Identification of hsa_circ_0002024 as a prognostic competing endogenous RNA (ceRNA) through the hsa_miR_129-5p/Anti-Silencing Function 1B Histone Chaperone (ASF1B) axis in renal cell carcinoma

Chen, Zhe; Ou, Dehua; Huang, Zhuangkai; Shen, Peilin

doi:10.1080/21655979.2021.1974650

Cited by 10 publications

(5 citation statements)

References 53 publications

(51 reference statements)

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“…Recent findings have greatly expanded our understanding of the role of ASF1B in the pathogenesis of various cancers, including prostate cancer, clear cell renal cell carcinoma, and cervical cancer [ 4 , 6 , 7 ]. Recent studies indicated that ASF1B was overexpressed in clear cell renal cell carcinoma, and its upregulation boosted cancer cell growth by activating the AKT pathway [ 4 , 28 ]. Han et al revealed that knockdown of ASF1B induced prostate cancer cell apoptosis by repressing the PI3K/Akt pathway [ 6 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-520d-3p suppresses melanoma cells proliferation by inhibiting the anti-silencing function 1B histone chaperone

Shi

et al. 2021

Bioengineered

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As the most common and aggressive malignant form of skin cancer, melanoma has a poor prognosis in its late stage. MicroRNA (miR)-520d-3p has been reported as a key modulator that regulates the development of different types of cancer, but its role in melanoma remains unclear. The purpose of this study was to investigate the role and mechanism of miR-520d-3p in melanoma. The expression of anti-silencing function 1B histone chaperone ( ASF1B ) and miR-520d-3p in melanoma tissues and cells was detected by reverse transcription-quantitative polymerase chain reaction. The interaction between ASF1B and miR-520d-3p was verified by luciferase activity detection. Cell counting kit-8, bromodeoxyuridine, fluorescein isothiocyanate, and cell adhesion assays were performed to detect cell viability, proliferation, apoptosis, and adhesion in melanoma cells. ASF1B expression was evidently increased, whereas miR-520d-3p level was downregulated in melanoma tissues and cells. Overexpression of ASF1B enhanced cell growth and adhesion and hampered cell apoptosis in melanoma cells. Furthermore, miR-520d-3p suppressed the tumorigenic effects of melanoma cells. Moreover, miR-520d-3p suppressed the expression of ASF1B to suppress melanoma tumorigenesis. In conclusion, we have found out that miR-520d-3p suppressed melanoma tumorigenesis by inhibiting ASF1B , which could be a promising target for melanoma therapy.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-520d-3p suppresses melanoma cells proliferation by inhibiting the anti-silencing function 1B histone chaperone

Shi

et al. 2021

Bioengineered

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“…Accumulating evidence has shown that up-regulation of ASF1B stimulated cancer cell proliferation, DNA replication and migration, accompanied by restrained cell cycle arrest and apoptosis ( Misiewicz-Krzeminska et al, 2013 ; Han et al, 2018 ; Zhou et al, 2019 ; Liu X. et al, 2020 ; Zhang et al, 2021 ), which was also consistent with our enrichment analysis of module genes ( Figure 2A ). In addition, several studies have underlined the important prognostic impact of ASF1B on a variety of cancers ( Corpet et al, 2011 ; Chen Z. et al, 2021 ; Feng et al, 2021 ). Another exciting finding was that ASF1B could regulate immune infiltration through affecting immune-related genes and pathways such as antigen processing and presentation and natural killer cell-mediated cytotoxicity ( Hu et al, 2021 ; Zhan et al, 2021 ), conferring its strong hints on potential immunotherapeutic target for several malignancies.…”

Section: Resultsmentioning

confidence: 99%

Identification of Survival-Associated Hub Genes in Pancreatic Adenocarcinoma Based on WGCNA

Huang¹,

Ye²,

Wang³

et al. 2022

Front. Genet.

