ArticleCancer management and research2020
miR-665 Suppresses the Epithelial-Mesenchymal Transition and Progression of Gastric Cancer by Targeting
Article in Cancer management and 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.
- The functional role of the extracellular matrix in inflammatory bowel disease associated gut fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- MicroRNA-665 and its potential role in drug response and survival outcomes in multiple myeloma: a preliminary study.Frontiers in pharmacology · 2025Article
- Deregulated circRNAs in Epithelial Ovarian Cancer With Activity in PreclinicalCancer genomics & proteomics · 2024Review
- A novel circular RNA, circMAML3, promotes tumor progression of prostate cancer by regulating miR-665/MAPK8IP2 axis.Cell death discovery · 2023Article
- Review
- Interfering HMGB3 release from cancer-associated fibroblasts by miR-200b represses chemoresistance and epithelial-mesenchymal transition of gastric cancer cells.Journal of gastrointestinal oncology · 2022Article
- LncRNA RPSAP52 promotes cell proliferation and inhibits cell apoptosis via modulating miR-665/STAT3 in gastric cancer.Bioengineered · 2022Article
- Circ_0078767 Inhibits the Progression of Non-Small-Cell Lung Cancer by Regulating the GPX3 Expression by Adsorbing miR-665.International journal of genomics · 2022Article
- MicroRNA-1269b inhibits gastric cancer development through regulating methyltransferase-like 3 (METTL3).Bioengineered · 2021Article
- Downregulation of MIAT reduces the proliferation and migratory and invasive abilities of retinoblastoma cells by sponging miR-665 and regulating LASP1.Experimental and therapeutic medicine · 2021Article
- MicroRNAs in Epithelial-Mesenchymal Transition Process of Cancer: Potential Targets for Chemotherapy.International journal of molecular sciences · 2021Review
- MicroRNA-665 regulates the proliferation, apoptosis and adhesion of gastric cancer cells by binding to cadherin 3.Oncology letters · 2021Article
- LncRNA DCST1-AS1 Promotes Endometrial Cancer Progression by Modulating the MiR-665/HOXB5 and MiR-873-5p/CADM1 Pathways.Frontiers in oncology · 2021Article
- CircRNA_100876 Is Upregulated in Gastric Cancer (GC) and Promotes the GC Cells' Growth, Migration and Invasion via miR-665/YAP1 Signaling.Frontiers in genetics · 2020Article
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5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastric cancer (GC) is one of the most common aggressive cancers and is characterized by high mortality. Increasing evidence has shown that microRNA-665 (miRNA-665) serves as inhibiting-miRNA in cancers. However, the role of miR-665 in GC is yet unclear.
methodsmiR-665 was first analyzed using bioinformatics. Subsequent quantitative real-time PCR was used to detect miR-665 expression levels in different GC cell lines and tissues. The function of miR-665 in GC cells was determined via Cell Counting Kit 8, colony formation, wound healing, and transwell assays. Furthermore, Western blotting was utilized to measure the expression level of epithelial-mesenchymal transition (EMT)-related proteins. The target prediction and luciferase reporter assays were performed to confirm the binding between miR-665 and 3'-UTR of the
resultsThe expression of miR-665 was significantly decreased in GC patients and GC cell lines. Clinical and pathological analyses showed that the low expression of miR-665 was significantly associated with high TNM stage (P = 0.007), distant metastasis (P = 0.031), and poor differentiation (P = 0.029). Endogenic mimics of miR-665 remarkably suppressed GC cell proliferation, migration, invasion, and EMT in in vitro experiments. Inhibition of miR-665 expression induced the opposite effects. The results of the bioinformatics analysis and dual-luciferase assay showed that miR-665 targeted the 3'-UTR of the
conclusionThe overall study results demonstrated that miR-665 inhibits tumor progression and EMT in GC by targeting
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