کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
11010964 | 1804489 | 2019 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
MicroRNA-645 represses hepatocellular carcinoma progression by inhibiting SOX30-mediated p53 transcriptional activation
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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
Amount of evidence demonstrate that aberrant microRNAs (miRNAs) are involved in tumorigenesis and progression in hepatocellular carcinoma (HCC). Among them, miR-645 is recently recognized as cancer-related miRNA and its significance in HCC remains largely unknown. In this study, we reported for the first that miR-645 expression was markedly elevated in HCC tissues and cell lines, and its up-regulation was associated with malignant clinical features, including tumor size and venous infiltration and poor prognosis. Our data revealed that miR-645 promoted cell proliferation, colony formation and inhibited apoptosis by gain- and loss-of function experiments in vitro. In vivo assays showed that miR-645 overexpression enhanced tumor growth. Moreover, miR-645 directly bound to the SOX30 3â²-UTR and post-transcriptionally repressed SOX30 expression in HCC cells. Furthermore, miR-645 inversely correlated with SOX30 expression in HCC tissues. Restoration of SOX30 expression at least partially abolished the biological effects of miR-645 on HCC cells. SOX30 regulated HCC progression through aberrant activation of p53 by directly binding to its promoter. Taken together, this research supports the first evidence that miR-645 exerts an oncogenic role in HCC progression and may be a therapeutic target for HCC treatment.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Journal of Biological Macromolecules - Volume 121, January 2019, Pages 214-222
Journal: International Journal of Biological Macromolecules - Volume 121, January 2019, Pages 214-222
نویسندگان
Jie Tao, Zhikui Liu, Yufeng Wang, Liang Wang, Guozhi Yin, Wei Yang, Kangsheng Tu, Qingguang Liu,