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microRNA-93, upregulated in serum of nasopharyngeal carcinoma patients, promotes tumor cell proliferation by targeting PDCD4
Deregulation of microRNAs (miRs) has been demonstrated to contribute to the development and malignant progression of nasopharyngeal carcinoma (NPC). Recently, miR-93 was reported to be significantly upregulated in NPC tissues and cell lines, and promote the proliferation, migration and invasion of N...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7086147/ https://www.ncbi.nlm.nih.gov/pubmed/32256737 http://dx.doi.org/10.3892/etm.2020.8520 |
Sumario: | Deregulation of microRNAs (miRs) has been demonstrated to contribute to the development and malignant progression of nasopharyngeal carcinoma (NPC). Recently, miR-93 was reported to be significantly upregulated in NPC tissues and cell lines, and promote the proliferation, migration and invasion of NPC cells in vitro, as well as tumor growth in vivo. However, whether there is any clinical value of serum miR-93 expression in NPC still remains unclear. Therefore, the present study aimed to explore the clinical significance of serum miR-93 expression in NPC. A total of 85 serum samples from NPC patients and 30 from healthy controls were collected. Reverse transcription-quantitative polymerase chain reaction data demonstrated that the serum expression of miR-93 was significantly increased in NPC patients, when compared with those in healthy controls. Following receiving chemo-radiotherapy, the serum miR-93 levels were significantly decreased in NPC patients. Furthermore, the increased serum levels of miR-93 were significantly associated with advanced grade, clinical stage, lymph node metastasis, as well as worse 5-year overall survival of NPC patients. Furthermore, the serum miR-93 expression was demonstrated to be an independent factor for predicating the prognosis of NPC. In vitro experiments demonstrated that knockdown of miR-93 caused a decrease in NPC cell proliferation, whereas overexpression of miR-93 promoted NPC cell proliferation. PDCD4 was then identified as a direct target of miR-93 in NPC cells. Overexpression of PDCD4 significantly eliminated the promoting effects of miR-93 overexpression on NPC cell proliferation. Taken together, these findings suggest that the serum miR-93 expression could be used as a predicator for the clinical outcome of NPC patients, and suggest that miR-93 may also become a potential therapeutic target for NPC treatment. |
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