated the mRNA expression and mutation profiles of gastric cancer patients with neurotropic tropomyosin receptor kinase (NTRK) 1-3 overexpression (defined as a ≥2.0-fold change). Furthermore, we screened eight TRK inhibitors in NCI-N87, SNU16, MKN28, MKN7, and AGS cells. Among these inhibitors, entrectinib showed the highest inhibitory activity; therefore, this drug was selected for analysis of its therapeutic mechanisms in gastric cancer. Entrectinib treatment induced apoptosis in NTRK1-3-expressing and VEGFR2-expressing NCI-N87 and AGS cells, but it had no effect on NTRK1-3-, VEGFR2-, TGFBR1-, and CD274-expressing MKN7 cells. SNU16 and MKN28 cells with low NTRK1-3 expression were not affected by entrectinib. Therefore, a mechanistic study was conducted in NCI-N87 (high expression of NTRK1-3 but mutation of NTRK3), AGS (high expression of NTRK1-3) and MKN28 (low expression of NTRK1-3) gastric cancer cell lines. Entrectinib treatment significantly reduced expression levels of phosphorylated NFκB, AKT, ERK, and β-catenin in NCI-N87 and AGS cells, whereas it upregulated the expression levels of ECAD in NCI-N87 cells. Together, these results suggest that entrectinib has anti-cancer activity not only in GC cells overexpressing pan NTRK but also in VEGFR2 GC cells via the inhibition of the pan NTRK and VEGFR signaling pathways.

scholarly journals Transcriptomic profiling of single circulating tumor cells provides insight into human metastatic gastric cancer

2022 ◽  
Vol 5 (1) ◽  
Author(s):  
Ryo Negishi ◽  
Hitomi Yamakawa ◽  
Takeru Kobayashi ◽  
Mayuko Horikawa ◽  
Tatsu Shimoyama ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Single Cell ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Transcriptome Analysis ◽  
Epithelial Mesenchymal Transition ◽  
Metastatic Gastric Cancer ◽  
Isolation Technique ◽  
Mesenchymal Transition ◽  
Single Ctcs

AbstractTranscriptome analysis of circulating tumor cells (CTCs), which migrate into blood vessels from primary tumor tissues, at the single-cell level offers critical insights into the biology of metastasis and contributes to drug discovery. However, transcriptome analysis of single CTCs has only been reported for a limited number of cancer types, such as multiple myeloma, breast, hepatocellular, and prostate cancer. Herein, we report the transcriptome analysis of gastric cancer single-CTCs. We utilized an antigen-independent strategy for CTC isolation from metastatic gastric cancer patients involving a size-dependent recovery of CTCs and a single cell isolation technique. The transcriptomic profile of single-CTCs revealed that a majority of gastric CTCs had undergone epithelial-mesenchymal transition (EMT), and indicated the contribution of platelet adhesion toward EMT progression and acquisition of chemoresistance. Taken together, this study serves to employ CTC characterization to elucidate the mechanisms of chemoresistance and metastasis in gastric cancer.

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
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