ArticleJournal of translational medicine2014
MicroRNA-362 induces cell proliferation and apoptosis resistance in gastric cancer by activation of NF-κB signaling.
Article in Journal of translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 92 citations in OpenAlex.
- Mechanisms of chemoresistance in gastric cancer: interplay between microRNAs and the tumor microenvironment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Article
- Cancer-associated fibroblast miR-148a-5p/CALD1/collagen VI pathway promotes proliferation in Helicobacter pylori-positive gastric cancer.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Three possible diagnostic biomarkers for gastric cancer: miR-362-3p, miR-362-5p and miR-363-5p.Biomarkers in medicine · 2024Article
- Mechanism of cisplatin resistance in gastric cancer and associated microRNAs.Cancer chemotherapy and pharmacology · 2023Review
- ER Negative Breast Cancer and miRNA: There Is More to Decipher Than What the Pathologist Can See!Biomedicines · 2023Review
- Review
- miR-874-3p mitigates cisplatin resistance through modulating NF-κB/inhibitor of apoptosis protein signaling pathway in epithelial ovarian cancer cells.Molecular and cellular biochemistry · 2022Article
- Contribution of MicroRNAs in Chemoresistance to Cisplatin in the Top Five Deadliest Cancer: An Updated Review.Frontiers in pharmacology · 2022Review
- NF-κB in Gastric Cancer Development and Therapy.Biomedicines · 2021Review
- Inhibitory feedback control of NF-κB signalling in health and disease.The Biochemical journal · 2021Review
- Cascades between miRNAs, lncRNAs and the NF-κB signaling pathway in gastric cancer (Review).Experimental and therapeutic medicine · 2021Review
- MicroRNAs as the critical regulators of cisplatin resistance in gastric tumor cells.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2021Review
- Knockdown of microRNA-130b improves doxorubicin sensitivity in bladder urothelial carcinoma by negatively regulating cylindromatosis expression.Archives of medical science : AMS · 2021Article
- Mechanisms of Action And Clinical Implications of MicroRNAs in the Drug Resistance of Gastric Cancer.Frontiers in oncology · 2021Review
- MicroRNA-362 negatively and positively regulates SMAD4 expression in TGF-β/SMAD signaling to suppress cell migration and invasion.International journal of medical sciences · 2021Article
- The role of deubiquitinating enzymes in gastric cancer.Oncology letters · 2020Review
- Comparison of microRNA Expression Profile in Chronic Myeloid Leukemia Patients Newly Diagnosed and Treated by Allogeneic Hematopoietic Stem Cell Transplantation.Frontiers in oncology · 2020Article
- Long non‑coding RNA MEG‑3 suppresses gastric carcinoma cell growth, invasion and migration via EMT regulation.Molecular medicine reports · 2019Article
- MicroRNA-362 Inhibits Cell Proliferation and Invasion by Directly Targeting SIX1 in Colorectal Cancer.Yonsei medical journal · 2019Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAccording to cancer-related microRNA (miRNA) expression microarray research available in public databases, miR-362 expression is elevated in gastric cancer. However, the expression and biological role of miR-362 in gastric progression remain unclear.
methodsmiR-362 expression levels in gastric cancer tissues and cell lines were determined using real-time PCR. The roles of miR-362, in promoting gastric cancer cell proliferation and apoptosis resistance, were assessed by different biological assays, such as colony assay, flow cytometry and TUNEL assay. The effect of miR-362 on NF-κB activation was investigated using the luciferase reporter assay, fluorescent immunostaining.
resultsMiR-362 overexpression induced cell proliferation, colony formation, and resistance to cisplatin-induced apoptosis in BGC-823 and SGC-7901 gastric cancer cells. MiR-362 increased NF-κB activity and relative mRNA expression of NF-κB-regulated genes, and induced nuclear translocation of p65. Expression of the tumor suppressor CYLD was inhibited by miR-362 in gastric cancer cells; miR-362 levels were inversely correlated with CYLD expression in gastric cancer tissue. MiR-362 downregulated CYLD expression by binding its 3' untranslated region. NF-κB activation was mechanistically associated with siRNA-mediated downregulation of CYLD. MiR-362 inhibitor reversed all the effects of miR-362.
conclusionThe results suggest that miR-362 plays an important role in repressing the tumor suppressor CYLD and present a novel mechanism of miRNA-mediated NF-κB activation in gastric cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.