کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2815866 1569844 2015 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Lentiviral DDX46 knockdown inhibits growth and induces apoptosis in human colorectal cancer cells
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی ژنتیک
پیش نمایش صفحه اول مقاله
Lentiviral DDX46 knockdown inhibits growth and induces apoptosis in human colorectal cancer cells
چکیده انگلیسی


• DDX46 is highly expressed in human colorectal cancer tissues.
• The cellular localization of DDX46 is focused in the nucleus of epithelial cells.
• DDX46 silencing inhibits cell proliferation and induces apoptosis in human colorectal cancer cells.

Colorectal cancer (CRC) is one of the leading causes of cancer related deaths worldwide. RNA helicases have been widely implicated in various types of cancer development. DDX46 belongs to the DEAD box family of RNA helicases, which are involved in the regulation of secondary RNA structures. The expression pattern of DDX46 in cancer tissues and the role of DDX46 in CRC progression have not been determined. In this study, we detected DDX46 protein expression in human CRC and adjacent tissues using immunohistochemistry. Our results showed that 87.04% of the columnar adenocarcinoma cases displayed high levels of focal nuclear DDX46 staining, and DDX46 protein expression was strongly increased in CRC tissues compared to adjacent tissues. Next, DDX46 RNAi lentivirus (DDX46-RNAi-LV) was used to silence the expression of DDX46 in the human colon carcinoma cells. Cells treated with the DDX46-RNAi-LV exhibited markedly reduced cell proliferation assessed by the MTT assay and visualized colony formation. Moreover, DDX46 silencing resulted in apoptotic induction via increased expression of cleaved caspase-3 and PARP. These results indicate that DDX46 is critical for CRC cell proliferation and is a potential therapeutic target for CRC treatment.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 560, Issue 2, 15 April 2015, Pages 237–244
نویسندگان
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