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LncRNA FOXD2-AS1 promotes hemangioma progression through the miR-324-3p/PDRG1 pathway.

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.

SUBMITTER: Zhao T

PROVIDER: S-EPMC7247140 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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lncRNA FOXD2-AS1 promotes hemangioma progression through the miR-324-3p/PDRG1 pathway.

Zhao Tiancheng T Zhang Jiayu J Ye Cong C Tian Leilei L Li Yezhou Y

Cancer cell international 20200524

<h4>Background</h4>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.<h4>Methods</h4>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 FOX ...[more]

PMID: 32489325

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Project description:Accumulating evidences revealed that long noncoding RNAs (lncRNAs) have been participated in cancer malignant progression, including glioblastoma multiforme (GBM). Despite much studies have found the precise biological role in the regulatory mechanisms of GBM, however the molecular mechanisms, particularly upstream mechanisms still need further elucidated. RT-QPCR, cell transfection, western blotting and bioinformatic analysis were executed to detect the expression of EGR1, HNF1A-AS1, miR-22-3p and ENO1 in GBM. Cell proliferation assay, colony formation assay, wound healing, migration and invasion assays were performed to detect the malignant characters of GBM cells. The molecular regulation mechanism was confirmed by luciferase reporter assay, ChIP and RIP. Finally, orthotopic mouse models were established to examine the effect of HNF1A-AS1 in vivo. In the current study, we analyzed clinical samples to show that the HNF1A-AS1 expression is upregulated and associated with poor patient survival in GBM. Functional studies revealed that HNF1A-AS1 knockdown markedly inhibits malignant phenotypes of GBM cells, whereas overexpression of HNF1A-AS1 exerts opposite effect. Mechanistically, the transcription factor EGR1 forced the HNF1A-AS1 expression by directly binding the promoter region of HNF1A-AS1. Furthermore, combined bioinformatics analysis with our mechanistic work, using luciferase reporter assays and RIP, we first demonstrated that HNF1A-AS1 functions as a competing endogenous RNA (ceRNA) with miR-22-3p to regulate ENO1 expression in GBM cells. HNF1A-AS1 directly binds to miR-22-3p and significantly inhibits miR-22-3p expression, while ENO1 expression was increased. miR-22-3p inhibitor offsets the HNF1A-AS1 silencing induced suppression in malignant behaviors of GBM cells. ENO1 was verified as a direct target of miR-22-3p and its expression levels was negatively with the prognosis in GBM patients. Taken together, our study illuminated the definite mechanism of HNF1A-AS1 in promoting GBM malignancy, and provided a novel therapeutic target for further clinical application.

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LncRNA FOXD2-AS1 promotes hemangioma progression through the miR-324-3p/PDRG1 pathway.

Publications

lncRNA FOXD2-AS1 promotes hemangioma progression through the miR-324-3p/PDRG1 pathway.

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