Circular RNAs in nasopharyngeal carcinoma

Yang, Mingxiu; Huang, Weiguo

doi:10.1016/j.cca.2020.05.029

Cited by 24 publications

(16 citation statements)

References 131 publications

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“…CircRNA is closely related to human diseases, especially in tumors. CircRNA can be secreted into body fluids, such as saliva, blood, and exosomes [ 21 , 22 ]. In clinical standard blood samples, hundreds of circRNA are more abundant than the corresponding linear mRNAs, so circRNA can be used as a new tumor marker in clinical detection [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

The Regulation of circRNA RNF13/miRNA‐1224‐5p Axis Promotes the Malignant Evolution in Acute Myeloid Leukemia

Zhang

Wang

et al. 2020

BioMed Research International

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Objective. To study the biological function of circular RNA RNF13 (circRNF13) in acute myeloid leukemia (AML) and its relationship with prognosis. Methods. We constructed stable AML cell lines with downregulated expression of circRNF13, and then, we explored the effect of downregulation of circRNF13 expression on the proliferation, migration, and invasion through qRT-PCR, MTT curve, colony formation, transwell migration and invasion experiment, cell cycle, apoptosis, Caspase 3/7 assay, and other experiments. We also studied the expression of C-myc and Tenascin-C by qRT-PCR to explore the role of circRNF13. Results. When the expression of circRNF13 was downregulated, the proliferation rate of AML cells decreased significantly, the cell cycle was blocked to G1 phase, and apoptosis rate increased significantly. C-myc related to cell proliferation decreased significantly at RNA level. Furthermore, when the expression of circRNF13 was downregulated, the migration and invasion ability of AML cells was significantly reduced, and the expression of Tenascin-C related to migration and invasion also decreased significantly. The luciferase reporter assay system confirmed that miRNA-1224-5p was the direct target of circRNF13. Conclusion. CircRNF13 inhibited the proliferation, migration, and invasion of AML cells by regulating the expression of miRNA-1224-5p. This study provides some clues for the diagnosis and treatment of AML.

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Section: Discussionmentioning

confidence: 99%

The Regulation of circRNA RNF13/miRNA‐1224‐5p Axis Promotes the Malignant Evolution in Acute Myeloid Leukemia

Zhang

Wang

et al. 2020

BioMed Research International

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“…Future research should be aimed to explore the molecular mechanism of NPC metastasis and proliferation and find the molecules active in the mechanism [ 27 , 28 ]. Recent studies have shown that non-coding RNA, including microRNA [ 29 ], long non-coding RNA [ 30 ], and circRNA [ 31 ] play an important role in the occurrence and development of NPC. Among them, circCRIM1 [ 32 ], circTGFBR2 , circHIPK3 [ 33 ] and circ_0046263 [ 34 ] play an important role in the metastasis and proliferation of NPC.…”

Section: Discussionmentioning

confidence: 99%

Splicing factor derived circular RNA circCAMSAP1 accelerates nasopharyngeal carcinoma tumorigenesis via a SERPINH1/c-Myc positive feedback loop

