ArticleMolecular medicine reports2015
MicroRNA‑205 promotes the tumorigenesis of nasopharyngeal carcinoma through targeting tumor protein p53-inducible nuclear protein 1.
Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- MiRNA signatures in nasopharyngeal carcinoma: molecular mechanisms and therapeutic perspectives.American journal of cancer research · 2023Review
- Induction of p27 contributes to inhibitory effect of isorhapontigenin (ISO) on malignant transformation of human urothelial cells.Cell cycle (Georgetown, Tex.) · 2022Article
- Effect of miR-184 and miR-205 on the tumorigenesis of conjunctival mucosa associated lymphoid tissue lymphoma through regulating RasL10B and TNFAIP8.International journal of ophthalmology · 2022Article
- Identification of a 7-microRNA signature in plasma as promising biomarker for nasopharyngeal carcinoma detection.Cancer medicine · 2020Observational
- miR-205-5p inhibits cell migration and invasion in prostatic carcinoma by targeting ZEB1.Oncology letters · 2018Article
- MicroRNA-342 inhibits cell proliferation and invasion in nasopharyngeal carcinoma by directly targeting ZEB1.Oncology letters · 2018Article
- Relevance of MicroRNA200 Family and MicroRNA205 for Epithelial to Mesenchymal Transition and Clinical Outcome in Biliary Tract Cancer Patients.International journal of molecular sciences · 2016Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nasopharyngeal carcinoma (NPC) is a common type of cancer in southern China, miRNAs have been shown to be involved in the tumorigenesis of multiple cancer types. The present study aimed to explore the potential role of miR‑205 in NPC. Reverse transcription quantitative polymerase chain reaction was used to determine the expression levels of miR‑205 in 20 fresh NPC specimens and 20 normal nasopharyngeal tissues. The function of miR‑205 in the proliferation, migration, invasion and apoptosis of NPC‑derived cells was detected by MTT assay, colony formation assay, wound healing assay, Transwell assay and flow cytometry. Furthermore, a target gene of miR‑205 was identified using the luciferase reporter assay. The expression of miR‑205 was increased in NPC tissues compared with that in normal tissues. Overexpression of miR‑205 was found to promote the proliferation, migration and invasion of NPC‑derived cells, while apoptosis was suppressed. Tumor protein p53-inducible nuclear protein 1 was identified as a target gene of miR‑205. Overall, the present study demonstrated that miR‑205 may function as an oncogene in NPC tumorigenesis.
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Registered trials
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