Pancreatic adenocarcinoma upregulated factor (PAUF) confers resistance to pancreatic cancer cells against oncolytic parvovirus H-1 infection through IFNA receptor-mediated signaling

Kaowinn, Sirichat; Cho, Il-Rae; Moon, Jeong; Jun, Seung Won; Kim, Chang Seok; Kang, Ho Young; Kim, Manbok; Koh, Sang Seok; Chung, Young‐Hwa

doi:10.1016/j.bbrc.2015.02.107

Cited by 5 publications

(3 citation statements)

References 29 publications

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“…Cell signaling: Intercellular communication between tumor cells has been well studied in the context of tumor progression and resistance to various immunotherapies, where tumor cells have been found to communicate and influence neighboring tumor cells via secreting cytokines, growth factors, metabolites, and extracellular vesicles to promote a protumoral environment [58]. Soluble signals released by infected cells can protect surrounding cells from viral infection, e.g., interferon responses [28,29,[59][60][61][62][63][64][65][66][67]. Secretion of interferons by tumor cells infected with oncolytic viruses and the subsequent activation of the interferon-receptor (IFNR)-based Janus-kinase (JAK-STAT) pathway in surrounding tumor cells has been demonstrated; thus, also in this context, this pathway is an important mode of antiviral resistance [68].…”

Section: Discussionmentioning

confidence: 99%

Resistance Mechanisms Influencing Oncolytic Virotherapy, a Systematic Analysis

2021

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Resistance to therapy is a frequently observed phenomenon in the treatment of cancer, and as with other cancer therapeutics, therapies based on oncolytic viruses also face the challenges of resistance, such as humoral and cellular antiviral responses, and tumor-associated interferon-mediated resistance. In order to identify additional mechanisms of resistance that may contribute to therapeutic failure, we developed a systematic search strategy for studies published in PubMed. We analyzed 6143 articles on oncolytic virotherapy and found that approximately 8% of these articles use resistance terms in the abstract and/or title. Of these 439 articles, 87 were original research. Most of the findings reported pertain to resistance mediated by tumor-cell-dependent interferon signaling. Yet, mechanisms such as epigenetic modifications, hypoxia-mediated inhibition, APOBEC-mediated resistance, virus entry barriers, and spatiotemporal restriction to viral spread, although not frequently assessed, were demonstrated to play a major role in resistance. Similarly, our results suggest that the stromal compartment consisting of, but not limited to, myeloid cells, fibroblasts, and epithelial cells requires more study in relation to therapy resistance using oncolytic viruses. Thus, our findings emphasize the need to assess the stromal compartment and to identify novel mechanisms that play an important role in conferring resistance to oncolytic virotherapy.

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Section: Discussionmentioning

confidence: 99%

Resistance Mechanisms Influencing Oncolytic Virotherapy, a Systematic Analysis

2021

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“…IFNA2, promyelocytic leukemia (PML), IFNα, IFN lambda 1 (IFNL1/IL29) and IRF7 are extracted as 5 top upstream regulators (Table VII). Activation of IFNα receptor-mediated signaling induced the oncogene PDAC up-regulated factor (PAUF) and made PDAC resistant to oncolytic parvovirus H-1 infection (27). Swayden demonstrated an alteration of PML protein sumoylation was associated with both gemcitabine and oxaliplatin resistance in pancreatic cancer MIAPaCa cells (28).…”

Section: Tlr3 Ligand Poly(i-c) Enhances the Cytotoxicity Of Tkis In Human Pancreatic Cancer Cell Linesmentioning

confidence: 99%

Involvement of the Interferon Signaling Pathways in Pancreatic Cancer Cells

et al. 2020

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Background/Aim: To examine interferon (IFN) signaling pathways in human pancreatic cancer cells and their therapeutic application for pancreatic ductal adenocarcinoma (PDAC). Materials and Methods: We examined the effects of IFNα on cytotoxicity, migration, as well as on the levels of tolllike receptor (TLR) signaling pathway-associated genes expression in pancreatic cancer cells. We also examined the additive effects of IFNα and poly(I-C) on tyrosine kinase inhibitor (TKI)-induced cytotoxicity. We performed transcriptome analysis (RNA-Seq) of clinical samples and compared the profile between pancreatic intraepithelial neoplasias (PanINs) and PDACs. Results: IFNα suppressed cell viability and cell migration, and affected TLR signaling pathways, in pancreatic cancer cells. TLR3 is one of the potential genes involved in IFNtreated pancreatic cancer cells. Furthermore, similar to IFN, extracellular addition of poly(I-C) enhanced TKI-induced cytotoxicity in pancreatic cancer cells. RNA-Seq analysis demonstrated that IFN signaling is one of the potential pathways involved in the progression of PanIN to PDAC. Conclusion: IFN signaling may be involved in the development of PDAC. Treatments that target the IFN and TLR3 signaling pathways may be therapeutic options against PDAC.

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“…Furthermore, ZG16B enhances angiogenesis and vascular permeability and then promotes tumor progression and metastasis of pancreatic cancer by stimulating CXCR4 expression and FAK activation [26][27][28]. Additionally, ZG16B helps pancreatic cancer cells to resist oncolytic parvovirus H-1 infection via IFNAR-mediated signaling [29]. As a special factor in pancreatic cancer, ZG16B promotes activation and maturation of DCs through TLR4 signaling pathway to mediate immune system activation; meanwhile, it could also increase and activate MDSCs to benefit tumor formation, showing a double-sided effect on the immunotherapy [30,31].…”

Section: Introductionmentioning

confidence: 99%

Identification of ZG16B as a prognostic biomarker in breast cancer

et al. 2020

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Zymogen granule protein 16B (ZG16B) has been identified in various cancers, while so far the association between ZG16B and breast cancer hasn’t been explored. Our aim is to confirm whether it can serve as a prognostic biomarker in breast cancer. In this study, Oncomine, Cancer Cell Line Encyclopedia (CCLE), Ualcan, and STRING database analyses were conducted to detect the expression level of ZG16B in breast cancer with different types. Kaplan–Meier plotter was used to analyze the prognosis of patients with high or low expression of ZG16B. We found that ZG16B was significantly upregulated in breast cancer. Moreover, ZG16B was closely associated with foregone biomarkers and crucial factors in breast cancer. In the survival analysis, high expression of ZG16B represents a favorable prognosis in patients. Our work demonstrates the latent capacity of ZG16B to be a biomarker for prognosis of breast cancer.

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Pancreatic adenocarcinoma upregulated factor (PAUF) confers resistance to pancreatic cancer cells against oncolytic parvovirus H-1 infection through IFNA receptor-mediated signaling

Cited by 5 publications

References 29 publications

Resistance Mechanisms Influencing Oncolytic Virotherapy, a Systematic Analysis

Resistance Mechanisms Influencing Oncolytic Virotherapy, a Systematic Analysis

Involvement of the Interferon Signaling Pathways in Pancreatic Cancer Cells

Identification of ZG16B as a prognostic biomarker in breast cancer

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