کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2816040 1159911 2015 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Functional linc-POU3F3 is overexpressed and contributes to tumorigenesis in glioma
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی ژنتیک
پیش نمایش صفحه اول مقاله
Functional linc-POU3F3 is overexpressed and contributes to tumorigenesis in glioma
چکیده انگلیسی


• Linc-POU3F3 levels were extraordinarily associated with the tumor WHO grade.
• Linc-POU3F3 and POU3F3 have reverse correlated with expression in glioma.
• Linc-POU3F3 affects colony formation and cell proliferation of glioma cells.
• Linc-POU3F3 could serve as a position marker, recruiting regulators to target gene.

Growing number of long intergenic noncoding RNAs (lincRNAs) have recently been identified in mammals as new modulators in cancer origination and progression involved in a broad range of biological processes. Long intergenic noncoding RNA POU3F3 (linc-POU3F3) has been characterized as a highly conserved functional transcription regulator in esophageal squamous cell carcinoma. The contributions of this lincRNA to glioblastoma remain unknown. In this present study, we investigated the expression pattern and functional role of linc-POU3F3 in glioma by using real-time PCR and gain-/loss-of-function studies. The results revealed that linc-POU3F3 levels were extraordinarily associated with the tumor WHO grade. In related biochemical assays, overexpression of linc-POU3F3 promotes cell viability and proliferation in glioma cells, whereas knockdown of linc-POU3F3 showed the opposite effect. As expected, we also found that linc-POU3F3 expression was negatively correlated with the mRNA level of POU3F3 (the evolutionarily conserved neighbor gene of linc-POU3F3). Our results indicate that linc-POU3F3 might affect glioma development via altering expression level of POU3F3, and lead us to believe that linc-POU3F3 may also have a crucial regulatory role in glioma progression.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 554, Issue 1, 1 January 2015, Pages 114–119
نویسندگان
, , , , ,