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长链非编码RNA LINC00525通过吸附miR-338-3p调控人胶质瘤细胞的增殖及上皮-间质转化。

Long non-coding RNA LINC00525 regulates the proliferation and epithelial to mesenchymal transition of human glioma cells by sponging miR-338-3p.

作者信息

Wan Yilv, Liang Feng, Wei Minjun, Liu Ying

机构信息

Deparment of Neurosurgery, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.

Deparment of Stomatology, The First Affiliated Hospital of Nanchang University, Nanchang, 330006, Jiangxi, China.

出版信息

AMB Express. 2020 Aug 28;10(1):156. doi: 10.1186/s13568-020-01094-4.

Abstract

Long non-coding RNA (LncRNA) LINC00525 has been shown to be upregulated in several human cancers and deduced to possess caner regulatory role. The regulation of molecular mechanics of human glioma by lncRNA-LINC00525 through microRNA sponging in glioma is elusive. The lncRNA-LINC00525 showed significant (P < 0.05) upregulation in glioma cancer cells. The upregulation of lncRNA-LINC00525 was upto 6.6-fold in glioma cells relative to the normal cells. Knockdown of lncRNA-LINC00525 significantly declined the proliferation of the glioma cancer cells. Additionally, the colony formation was inhibited by around 60% in glioma cells. The wound healing and transwell assays revealed significant (P < 0.05) inhibition of migration and invasion potential under lncRNA-LINC00525 knockdown. The western blotting study of biomarkers of epithelial to mesenchymal transition (EMT) revealed that lncRNA-LINC00525 gene silencing reduced the expression of mesenchymal molecular markers but increased the protein levels of epithelial markers. miR-338-3p was predicted to be interacting with lncRNA-LINC00525 in glioma and was shown to mediated the regulatory role of lncRNA-LINC00525. Taken together, the results of present study are supportive of the prognostic applicability of lncRNA-LINC00525 against human glioma together with its therapeutic potential against the said malignancy.

摘要

长链非编码RNA(LncRNA)LINC00525已被证明在多种人类癌症中上调,并被推断具有癌症调节作用。lncRNA-LINC00525通过在胶质瘤中充当微小RNA海绵对人类胶质瘤分子机制的调节尚不清楚。lncRNA-LINC00525在胶质瘤癌细胞中显示出显著上调(P < 0.05)。相对于正常细胞,lncRNA-LINC00525在胶质瘤细胞中的上调高达6.6倍。敲低lncRNA-LINC00525显著降低了胶质瘤癌细胞的增殖。此外,胶质瘤细胞中的集落形成受到约60%的抑制。伤口愈合和Transwell实验表明,敲低lncRNA-LINC00525后,细胞的迁移和侵袭能力受到显著抑制(P < 0.05)。上皮-间质转化(EMT)生物标志物的蛋白质印迹研究表明,lncRNA-LINC00525基因沉默降低了间质分子标志物的表达,但增加了上皮标志物的蛋白质水平。预测miR-338-3p在胶质瘤中与lncRNA-LINC00525相互作用,并介导lncRNA-LINC00525的调节作用。综上所述,本研究结果支持lncRNA-LINC00525对人类胶质瘤的预后适用性及其对所述恶性肿瘤的治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/15a3/7455684/20364a7e1ec7/13568_2020_1094_Fig1_HTML.jpg

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