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MiR-205 determines the radioresistance of human nasopharyngeal carcinoma by directly targeting PTEN
- Source :
- Cell Cycle. 11:785-796
- Publication Year :
- 2012
- Publisher :
- Informa UK Limited, 2012.
-
Abstract
- Radiotherapy is the primary treatment for nasopharyngeal carcinoma (NPC), but radioresistance severely reduces NPC radiocurability. Here, we have established a radio-resistant NPC cell line, CNE-2R, and investigate the role of miRNAs in radioresistance. The miRNAs microarray assay reveals that miRNAs are differentially expressed between CNE-2R and its parental cell line CNE-2. We find that miR-205 is elevated in CNE-2R. A target prediction algorithm suggests that miR-205 regulates expression of PTEN, a tumor-suppressor. Introducing miR-205 into CNE-2 cells suppresses PTEN protein expression, followed by activation of AKT, increased number of foci formation and reduction of cell apoptosis post-irradiation. On the other hand, knocking down miR-205 in CNE-2R cells compromises the inhibition of PTEN and increases cell apoptosis. Significantly, immunohistochemistry studies demonstrate that PTEN is downregulated at late stages of NPC, and that miR-205 is significantly elevated followed the radiotherapy. Our data conclude that miR-205 contributes to radioresistance of NPC by directly targeting PTEN. Both miR-205 and PTEN are potential predictive biomarkers for radiosensitivity of NPC and may serve as targets for achieve successful radiotherapy in NPC.
- Subjects :
- Blotting, Western
Nasopharyngeal neoplasm
Radiation Tolerance
Cell Line, Tumor
Report
Radioresistance
microRNA
otorhinolaryngologic diseases
medicine
Humans
PTEN
Molecular Biology
Protein kinase B
Cell Proliferation
Nasopharyngeal Carcinoma
biology
Reverse Transcriptase Polymerase Chain Reaction
Cell growth
Carcinoma
PTEN Phosphohydrolase
Nasopharyngeal Neoplasms
Cell Biology
Flow Cytometry
medicine.disease
MicroRNAs
stomatognathic diseases
Nasopharyngeal carcinoma
Apoptosis
biology.protein
Cancer research
Developmental Biology
Subjects
Details
- ISSN :
- 15514005 and 15384101
- Volume :
- 11
- Database :
- OpenAIRE
- Journal :
- Cell Cycle
- Accession number :
- edsair.doi.dedup.....da68a36f89e1c667a801698930882eec
- Full Text :
- https://doi.org/10.4161/cc.11.4.19228