4.3 Article

Long non-coding RNA NEAT1 regulates epithelial membrane protein 2 expression to repress nasopharyngeal carcinoma migration and irradiation-resistance through miR-101-3p as a competing endogenous RNA mechanism

Journal

ONCOTARGET
Volume 8, Issue 41, Pages 70156-70171

Publisher

IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.19596

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Funding

  1. National Natural Science Foundation of China [81672553]
  2. China Postdoctoral Science Foundation [2016M602696]
  3. Sichuan Youth Science and Technology Foundation [2016JQ0060]
  4. Sichuan University [2015SCU04A13]

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The altered expression of long non-coding RNAs (lncRNAs) is often related to carcinogenesis, metastasis and resistance to radiation or chemotherapy. In the current study, cDNA microarray analysis found that NEAT1 expression was reduced in nasopharyngeal carcinoma (NPC) patients and that it regulated NPC progression. However, the detailed mechanisms of NEAT1 in NPC were unclear. NEAT1 repressed NPC cell growth, invasion and radiation resistance in vitro and tumor metastasis in vivo. In addition, the results of an approach integrating bioinformatics, luciferase reporter assays and RNA immunoprecipitation indicated that NEAT1 antagonized miR-101-3p through a competing endogenous RNA (ceRNA) mechanism and that the interaction between NEAT1 and EMP2 was miR-101-3p dependent. Our results showed a novel connection of NEAT1, miR-101-3p and EMP2 in NPC migration and radiation resistance.

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