ArticleTranslational cancer research2020
EDIL3 regulates gastric cancer cell migration, invasion and epithelial-mesenchymal transition via TGF-β1/XIST/miR-137 feedback loop.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
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- The Marine Triterpene Stellettin B Triggers Mitochondrial-to-Nuclear Translocation of AIF/EndoG and Reverses Epithelial-Mesenchymal Transition to Inhibit Oral Cancer Progression.International journal of medical sciences · 2026Article
- Elucidating the multiscale mechanisms and therapeutic targets of caffeic acid in gastric cancer: a synergy of computational and experimental approaches.Frontiers in molecular biosciences · 2025Article
- Nischarin inhibits the epithelial-mesenchymal transition process and angiogenesis in breast cancer cells by inactivating FAK/ERK signaling pathway via EGF like repeats and discoidin domains 3.Molecular biology reports · 2024Article
- Key genes and molecular mechanisms related to Paclitaxel Resistance.Cancer cell international · 2024Review
- Oncogenic and immunological role of EDIL3 in human tumours: From pan-cancer analysis to validation in gastric cancer.Heliyon · 2024Article
- Epidermal Growth Factor-Like Repeats and Discoidin I-Like Domains 3 Deficiency Attenuates Dilated Cardiomyopathy by Inhibiting Ubiquitin Specific Peptidase 10 Dependent Smad4 Deubiquitination.Journal of the American Heart Association · 2024Article
- Article
- EMT-related gene classifications predict the prognosis, immune infiltration, and therapeutic response of osteosarcoma.Frontiers in pharmacology · 2024Article
- ZNF643/ZFP69B Exerts Oncogenic Properties and Associates with Cell Adhesion and Immune Processes.International journal of molecular sciences · 2023Article
- EDIL3 as an Angiogenic Target of Immune Exclusion Following Checkpoint Blockade.Cancer immunology research · 2023Article
- Syndecan-4 is a maestro of gastric cancer cell invasion and communication that underscores poor survival.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- EDIL3 is a potential prognostic biomarker that correlates with immune infiltrates in gastric cancer.PeerJ · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundHuman gastric cancer is a serious disease with high mortality rate all over the world. The one of difficulties in effective therapy of gastric cancer is metastasis. It has been reported that lncRNAs and miRNAs are involved in cancer metastasis. So, exploration of new molecular mechanism underlying gastric cancer metastasis involving in network of lncRNAs/miRNAs/effector proteins is important and meaningful for guiding the treatment of gastric cancer.
methodsMTT assay, flow cytometric analysis and colony formation assay were performed to evaluate AGS or MKN-45 cell proliferation, cycle distribution and colony formation, and RT-qPCR was used to examine the expressive abundances of EDIL3, XIST and miR-137. EDIL3 and epithelial-mesenchymal transition (EMT) related proteins were detected by western blot and migration and invasion were measured by transwell analysis. Meanwhile, Dual-luciferase reporter gene assay was used to confirm XIST binding to miR-137, and miR-137 binding to EDIL3. AGS cells were used to establish the xenograft tumor model to verify the role of EDIL3 in tumorigenesis in nude mice.
resultsExpression levels of EDIL3 was increased in gastric cancer tissues and cell lines. Downregulation of EDIL3 or XIST and overexpression of miR-137 inhibited proliferation, migration, invasion and EMT in AGS and MKN-45 cells. XIST could specifically bind to miR-137, and EDIL3 was a target gene of miR-137. Moreover, TGF-β1 stimulated XIST expression, inhibited miR-137 expression and induced migration, invasion and EMT. We also found that overexpression of EDIL3 elevated levels of TGF-β1 and induced migration, invasion and EMT, which were reversed by TGF-β1 inhibition. EDIL3 knockdown suppressed migration, invasion and EMT, which were reversed by XIST. Overexpression of miR-137 inhibited proliferation, migration, invasion and EMT, which were reversed by EDIL3 overexpression.
conclusionsEDIL3 regulates gastric cancer cell migration, invasion and EMT, which is involved in the regulation of TGF-β1/XIST/miR-137 feedback loop, and EDIL3 knockdown inhibits tumor growth in nude mice. These findings indicate that the EDIL3 mediated molecular feedback loop may be developed as drug targets for the gastric carcinoma treatment.
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