ArticleExperimental and therapeutic medicine2018
MicroRNA-663b promotes cell proliferation and epithelial mesenchymal transition by directly targeting SMAD7 in nasopharyngeal carcinoma.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Occlusion enhanced pan-cancer classification via deep learning.BMC bioinformatics · 2024Article
- Hsa_circ_0004214 involved in the epithelial-mesenchymal transition induced by beryllium sulfate through modulating JAK-STAT signaling pathway.Toxicology research · 2024Article
- Extracellular Vesicle MicroRNAs From Corneal Stromal Stem Cell Enhance Stemness of Limbal Epithelial Stem Cells by Targeting the Notch Pathway.Investigative ophthalmology & visual science · 2023Article
- An Overview of Epithelial-to-Mesenchymal Transition and Mesenchymal-to-Epithelial Transition in Canine Tumors: How Far Have We Come?Veterinary sciences · 2022Review
- Effect of microRNA-663b on migration, invasion and epithelial‑mesenchymal transition of oral squamous cell carcinoma cells.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2022Article
- Cervical cancer-derived exosomal miR-663b promotes angiogenesis by inhibiting vinculin expression in vascular endothelial cells.Cancer cell international · 2021Article
- Exosomal miR‑663b exposed to TGF‑β1 promotes cervical cancer metastasis and epithelial‑mesenchymal transition by targeting MGAT3.Oncology reports · 2021Article
- MicroRNA-663b enhances migration and invasion by targeting adenomatous polyposis coli 2 in colorectal carcinoma cells.Oncology letters · 2020Article
- Downregulation of miRNA-663b protects against hypoxia-induced injury in cardiomyocytes by targeting BCL2L1.Experimental and therapeutic medicine · 2020Article
- miR-663b promotes colorectal cancer progression by activating Ras/Raf signaling through downregulation of TNK1.Human cell · 2020Article
- The role of contextual signal TGF-β1 inducer of epithelial mesenchymal transition in metastatic lung adenocarcinoma patients with brain metastases: an update on its pathological significance and therapeutic potential.Contemporary oncology (Poznan, Poland) · 2019Review
- Expression and Role of MicroRNA-663b in Childhood Acute Lymphocytic Leukemia and its Mechanism.Open medicine (Warsaw, Poland) · 2019Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRs) serve important roles in the development of various types of human cancer, including nasopharyngeal carcinoma (NPC). In the present study, the expression levels of miR-663b in NPC were investigated and its role and underlying mechanisms were examined. Reverse transcription-quantitative polymerase chain reaction was performed to assess miR-663b expression levels in NPC tissues and C666-1 cells. TargetScan was applied to predict the putative targets of miR-663b and the dual luciferase reporter assay was used to confirm the predictions. To investigate the role of miR-663b in NPC, the NPC C666-1 cell line was transfected with miR-663b mimics, miR-663b inhibitors or negative control. The Cell Counting kit-8 assay was performed for cell proliferation detection and western blot analysis was applied to determine the expression levels of epithelial mesenchymal transition (EMT)-associated proteins. Results indicated that when compared with the adjacent normal tissues and the normal nasopharyngeal epithelial cells, miR-663b expression levels were significantly upregulated in the NPC tissues and the NPC cells (P<0.01). Notably, SMAD7 is a target gene of miR-663b and may be inhibited by miR-663b. Results indicated that NPC cell proliferation was significantly promoted by miR-663b mimics and significantly inhibited by miR-663b inhibitors (P<0.05 and P<0.01). In addition, the results indicated that, when compared with the negative control group the expression levels of E-cadherin were significantly decreased, whereas the expression levels of N-cadherin, Vimentin and matrix metalloproteinase-9 were significantly increased in the cells of the miR-663b mimics group (P<0.05 and P<0.01). However, cells in the miR-663b inhibitors group exhibited the opposite effects. In conclusion, the results of the present study indicated that miR-663b functions as a tumor promoter in NPC via promoting NPC cell proliferation and EMT by directly targeting SMAD7.
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