scholarly journals miRNA Expression Profiling Regulates Epithelial Mesenchymal Transition in 125I Seed Irradiation of Gastric Carcinoma Cell

2021 ◽  
Author(s):  
Zhenhuan Ma ◽  
Zhen Li ◽  
Lei Zou ◽  
Guojian Li ◽  
Yan Bao ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cell ◽  
125I Seed ◽  
Control Groups ◽  
Gastric Carcinoma Cell ◽  
Smad Pathway ◽  
Mesenchymal Transition ◽  
Seed Irradiation ◽  
And Control

Abstract Backgroud The aim of this study is to examine miRNA profiling and miR-1285-3p participates in 125I seed irradiation of gastric carcinoma cell via the regulation of epithelial mesenchymal transition (EMT). Methods An in vitro I-125 seed irradiation model was established, followed by the small RNA-Sequencing to investigate the full spectrum of miRNAs that are response to I-125 seed implantation. Validation was performed with quantitative real time PCR (qRT-PCR). qRT-PCR was also employed to measure miR-1285-3p and EMT-related mRNAs expression. Western blotting assay was performed to test the expression of EMT-related proteins. Luciferase reporter assay was conducted to confirm the direct targeting of SMAD2/3 and SMAD4 by miR-1285-3p.Results A total of 1034 miRNAs were initially detected. Of these, 11 miRNAs were significantly differentially expressed between I-125 seed irradiation and control groups. Six miRNAs (hsa-miR-127-3p, hsa-miR-1285-3p, hsa-miR-296-5p, hsa-miR-421, hsa-miR-495-3p, and hsa-miR-548am-3p) were up regulation and five miRNAs (hsa-miR-17-5p, hsa-miR-193b-5p, hsa-miR-23b-5p, hsa-miR-483-5p, hsa-miR-92a-1-5p) were down regulation between I-125 seed irradiation treatment and control groups. EMT is involved in gastric cancer cells treatment with I-125 seed implantation, and downregulation of miR-1285-3p can repress EMT through its targeting of SMAD pathway, which make miR-1285-3p a novel target of I-125 therapeutic intervention for human gastric cancer.Conclusions This study revealed that miR-1285-3p inhibited EMT by targeting SMAD pathway in 125I seed irradiation of gastric carcinoma.

scholarly journals ADAM17 promotes epithelial-mesenchymal transition via TGF-β/Smad pathway in gastric carcinoma cells

2016 ◽  
Vol 49 (6) ◽  
pp. 2520-2528 ◽  
Author(s):  
Min Xu ◽  
Hailang Zhou ◽  
Chunli Zhang ◽  
Junbo He ◽  
Hong Wei ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Smad Pathway ◽  
Mesenchymal Transition

scholarly journals Pyruvate Kinase M2 Knockdown Suppresses Migration, Invasion, and Epithelial-Mesenchymal Transition of Gastric Carcinoma via Hypoxia-Inducible Factor Alpha/B-Cell Lymphoma 6 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Ning Li ◽  
Dandan Meng ◽  
Yue Xu ◽  
Ling Gao ◽  
Fengqian Shen ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Cell Lines ◽  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Hypoxia Inducible Factor ◽  
B Cell Lymphoma ◽  
Gastric Carcinoma Cell ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Gastric carcinoma is a common malignant cancer. Pyruvate kinase M2 (PKM2) is highly expressed in cancers, including gastric carcinoma. However, its function and molecular mechanism in gastric carcinoma remains unclear. Here, we aimed to explore the function and the underlying mechanism of PKM2 on malignant phenotypes in gastric carcinoma. In this study, the mRNA levels and protein levels of PKM2 in gastric carcinoma cell lines and normal gastric mucosa epithelial cell lines were detected using quantitative real-time PCR and western blot, respectively. PKM2 was downregulated by siRNA transfection. HIF-1α or BCL-6 was upregulated by corresponding overexpression plasmid. Cell viability was detected using CCK-8 assay. Cell invasion and migration were determined using transwell assay. Higher expression of PKM2 was observed in human gastric carcinoma cell lines MKN-45 and SGC-7901 than in the normal gastric mucosa epithelial cell line GES-1. PKM2 knockdown suppressed cancer cell invasion and migration and inhibited the epithelial-mesenchymal transition (EMT) phenotype by inhibiting E-cadherin and promoting vimentin and N-cadherin expression. Also, we observed that PKM2 knockdown suppressed the hypoxia-inducible factor alpha (HIF-1α) and B-cell lymphoma 6 (BCL-6) signaling pathway. HIF-1α overexpression reversed the function of PKM2 silencing on cell invasion, migration, EMT, and BCL-6 expression. BCL-6 overexpression also reversed the function of PKM2 silencing on cell invasion, migration, and EMT but did not affect HIF-1α expression. Taken together, data from our study suggest that PKM2 knockdown impeded cell migration, invasion, and EMT of gastric carcinoma cells via the HIF-1α/BCL-6 pathway.

Mucins and mucin-associated carbohydrate antigens expression in gastric carcinoma cell lines

1999 ◽  
Vol 435 (5) ◽  
pp. 479-485 ◽  
Author(s):  
F. Carvalho ◽  
Leonor David ◽  
Jean-Pierre Aubert ◽  
Anna López-Ferrer ◽  
Carme De Bolós ◽  
...  
Keyword(s):  
Gastric Carcinoma ◽  
Cell Lines ◽  
Carcinoma Cell ◽  
Gastric Carcinoma Cell ◽  
Carbohydrate Antigens ◽  
Carcinoma Cell Lines ◽  
Gastric Carcinoma Cell Lines

scholarly journals RON Mediates Tumor-Promoting Effects in Endometrial Adenocarcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Qin Yu ◽  
Jianzhang Wang ◽  
Tiantian Li ◽  
Xinxin Xu ◽  
Xinyue Guo ◽  
...  
Keyword(s):  
Nude Mice ◽  
Reproductive Tract ◽  
Epithelial Mesenchymal Transition ◽  
Endometrial Adenocarcinoma ◽  
Female Reproductive Tract ◽  
Migration And Invasion ◽  
Smad Pathway ◽  
Mesenchymal Transition ◽  
Adenocarcinoma Cells

Endometrial adenocarcinoma is one of the most prevalent female reproductive tract cancers in the world, and the development of effective treatment is still the main goal of its current research. Epithelial-mesenchymal transition (EMT) plays a significant part in the occurrence and development of epithelial carcinoma, including endometrial adenocarcinoma. Recepteur d’origine nantais (RON) induces EMT and promotes proliferation, migration, and invasion in various epithelial-derived cancers, but its role in endometrial adenocarcinoma is still poorly studied. The purpose of this study is to verify the overexpression of RON in endometrial adenocarcinoma and to explore its specific roles. RON expression in tumor lesions was verified by immunohistochemical staining, HEC-1B cells were used to construct stable cell lines with RON overexpression or knockdown to investigate the effects of RON on the function of endometrial adenocarcinoma cells, and xenotransplantation experiment was carried out in nude mice to explore the effect of RON on the growth of endometrial adenocarcinoma in vivo. This study revealed that RON could promote the proliferation, migration, and invasion of HEC-1B cells and induce EMT, and these effects were regulated through the Smad pathway. RON overexpression could promote growth of endometrial adenocarcinoma cells in nude mice, while its inhibitor BMS777607 could restrict this role. RON played an important role in endometrial adenocarcinoma and had a potential to become a new therapeutic target for endometrial adenocarcinoma.

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