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Pancreatic adenocarcinoma is one of the leading causes of cancer-related death worldwide. Since little clinical symptoms were shown in the early period of pancreatic adenocarcinoma, most patients were found to carry metastases when diagnosis. The lack of effective diagnosis biomarkers and therapeutic targets makes pancreatic adenocarcinoma difficult to screen and cure. The fundamental problem is we know very little about the regulatory mechanisms during carcinogenesis. Here, we employed weighted gene co-expression network analysis (WGCNA) to build gene interaction network using expression profile of pancreatic adenocarcinoma from The Cancer Genome Atlas (TCGA). STRING was used for the construction and visualization of biological networks. A total of 22 modules were detected in the network, among which yellow and pink modules showed the most significant associations with pancreatic adenocarcinoma. Dozens of new genes including PKMYT1, WDHD1, ASF1B, and RAD18 were identified. Further survival analysis yielded their valuable effects on the diagnosis and treatment of pancreatic adenocarcinoma. Our study pioneered network-based algorithm in the application of tumor etiology and discovered several promising regulators for pancreatic adenocarcinoma detection and therapy.

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“…Cenpf has a close relationship with MAPK (26, 27) and Wnt pathway (28). Antisilencing function 1b (Asf1b) had effects on cell proliferation, leading to abnormal nuclear structure and unique transcriptional features (29) and was often associated with various malignancies (30,31). According to the functional enrichment analysis, Asf1b was mainly enriched in the 'process utilizing autophagic mechanism' and 'biosynthesis of nucleotide sugars'.…”

Section: Discussionmentioning

confidence: 99%

Investigation on the molecular mechanism of SPA interference with osteogenic differentiation of bone marrow mesenchymal stem cells

Wen,

Zhu,

Yang

et al. 2024

Preprint

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The binding of Staphylococcus aureus protein A (SPA) to osteoblasts induces apoptosis and inhibits bone formation. Bone marrow derived mesenchymal stem cells (BMSC) has the ability to differentiate into bone, fat and cartilage. Hence, it was vital to analyze the molecular mechanism of SPA affecting osteogenic differentiation. We introduced transcript sequence data to screen out differentially expressed genes (DEGs) related to SPA interfered BMSC. Protein-protein interaction (PPI) network of DEGs was established to screen biomarkers associated with BMSC with SPA interference. ROC curve was plotted to evaluate the ability of biomarkers to distinguish between two groups of samples. We finally performed GSEA and regulatory analysis based on biomarkers. We identified 321 DEGs. Subsequently, 6 biomarkers (Cenpf, Kntc1, Nek2, Asf1b, Troap and Kif14) were identified via hubba algorithm in PPI. ROC analysis showed that six biomarkers could clearly distinguish normal differentiated and SPA interfered BMSC. Moreover, we found that these biomarkers was mainly enriched in the ‘Pyrimidine metabolism’ pathway. We also constructed ‘71 circRNAs-14 miRNAs-5 mRNAs’ and ‘10 lncRNAs-5 miRNAs-2 mRNAs’ networks. Kntc1 and Asf1b genes were associated with rno-miR-3571. Nek2 and Asf1b genes were associated with rno-miR-497-5p. Finally, we found significant lower expression of six biomarkers in SPA interfered group compared to the normal group by RT-qPCR. Overall, we obtained 6 biomarkers (Cenpf, Kntc1, Nek2, Asf1b, Troap and Kif14) related to SPA interfered BMSC, which laid a theoretical foundation for exploring the key factors of SPA affecting osteogenic differentiation.

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Identification of hsa_circ_0002024 as a prognostic competing endogenous RNA (ceRNA) through the hsa_miR_129-5p/Anti-Silencing Function 1B Histone Chaperone (ASF1B) axis in renal cell carcinoma

Cited by 10 publications

References 53 publications

MicroRNA-520d-3p suppresses melanoma cells proliferation by inhibiting the anti-silencing function 1B histone chaperone

MicroRNA-520d-3p suppresses melanoma cells proliferation by inhibiting the anti-silencing function 1B histone chaperone

Identification of Survival-Associated Hub Genes in Pancreatic Adenocarcinoma Based on WGCNA

Investigation on the molecular mechanism of SPA interference with osteogenic differentiation of bone marrow mesenchymal stem cells

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