Autor: |
Tiancheng Zhao, Jiayu Zhang, Cong Ye, Leilei Tian, Yezhou Li |
Jazyk: |
angličtina |
Rok vydání: |
2020 |
Předmět: |
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Zdroj: |
Cancer Cell International, Vol 20, Iss 1, Pp 1-8 (2020) |
Druh dokumentu: |
article |
ISSN: |
1475-2867 |
DOI: |
10.1186/s12935-020-01277-w |
Popis: |
Abstract Background Long non-coding RNAs (lncRNAs) FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) are reported could function as tumor promoter in several cancers. However, its role in hemangioma was not reported to yet. Methods Expression level of FOXD2-AS1 in hemangioma tissues and cells was explored using quantitative reverse-time PCR. Cell counting kit-8 (CCK-8) assay, colony formation assay, wound-healing assay, and transwell invasion assay were conducted to measure the roles of FOXD2-AS1. In addition, the levels of markers for proliferation and Epithelial-Mesenchymal Transition were investigated. Connection of FOXD2-AS1 and mcroRNA-324-3p (miR-324-3p) or miR-324-3p and p53 and DNA damage regulated 1 (PDRG1) was analyzed with bioinformatic analysis method and dual-luciferase activity reporter assay. Results Here, we found that FOXD2-AS1 was highly expressed in proliferating-phase hemangioma tissues compared with the involuting-phase hemangioma tissues. Functionally, FOXD2-AS1 knockdown suppressed cell proliferation, colony formation, migration, and invasion in vitro. Conversely, overexpression of FOXD2-AS1 promoted tumor growth in vitro. Mechanistically, FOXD2-AS1 inversely regulated miR-324-3p abundance in hemangioma cells. We also found FOXD2-AS1 acted as a competing endogenous RNA (ceRNA) by directly sponging miR-324-3p to regulate PDRG1 expression. In addition, the knockdown of PDRG1 reversed the stimulation effects of FOXD2-AS1 overexpression on HA cells. Conclusion To conclude, our study sheds novel light on the biological roles of FOXD2-AS1 in hemangioma, which may help the development of targeted therapy method for cancer. |
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