Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

Wang, Yipeng; Yang, Chunqing; Liu, Xiaobai; Zheng, Jian; Zhang, Fangfang; Wang, Di; Xue, Yixue; Li, Xiaozhi; Shen, Shuyuan; Shao, Lianqi; Yang, Yang; Liu, Libo; Ma, Jun; Liu, Yunhui

doi:10.1111/cas.14308

Cited by 15 publications

(19 citation statements)

References 54 publications

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“…LINC00520 has been shown to up-regulate and modulate the malignant phenotype of tumor cells in some malignant tumors [12,14,33]. LINC00520 promotes the proliferation, migration and invasion of glioma cells, but inhibits its apoptosis [34]. Wu et al reported that LINC00520 contribute to the metastasis of laryngeal h Representative bioluminescence images of mice after tail vein injection of stably expressing LINC00520 shRNA or control A375 cells.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA LINC00520 promotes the proliferation and metastasis of malignant melanoma by inducing the miR-125b-5p/EIF5A2 axis

Luan

Ding

Yuan

et al. 2020

J Exp Clin Cancer Res

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Background: Long intergenic non-protein coding RNA 520 (LINC00520), a novel identified lncRNA, has been shown to modulate the malignant phenotype of tumor cells in some malignant tumors. However, the exact role and molecular mechanism of LINC00520 in malignant melanoma has not been studied. Methods: The expression of LINC00520 in melanoma tissues were detected by using RNA-seq analysis and qRT-PCR. Melanoma cases from the public databases (The Cancer Genome Atlas (TCGA), GEO#GSE15605, GEO#GSE34460 and GEO#GSE24996) were included in this study. CCK-8 assay, EdU assay, transwell and scratch wound assay were used to explore the role of LINC00520 in melanoma cells. Luciferase reporter assays, MS2-RIP, RNA pull-down and RNA-ChIP assay were used to demonstrate the molecular biological mechanism of LINC00520 in melanoma. Results: We found that LICN00520 was found to be overexpressed in melanoma tissue. High expression of LICN00520 is a risk factor for the prognosis of melanoma patients. LINC00520 promotes the proliferation, invasion and migration of melanoma cells. LICN00520 exerted its oncogenic role by competitive binding miR-125b-5p to promote Eukaryotic initiation factor 5A2 (EIF5A2) expression. We also showed that LICN00520 promotes the growth and metastasis of melanoma in vivo through regulating miR-125b-5p/EIF5A2 axis. Conclusions: All results elucidated the role and molecular mechanism of LINC00520 in the malignant development of melanoma. LINC00520, a new oncogene in melanoma, maybe serve as a survival biomarkers or therapeutic target for melanoma patients.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA LINC00520 promotes the proliferation and metastasis of malignant melanoma by inducing the miR-125b-5p/EIF5A2 axis

Luan

Ding

Yuan

et al. 2020

J Exp Clin Cancer Res

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“…AP4 is required for c-Myc-mediated exit from cell cycle arrest in breast cancer cells [ 28 ], and siRNA-mediated knockdown of AP4 in gastric cancer cell lines leads to cell cycle arrest [ 32 ]. In glioma cells, the cell proliferation rate is positively correlated with the AP4 expression level, while the rate of apoptosis is negatively correlated with the AP4 level [ 71 ]. A similar correlation between AP4 expression levels and proliferation rate was also observed in colorectal cancer and prostate cancer cell lines [ 52 , 55 ].…”

Section: Ap4 Is Essential For Cell Cycle Regulation and Cellular Smentioning

confidence: 99%

“…Many studies showed that the 3′-UTR region of AP4 mRNA binds to various miRNAs ( Figure 2 ). These include: miR-15a, miR-16-1 and miR-302c in colorectal cancer [ 57 , 72 ], miR-608 in non-small cell lung cancer [ 53 ], and miR-520f-3p in glioma cells [ 71 ]. In these studies, the expression level of the identified miRNAs inversely correlates with the expression level of AP4, demonstrating that the binding of ncRNA to the 3′-UTR of AP4 leads to the degradation of AP4 mRNA and inhibition of EMT.…”

Section: Connections Between Non-coding Rnas and Ap4 In Cancermentioning

confidence: 99%

“…LINC00520 competes with AP4 mRNA for the binding of miR-520f-3p, and the expression of LINC00520 protects AP4 mRNA from degradation. miR-520f-3p, AP4, and LINC00520 therefore also form a feedback loop to mediate cancer progression in glioma [ 71 ]. It remains to be determined whether AP4 also forms regulatory feedback loops with ncRNA in other types of cancer.…”

