Long non-coding RNA H19 promotes glucose metabolism and cell growth in malignant melanoma via miR-106a-5p/E2F3 axis

Journal of Cancer Research and Clinical Oncology - Tập 144 - Trang 531-542 - 2018
Wenkang Luan1, Zhou Zhou2, Xin Ni3, Yun Xia1, Jinlong Wang1, Yulan Yan4, Bin Xu1
1Department of Plastic Surgery, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, China
2Department of Neurosurgery, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, China
3Department of Gastroenterology, Affiliated Hospital of Jiangsu University, Zhenjiang, China
4Department of Respiratory Medicine, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, China

Tóm tắt

lncRNA H19 has been considered as an oncogenic lncRNA in many human tumours. In the present study, we identify the role and molecular mechanism of lncRNA H19 in melanoma. QRT-PCR was used to detect the expression of lncRNA H19 and E2F3 was detected in melanoma tissues. Cell counting kit-8 (CCK8), representative metabolites analysis was used to explore the biological function of lncRNA H19, miR-106a-5p and E2F3 in melanoma cells. Bioinformatics, luciferase reporter assays, MS2-RIP and RNA pull-down assay was used to demonstrate the molecular mechanism of lncRNA H19 in melanoma. We further test the function of lncRNA H19 in vivo though Xenograft tumour assay. We found that lncRNA H19 was increased in melanoma tissue, and lncRNA H19 was correlated with poor prognosis of melanoma patients. miR-106a-5p acts as a tumour suppressor in melanoma by targeting E2F3. E2F3 affects the melanoma cell glucose metabolism and growth. We also demonstrated that lncRNA H19 may function as the sponge of miR-106a-5p to up-regulate E2F3 expression, and consequently promote the glucose metabolism and growth of melanoma. This result elucidates a new mechanism for lncRNA H19 in melanoma development and provides a survival indicator and potential therapeutic target for melanoma patients.

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