کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5589369 | 1569829 | 2017 | 20 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia
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کلمات کلیدی
TKIslncRNAFBSHULCFITCshRNAHOX transcript antisense RNAqRT-PCRCMLlncRNAsc-Myc - c-mycHCC - HCCPI3K/AKT - PI3K / AKTshort hairpin RNA - RNA موی سر کوتاهLong non-coding RNAs - RNA های بدون کدگذاری طولانیmiR-200a - به miR-200Aquantitative real time PCR - زمان واقعی PCR کمیfetal bovine serum - سرم جنین گاوBlast phase - فاز انفجارchronic phase - فاز مزمنfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتChronic myeloid leukemia - لوسمی میلوئید مزمنTyrosine kinase inhibitors - مهار کننده های تیروزین کینازHepatocellular carcinoma - کارسینوم هپاتوسلولار(کارسینوم سلولهای استخوانی)
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
ژنتیک
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia](/preview/png/5589369.png)
چکیده انگلیسی
Aberrant expression of long noncoding RNA (lncRNA) HULC is associated with various human cancers. However, the role of HULC in chronic myeloid leukemia (CML) is unknown. In this study, we found that HULC was remarkably overexpressed in both leukemia cell lines and primary hematopoietic cells derived from CML patients. The increase in HULC expression was positively correlated with clinical stages in CML. Moreover, the knockdown of HULC significantly inhibited CML cell proliferation and induced apoptosis by repressing c-Myc and Bcl-2. Furthermore, inhibition of HULC enhanced imatinib-induced apoptosis of CML cells. Further experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity. Furthermore, HULC could modulate c-Myc and Bcl-2 by miR-200a as an endogenous sponge. Taken together, these results reveal that HULC promotes oncogenesis in CML and suggest a potential strategy for the CML treatment.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 607, 5 April 2017, Pages 41-46
Journal: Gene - Volume 607, 5 April 2017, Pages 41-46
نویسندگان
Yinghao Lu, Yan Li, Xiao Chai, Qian Kang, Peng Zhao, Jie Xiong, Jishi Wang,