کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5505208 | 1400263 | 2017 | 19 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Functional evidence that the self-renewal gene NANOG regulates esophageal squamous cancer development
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Cancer cell molecular mimicry of stem cells (SC) follows with enhanced proliferative and renewal capacities. In support, numerous mediators of SC self-renewal have been evinced to exhibit oncogenic potential. More and more researches showed that the embryonic stem cell self-renewal genes express in various cancer cells. In this study, we sought to test the tumorigenic functions of NANOG, particularly, in esophageal cancer (EC). Using quantitative RT-PCR and western blotting, we confirmed that EC cells highly express NANOG mRNA and protein. We then constructed a shRNA-mediated plasmid to knockdown of NANOG mRNA. We observed that NANOG deficiency in Eca109Â cells decreased clone formation, cell proliferation, and showed G1 arrest. To further investigate the functions and mechanisms of NANOG in Eca109Â cells, we detected the changes of multiple signaling molecules when NANOG deficiency. We foud that NANOG deficiency affected multiple genes, particularly, supressed drug-resistance via down-regulated ABCG2 in Eca109Â cells, and caused G1 arrest by down-regulated cyclin D1 (CCND1) expression. The present loss-of-function work, establish the integral role for NANOG in Eca109Â cell proliferation, drug resistance, and shed light on its mechanisms of action.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 490, Issue 2, 19 August 2017, Pages 161-168
Journal: Biochemical and Biophysical Research Communications - Volume 490, Issue 2, 19 August 2017, Pages 161-168
نویسندگان
Li Deng, Xiaocong Xiang, Fei Yang, Dongqin Xiao, Kang Liu, Zhu Chen, Ruolan Zhang, Gang Feng,