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.

中文翻译：

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LINC01133通过使miR-4784海绵化以上调AHDC1来促进宫颈癌的进展。

宫颈癌是最致命的妇科肿瘤，发生率高，在恶性细胞过程中表现出异常表达的lncRNAs。公认的长基因间非蛋白质编码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LINC01133在宫颈癌中的功能和相应的机制。LINC01133表达谱通过挖掘癌症基因组图谱（TCGA）数据库和qRT-PCR分析进行了验证。揭示了LINC01133的一个明显上调的表达。CCK-8，锥虫蓝排除法，EdU和Transwell迁移分析的结果表明LINC01133对宫颈癌具有促进作用。LINCO1133也加剧了上皮-间质转化（EMT）。沉默LINCO1133可促进子宫颈癌细胞的凋亡率。在机械上，LINC01133充当ceRNA靶向miR-4784，以增强AHDC1表达。最后，LINCO1133 / miR-4784以依赖AHDC1的方式加剧了宫颈癌的恶性生长，侵袭性和EMT。