Downregulation of long noncoding RNA DGCR5 contributes to the proliferation, migration, and invasion of cervical cancer by activating Wnt signaling pathway
| Autor: | Yuan-Yuan Xiang, Shuxiong Lu, Yue Chang, Yun Liu |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Physiology Clinical Biochemistry Down-Regulation Mice Nude Uterine Cervical Neoplasms Apoptosis HeLa Small hairpin RNA 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Cell Movement Cell Line Tumor medicine Animals Humans Gene silencing Neoplasm Invasiveness Wnt Signaling Pathway Tumor Stem Cell Assay Cell Proliferation Cervical cancer Mice Inbred BALB C biology Cell growth Wnt signaling pathway Cell Biology medicine.disease biology.organism_classification Gene Expression Regulation Neoplastic 030104 developmental biology 030220 oncology & carcinogenesis Disease Progression Cancer research Female RNA Long Noncoding |
| Zdroj: | Journal of Cellular Physiology. 234:11662-11669 |
| ISSN: | 1097-4652 0021-9541 |
| DOI: | 10.1002/jcp.27825 |
| Popis: | Accumulating research works have reported that long noncoding RNAs (lncRNAs) are involved in various cancers, including cervical cancer. LncRNA DGCR5 has been identified in many cancers. However, the biological role of DGCR5 in cervical cancer remains barely known. We aimed to investigate the biological function of DGCR5 in cervical cancer progression. Here, in our current study, we observed that DGCR5 was downregulated in human cervical cancer cell lines (MS751, SiHa, HeLa, and HT-3) compared with the primary normal cervical squamous cells (NCSC1 and NCSC2). Then, DGCR5 was restrained by transfection with lenti-virus-short hairpin RNA (LV-shRNA) while induced by LV-DGCR5 in HeLa and C33A cells. Silence of DGCR5 obviously induced cervical cancer cell viability and cell proliferation. Reversely, upregulation of DGCR5 inhibited HeLa and C33A cell survival and proliferation. Furthermore, silencing of DGCR5 increased cervical cancer cell colony formation ability and decreased cell apoptosis, whereas its overexpression exhibited an opposite process. Moreover, DGCR5 suppressed migration and invasion capacity of cervical cancer cells. The Wnt signaling is integral in numerous biological processes. Here, we found that Wnt signaling was strongly activated in cervical cancer cells. Downregulation of DGCR5 contributed to cervical cancer progression by activating Wnt signaling. Subsequently, in vivo animal models were used to confirm that DGCR5 suppressed cervical cancer via targeting Wnt signaling. In conclusion, we reported that DGCR5 was involved in cervical cancer progression via modulating the Wnt pathway. |
| Databáze: | OpenAIRE |
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