کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3163924 1198754 2015 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
MicroRNA-24 induces cisplatin resistance by targeting PTEN in human tongue squamous cell carcinoma
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی دندانپزشکی، جراحی دهان و پزشکی
پیش نمایش صفحه اول مقاله
MicroRNA-24 induces cisplatin resistance by targeting PTEN in human tongue squamous cell carcinoma
چکیده انگلیسی


• MicroRNA-24 target PTEN.
• miR-24 plays an important role in the cell survival and cisplatin resistance of TSCC.
• miR-24 induces cisplatin resistance primarily through targeting PTEN/Akt pathway.

SummaryBackgroundmiR-24 is one of the most significantly up-regulated miRNAs in tongue squamous cell carcinoma (TSCC). PTEN plays an important role in the cell survival and cisplatin resistance of multiple cancers. However, it remains unclear what role does function and mechanism of miR-24 and PTEN play in TSCC.Methodology/principal findingsIn this study, miR-24 expression was detected in 79 cases of paired TSCC and normal tissues and 8 TSCC cell lines by real-time PCR and the relevance between miR-24 expression and clinicopathological parameters were analyzed. Further, we demonstrated that deregulation of miR-24 was found to associate with high grade and late stage tumor. In addition, miR-24 induces cell survival and cisplatin resistance through targeting 3′-UTR region of the PTEN, which leads to downregulation of PTEN protein and activation of Akt pro-survival pathway.Conclusions/significanceIn conclusion, our results demonstrated that deregulation of miR-24 is a recurrent event in human tongue squamous cell carcinoma and associate with tumor progression and that miR-24 induces cell survival and cisplatin resistance primarily through targeting PTEN/Akt pathway. Thus, miR-24 could be important targets for intervention of this malignancy.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Oral Oncology - Volume 51, Issue 11, November 2015, Pages 998–1003
نویسندگان
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