Abstract
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.