4.5 Article

MicroRNA-148b suppresses proliferation, migration, and invasion of nasopharyngeal carcinoma cells by targeting metastasis-associated gene 2

期刊

ONCOTARGETS AND THERAPY
卷 10, 期 -, 页码 2815-2822

出版社

DOVE MEDICAL PRESS LTD
DOI: 10.2147/OTT.S135664

关键词

miR-148b; metastasis-associated gene 2; proliferation; invasion; nasopharyngeal carcinoma

资金

  1. Medical Scientific Research Foundation of Guangdong Province, China [A2016529, A2015105]
  2. Administration of Traditional Chinese Medicine of Guangdong Province, China [A20171148]
  3. National Natural Science Foundation of China [81201763]
  4. National Natural Science Foundation of Guangdong, China [2016A030310357]
  5. Science Research Foundation of Guangdong Medical University, China [M2015011]

向作者/读者索取更多资源

Purpose: MicroRNAs (miRNAs) play important roles in tumorigenesis and metastasis by regulating genes expression. MiRNA-148b (miR-148b) had been reported to inhibit tumor progression in some kinds of cancers, but the functions of miR-148b in nasopharyngeal carcinoma (NPC) remain largely unknown. The aim of this study was to investigate the functional role of miR-148b in NPC. Methods: Expression of miR-148b in NPC tissues and cell lines was detected by quantitative reverse transcription polymerase chain reaction. MiR-148b was overexpressed in CNE2 and C666-1 cells by miR-148b mimic transfection. The effects of miR-148b on cell proliferation, migration, and invasion were determined by colony formation assays, cell viability assays, and transwell assays. The target gene of miR-148b was investigated by luciferase assays, and the rescue experiment was performed. Results: MiR-148b was downregulated in NPC tissues and cell lines. Ectopic miR-148b expression significantly inhibited proliferation, migration, and invasion of CNE2 and C666-1 cells. We identified that metastasis-associated gene 2 (MTA2) is a direct target of miR-148b. Rescue experiment demonstrated that the tumor-suppressive effects of miR-148b on C666-1 cell were partly reversed by restoration of MTA2 expression. Moreover, miR-148b expression was negatively related to mRNA level of MTA2 in NPC tissues. Conclusion: Our findings elucidate that miR-148b negatively regulates the growth, migration, and invasion of NPC cells, at least in part, by targeting MTA2. The present study indicates that miR-148b is a potential therapeutic agent for NPC.

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