Wang

Yan

et al. 2022

Mol Cancer

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Background Circular RNAs play an important role in tumor genesis and progression, but they have not been sufficiently studied in patients with nasopharyngeal carcinoma (NPC). Methods The circular RNA, circCAMSAP1, was screened in NPC cells by RNA sequencing analysis. The expression of circCAMSAP1 in NPC tissues was examined by real-time quantitative polymerase chain reaction (RT-qPCR) and in situ hybridization. Wound-healing, transwell, MTT and flow cytometry assays, and nude mouse tumor models were used to explore the effect of circCAMSAP1 on proliferation and metastasis of NPC in vitro or in vivo. The downstream proteins regulated by circCAMSAP1 were screened using mass spectrometry. The interaction between circCAMSAP1 and the SERPINH1 mRNA was identified using the circular RNA immunoprecipitation method and the luciferase reporter assay. The interaction between SERPINH1 and transcription factor c-Myc was verified through Co-immunoprecipitation (Co-IP) and immunofluorescence. The effect of c-Myc on the generation of circCAMSAP1 was examined through RT-qPCR and chromatin immunoprecipitation. Finally, the splicing factors that promote the production of circCAMSAP1 were explored by RT-qPCR and RNA immunoprecipitation (RIP). Results We found that circCAMSAP1 was highly expressed in NPC tissues and promoted NPC proliferation and metastasis. Additionally, circCAMSAP1 promoted SERPINH1 expression through improved SERPINH1 mRNA stability by binding to the 3′-untranslated region (3’UTR) of SERPINH1. Highly expressed SERPINH1 reduced the ubiquitination-degradation rate of c-Myc, causing increased tumorigenesis. Meanwhile, c-Myc, cooperating with splicing factor 10 (SRSF10), could also promote CAMSAP1 pre-mRNA transcription and back-splicing, forming a positive feedback of circCAMSAP1 production, resulting in the proliferation and metastasis of NPC. Conclusions Our findings revealed that circCAMSAP1 promotes NPC proliferation and metastasis by binding to the 3’UTR of SERPINH1, suggesting that the positive feedback of circCAMSAP1-SERPINH1-c-Myc may serve as a prognostic biomarker or therapeutic target in patients with NPC.

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“…NPC is a geographically distributed head and neck epithelial tumor with poor clinical e cacy and high metastasis tendency in advanced stage [22]. LncRNA HCP5 is reported to commonly act as an oncogenic role in human malignant tumors [23].…”

Section: Discussionmentioning

confidence: 99%

Regulatory mechanism of lncRNA HCP5 in nasopharyngeal carcinoma cell proliferation and apoptosis via the miR-140-5p/NPR3 axis

Huang

Deng

et al. 2020

Preprint

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Objectives Nasopharyngeal carcinoma (NPC) is malignant tumor frequently occurring in east and southeast Asia. This study investigated the underlying mechanism of lncRNA HCP5 in NPC cell proliferation and apoptosis. Methods LncRNA HCP5 expression in NPC cells and tissues was detected. SUNE-1 cells were transfected with HCP5 silencing and CNE-1 cells were transfected with overexpressing HCP5, and then cell proliferation and apoptosis were measured. Subcellular localization of HCP5 was analyzed. The binding relationship between lncRNA HCP5 and miR-140-5p, and miR-140-5p and NPR3 were predicted and verified. Expressions of miR-140-5p and NPR3 in NPC cells were detected. SUNE-1 cells and CNE-1 cells were transfected with miR-140-5p mimic, and si-HCP5-transfected SUNE-1 cells were treated with miR-140-5p inhibitor. Then the proliferation and apoptosis of NPC cells were detected. Results LncRNA HCP5 was elevated in NPC tissues and cells. HCP5 silencing suppressed NPC cell proliferation and enhanced apoptosis. HCP5 was mainly located in the cytoplasm of NPC cells. HCP5 promoted NPR3 expression by competitively binding to miR-140-5p. Overexpression of miR-140-5p weakened proliferation and facilitated apoptosis of NPC cells. miR-140-5p inhibitor partially restored the effects of HCP5 silencing on NPC cells. Conclusion LncRNA HCP5 upregulated NPR3 expression via sponging miR-140-5p, thereby suppressing NPC cell proliferation and promoting apoptosis. This study may offer new insights into NPC treatment.

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Circular RNAs in nasopharyngeal carcinoma

Cited by 24 publications

References 131 publications

The Regulation of circRNA RNF13/miRNA‐1224‐5p Axis Promotes the Malignant Evolution in Acute Myeloid Leukemia

The Regulation of circRNA RNF13/miRNA‐1224‐5p Axis Promotes the Malignant Evolution in Acute Myeloid Leukemia

Splicing factor derived circular RNA circCAMSAP1 accelerates nasopharyngeal carcinoma tumorigenesis via a SERPINH1/c-Myc positive feedback loop

Regulatory mechanism of lncRNA HCP5 in nasopharyngeal carcinoma cell proliferation and apoptosis via the miR-140-5p/NPR3 axis

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