Human alpha and beta herpesviruses and cancer: passengers or foes?

Golais, F; Mrázová, Veronika

doi:10.1007/s12223-020-00780-x

Cited by 14 publications

(4 citation statements)

References 125 publications

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“…In fact, even HSV-1 and HSV-2 are reported to act as cofactors for malignant transformation in several tumor malignancies including thyroid tumors, prostate cancer, and elevated incidences for melanoma, as well as cervical cancer in combination with HPV. [122][123][124][125] As a major cause for a putative malignant transformation mediated by HSV-1/2, the oncogenic and antiapoptotic viral protein ICP10PK is discussed. 126 VZV is also speculated to elevate the risk for certain malignancies mediated by its antiapoptotic IE63 protein.…”

Section: Resultsmentioning

confidence: 99%

Molecular mechanisms of human herpes viruses inferring with host immune surveillance

Jasinski‐Bergner

Mandelboim

Seliger

2020

J Immunother Cancer

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Several human herpes viruses (HHVs) exert oncogenic potential leading to malignant transformation of infected cells and/or tissues. The molecular processes induced by viral-encoded molecules including microRNAs, peptides, and proteins contributing to immune evasion of the infected host cells are equal to the molecular processes of immune evasion mediated by tumor cells independently of viral infections. Such major immune evasion strategies include (1) the downregulation of proinflammatory cytokines/chemokines as well as the induction of anti-inflammatory cytokines/chemokines, (2) the downregulation of major histocompatibility complex (MHC) class Ia directly as well as indirectly by downregulation of the components involved in the antigen processing, and (3) the downregulation of stress-induced ligands for activating receptors on immune effector cells with NKG2D leading the way. Furthermore, (4) immune modulatory molecules like MHC class Ib molecules and programmed cell death1 ligand 1 can be upregulated on infections with certain herpes viruses. This review article focuses on the known molecular mechanisms of HHVs modulating the above-mentioned possibilities for immune surveillance and even postulates a temporal order linking regular tumor immunology with basic virology and offering putatively novel insights for targeting HHVs.

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Section: Resultsmentioning

confidence: 99%

Molecular mechanisms of human herpes viruses inferring with host immune surveillance

Jasinski‐Bergner

Mandelboim

Seliger

2020

J Immunother Cancer

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“…In vitro and in vivo experiments have shown that SENPs are a suitable target for anti-tumor therapy ( 27 ). HSV-1 is also involved in tumorigenesis ( 28 ). Therefore, we speculate that the brown and yellow module genes play an important role in drug resistance and PCa progression through these pathways.…”

Section: Discussionmentioning

confidence: 99%

Identification of bicalutamide resistance-related genes and prognosis prediction in patients with prostate cancer

Wang

Pan

et al. 2023

Front. Endocrinol.

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BackgroundProstate cancer (PCa) is the second most common type of cancer and the fifth leading cause of cancer-related death in men. Androgen deprivation therapy (ADT) has become the first-line therapy for inhibiting PCa progression; however, nearly all patients receiving ADT eventually progress to castrate-resistant prostate cancer. Therefore, this study aimed to identify hub genes related to bicalutamide resistance in PCa and provide new insights into endocrine therapy resistance.MethodsThe data were obtained from public databases. Weighted correlation network analysis was used to identify the gene modules related to bicalutamide resistance, and the relationship between the samples and disease-free survival was analyzed. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were performed, and hub genes were identified. The LASSO algorithm was used to develop a bicalutamide resistance prognostic model in patients with PCa, which was then verified. Finally, we analyzed the tumor mutational heterogeneity and immune microenvironment in both groups.ResultsTwo drug resistance gene modules were identified. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses revealed that both modules are involved in RNA splicing. The protein–protein interaction network identified 10 hub genes in the brown module LUC7L3, SNRNP70, PRPF3, LUC7L, CLASRP, CLK1, CLK2, U2AF1L4, NXF1, and THOC1) and 13 in the yellow module (PNN, PPWD1, SRRM2, DHX35, DMTF1, SALL4, MTA1, HDAC7, PHC1, ACIN1, HNRNPH1, DDX17, and HDAC6). The prognostic model composed of RNF207, REC8, DFNB59, HOXA2, EPOR, PILRB, LSMEM1, TCIRG1, ABTB1, ZNF276, ZNF540, and DPY19L2 could effectively predict patient prognosis. Genomic analysis revealed that the high- and low-risk groups had different mutation maps. Immune infiltration analysis showed a statistically significant difference in immune infiltration between the high- and low-risk groups, and that the high-risk group may benefit from immunotherapy.ConclusionIn this study, bicalutamide resistance genes and hub genes were identified in PCa, a risk model for predicting the prognosis of patients with PCa was constructed, and the tumor mutation heterogeneity and immune infiltration in high- and low-risk groups were analyzed. These findings offer new insights into ADT resistance targets and prognostic prediction in patients with PCa.

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“…Recently identified herpes virus-associated growth factors with both transforming and transformation-suppressing activities are considered to be significant factors in tumor formation. Furthermore, in two cancer cases, serous ovarian carcinoma and certain prostate tumors, virus-encoded microRNAs were identified as potential cofactors in tumor formation ( 5 ) . Further research is needed to understand the mechanisms involved and potential therapeutic interventions.…”

Section: Discussionmentioning

confidence: 99%

Integrated analysis of differentially expressed genes implicated in ovarian cancer progression

Gür,

Külcü Sarıkaya,

Sünnetçi Akkoyunlu

2023

tjod

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Objective: Ovarian cancer (OC) is a common gynecological malignancy associated with high morbidity and generally poor prognosis despite treatment. The aim of this study was to understand the influence of gene expression differences and pathways in OC development and progression. Materials and Methods: One hundred and thirty-three OC samples and 34 normal ovarian tissues were included in the study from the Gene Expression Omnibus database. GeneSpring Software was used to obtain differentially expressed genes (DEGs) in all stages comparing tumor and normaltissue. DEGs were analyzed using the DAVID interface for Kyoto Encyclopedia of Genes and Genomes pathway analysis. Most most connected genes were selected as hub genes for each stage using the STRING application in Cytoscape software. Results: DEGs were found to be associated with cell cycle and herpes simplex virus infection pathways. A total of 19 genes ( ACTB, AKT1, ALB, CTNNB1, EGFR, EP300, ESR1, FN1, GAPDH, HSPA4, IL6, JUN, MYC, PTEN, RPS27A, SRC, TNF, TP53 and UBC ) were identified as hub genes. Among the hub genes, the TP53 gene was found to have the highest level of connections in all stages. EGFR, RPS27A, and AKT1 were found to have high numbers of connections in stages II, III, and IV, respectively. Conclusion: The results of the current study may provide new insights into OC pathogenesis and suggest potential prognostic and therapeutic targets.

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Human alpha and beta herpesviruses and cancer: passengers or foes?

Cited by 14 publications

References 125 publications

Molecular mechanisms of human herpes viruses inferring with host immune surveillance

Molecular mechanisms of human herpes viruses inferring with host immune surveillance

Identification of bicalutamide resistance-related genes and prognosis prediction in patients with prostate cancer

Integrated analysis of differentially expressed genes implicated in ovarian cancer progression

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