Section: Connections Between Non-coding Rnas and Ap4 In Cancermentioning

confidence: 99%

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Transcription Factor AP4 Mediates Cell Fate Decisions: To Divide, Age, or Die

Wong

Joyson

Hermeking

et al. 2021

Cancers

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Activating Enhancer-Binding Protein 4 (AP4)/transcription factor 4 (TFAP4) is a basic-helix-loop-helix-leucine-zipper transcription factor that was first identified as a protein bound to SV40 promoters more than 30 years ago. Almost 15 years later, AP4 was characterized as a target of the c-Myc transcription factor, which is the product of a prototypic oncogene that is activated in the majority of tumors. Interestingly, AP4 seems to represent a central hub downstream of c-Myc and N-Myc that mediates some of their functions, such as proliferation and epithelial-mesenchymal transition (EMT). Elevated AP4 expression is associated with progression of cancer and poor patient prognosis in multiple tumor types. Deletion of AP4 in mice points to roles of AP4 in the control of stemness, tumor initiation and adaptive immunity. Interestingly, ex vivo AP4 inactivation results in increased DNA damage, senescence, and apoptosis, which may be caused by defective cell cycle progression. Here, we will summarize the roles of AP4 as a transcriptional repressor and activator of target genes and the contribution of protein and non-coding RNAs encoded by these genes, in regulating the above mentioned processes. In addition, proteins interacting with or regulating AP4 and the cellular signaling pathways altered after AP4 dysregulation in tumor cells will be discussed.

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“…High TFAP4 expression predicts poor outcomes in colorectal cancer patients (28). LncRNA LINC00520 sponges miR-520f-3p by targeting TFAP4 to promote the progression of glioma malignancy (29). However, the regulatory mechanism underlying the association of TTN-AS1 with the miR-16-1-3p/TFAP4 axis in OS is unclear.…”

Section: Introductionmentioning

confidence: 99%

Silencing of the Long Non-Coding RNA TTN-AS1 Attenuates the Malignant Progression of Osteosarcoma Cells by Regulating the miR-16-1-3p/TFAP4 Axis

et al. 2021

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ObjectivesOsteosarcoma (OS) is a type of bone malignancy. This study attempted to explore the effect of long non-coding RNA TTN-AS1 (TTN-AS1) on OS and to determine its molecular mechanisms.MethodsThe expression of TTN-AS1, microRNA-16-1-3p (miR-16-1-3p), and transcription factor activating enhancer binding protein 4 (TFAP4) in OS was assessed using qRT-PCR. The OS cell proliferation, migration, and invasion were measured using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), wound-healing, and transwell assays. N-cadherin and MMP-2 protein level was determined with western blot. Interactions between TTN-AS1 and miR-16-1-3p or TFAP4 and miR-16-1-3p were confirmed using the dual-luciferase reporter assay. Additionally, an OS xenograft tumor model was constructed to assess the effect of TTN-AS1 on tumor growth.ResultsTTN-AS1 and TFAP4 expression was increased in OS, while miR-16-1-3p expression was decreased. TTN-AS1 silencing restrained OS cell proliferation, migration, invasion, N-cadherin and MMP-2 protein expression, and hindered tumor growth. MiR-16-1-3p overexpression retarded the malignant behavior of OS cells. TTN-AS1 played a carcinostatic role by down-regulating miR-16-1-3p in the OS cells. Moreover, miR-16-1-3p inhibition or TFAP4 elevation weakened the suppressive effect of TTN-AS1 silencing on OS cell tumor progression.ConclusionTTN-AS1 promoted the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of OS cells via mediating the miR-16-1-3p/TFAP4 axis. TTN-AS1 may be a critical target for improving OS.

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Transcription factor AP‐4 (TFAP4)‐upstream ORF coding 66 aa inhibits the malignant behaviors of glioma cells by suppressing the TFAP4/long noncoding RNA 00520/microRNA‐520f‐3p feedback loop

Cited by 15 publications

References 54 publications

Long non-coding RNA LINC00520 promotes the proliferation and metastasis of malignant melanoma by inducing the miR-125b-5p/EIF5A2 axis

Long non-coding RNA LINC00520 promotes the proliferation and metastasis of malignant melanoma by inducing the miR-125b-5p/EIF5A2 axis

Transcription Factor AP4 Mediates Cell Fate Decisions: To Divide, Age, or Die

Silencing of the Long Non-Coding RNA TTN-AS1 Attenuates the Malignant Progression of Osteosarcoma Cells by Regulating the miR-16-1-3p/TFAP4 Axis

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