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LINC01133 promotes the progression of cervical cancer by sponging miR-4784 to up-regulate AHDC1

机译:LINC01133通过海绵miR-4784提升宫颈癌进展到上调AHDC1

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摘要

Cervical cancer, as the deadliest gynecological tumor with high risk of incidence, manifests aberrantly expressed lncRNAs in the malignant cellular processes. Long intergenic non-protein coding RNA 1133 (LINC01133) has been acknowledged to actively participate in aggressive tumor phenotypes. Our study focused on the identification of the function and corresponding mechanism of the novel molecule, LINC01133 in cervical cancer. LINC01133 expression profile was validated by digging The Cancer Genome Atlas (TCGA) database and qRT-PCR analysis. A considerably up-regulated expression of LINC01133 was unveiled. The results of CCK-8, trypan blue exclusion, EdU and transwell migration assays manifested the facilitating property of LINC01133 in cervical cancer. The epithelial–mesenchymal transition (EMT) was also exacerbated by LINCO1133. Apoptotic rate of cervical cancer cells was promoted after silencing LINCO1133. Mechanically, LINC01133 functioning as a ceRNA targeted miR-4784 to augment AHDC1 expression. Finally, LINCO1133/miR-4784 aggravated the malignant growth and aggressiveness and EMT of cervical cancer in an AHDC1-dependant way.
机译:宫颈癌,作为最致命的妇科肿瘤,发病率高,表达恶性细胞过程中的异常表达LNCRNA。已经承认,长期非蛋白质编码RNA 1133(LINC01133)积极参与侵袭性肿瘤表型。我们的研究重点是鉴定新型分子的功能和相应机制,LINC01133在宫颈癌中。通过挖掘癌症基因组Atlas(TCGA)数据库和QRT-PCR分析来验证LINC01133表达谱。揭开了LINC01133的大量上调表达。 CCK-8,台盼蓝排除,EDU和Transwell迁移测定的结果表现出宫颈癌LINC01133的促进性质。上皮 - 间充质转换(EMT)也被Linco1133加剧。沉默LINCO1133后促进了宫颈癌细胞的凋亡率。机械地,LINC01133用作CERNA目标MIR-4784以增强AHDC1表达。最后,LINCO1133 / MIR-4784以AHDC1依赖的方式加剧了宫颈癌的恶性生长和侵袭性和EMT。

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