Abstract
Background:
Cervical cancer (CC) is regarded as one of the most common gynecological malignancies. LncRNA DLX6-AS1 has been proven vital in various cancers, whereas its exact function is still largely unestablished in CC.
Materials and Methods:
The expression pattern of DLX6-AS1 and miR-16-5p in CC cells was determined by real-time quantitative polymerase chain reaction (RT-qPCR). ARPP19 expression was assessed by RT-qPCR and Western blot assays in CC cells. The precise function of DLX6-AS1 in CC was detected by Cell-Counting Kit-8 (CCK-8), 5-ethynyl-2′-deoxyuridine (EdU), caspase-3 activity, transwell, and Western blot experiments. RNA immunoprecipitation (RIP) and luciferase reporter assays were employed to certify the combination between miR-16-5p and DLX6-AS1 (or ARPP19). Nuclear cytoplasmic segmentation determined the localization of DLX6-AS1 in CC cells. A xenograft mouse model assay studied the influences of DLX6-AS1 silencing on CC progression in vivo.
Results:
Elevated DLX6-AS1 expression was disclosed in CC cells. DLX6-AS1 silence attenuated proliferation, migration, and epithelial–mesenchymal transition program as well as enhanced CC cell apoptosis. DLX6-AS1 was uncovered to sponge and negatively modulate miR-16-5p in CC. Besides, ARPP19 was uncovered as a downstream target gene of miR-16-5p in CC. Rescue experiments indicated that DLX6-AS1 enhanced the cellular process of CC cells through upregulating ARPP19. Moreover, in vivo assay confirmed that DLX6-AS1 promoted CC growth.
Conclusions:
DLX6-AS1 accelerates the progression of CC through sponging miR-16-5p and upregulates ARPP19, which offers a novel insight into prognosis and remedy of CC.
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Supplementary Material
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