Inflammation, Immunity, and Cancer

Singh, Rajesh; Mishra, Manoj K.; Aggarwal, Himanshu

doi:10.1155/2017/6027305

Cited by 159 publications

(140 citation statements)

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“…Chronic inflammation is involved in the development of a wide variety of tumors. 15 , 16 In cervical cancer patients, IL-6 and IL-8 concentrations in cervicovaginal washings are significantly higher than those in cervical intraepithelial neoplasia patients and controls. 17 – 19 In most patients, local IL-6 and IL-8 levels were also higher in serum.…”

Section: Introductionmentioning

confidence: 93%

FPR1 mediates the tumorigenicity of human cervical cancer cells

Cao¹,

Zhang²

2018

CMAR

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PurposeThe present study aimed to investigate the role of FPR1 and the downstream effectors such as NF-κB and IL-6/8 in the development of cervical cancer.Patients and methodsFPR1 protein expression was detected via immunohistochemical staining in tissue microarrays containing cervical cancer tissues from 185 patients. Following FPR1 silencing in SiHa cells using lentiviral siRNA delivery, biological characteristics and tumor formation were evaluated in vitro and in vivo, respectively. Phosphorylated NF-κB levels were detected by Western blotting, while IL-6 and IL-8 secretion were detected by ELISA in both FPR1 knockdown and control SiHa cells. Human umbilical vein endothelial cell tube formation assays were performed to evaluate the angiogenesis-promoting ability of IL-6 and IL-8 secretion in FPR1 knockdown and control SiHa cells. Neovascularization, proliferation and apoptosis markers were detected by immunohistochemical staining to analyze the tumorigenic role of FPR1.ResultsImmunohistochemistry of cervical cancer tissues from 185 patients revealed high FPR1 expression levels in patients with advanced-stage disease and/or poor prognosis. Compared with control cells, cervical cancer cells in which FPR1 was silenced exhibited inhibition of cell invasion, migration and proliferation and higher levels of apoptosis. NF-κB was inhibited in FPR1 knockdown in SiHa cells. IL-6/8 upregulation by FPR1 activation stimulated angiogenesis. FPR1 deficiency inhibited the tumorigenicity of cervical cancer cells in nude mice. FPR1, IL-6, IL-8, CD31 and Ki67 levels were all reduced, whereas cleaved caspase-3 was upregulated, in the FPR1 knockdown group compared with the levels in the control group.ConclusionHigh FPR1 expression was associated with advanced stage and poor prognosis in cervical cancer patients. FPR1 activation induced NF-κB nuclear translocation to promote cervical cancer development through the upregulation of IL-6 and IL-8 expression. Inhibiting FPR1 activity may thus have potential therapeutic value in cervical cancer patients.

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Section: Introductionmentioning

confidence: 93%

FPR1 mediates the tumorigenicity of human cervical cancer cells

Cao¹,

Zhang²

2018

CMAR

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“…Cancer-associated inflammation involves crosstalk between malignant and non-malignant cells in an autocrine and paracrine fashion through mediators such as cytokines, chemokines and prostaglandins [21]. With the combined force of genetic alteration, inflammatory tumor microenvironments contribute towards tumor growth and distant metastasis [22]. Furthermore, the carcinogenic effect of inflammatory response could be inhibited by using anti-inflammatory drugs [23].…”

Section: Vcna Cav1 Epcam Egf Gpc3 Col1a1 Timp1 Ccl5 Csf1r DCmentioning

confidence: 99%

Identification of potential novel differentially-expressed genes and their role in invasion and migration in renal cell carcinoma

Shi

Qin

Wang

et al. 2020

Aging

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Clear cell renal cell carcinoma (ccRCC) remains one of the most common cancer types globally, and while it has been extensively studied, the molecular basis for its pathology remains incompletely understood. Herein, we profiled three previously published datasets (GSE66272, GSE100666, and GSE105261) in a single integrated analysis aimed at identifying disease-associated patterns of gene expression that may offer mechanistic insight into the drivers of this disease. We pooled expression data from 39 normal kidney samples and 39 kidney tumors, leading us to identify 310 differentially expressed genes (DEGs) that were linked to kidney cancer in all three analyzed datasets. Of these genes, 133 and 177 were up-and downregulated, respectively, in cancer samples. We then incorporated these DEGs into a protein-protein interaction network with the STRING and Cytoscape tools, and we were able to identify signaling pathways significantly enriched for these DEGs. The relationship between DEG expression and ccRCC patient survival was further evaluated using a Kaplan-Meier approach, leading us to identify TIMP1 as an independent prognostic factor in ccRCC patients. When TIMP1 expression was disrupted in ccRCC cell lines, this impaired their migratory and invasive capabilities. In summary, we employed an integrative bioinformatics approach to identify ccRCC-related DEGs and associated signaling pathways. Together these findings offer novel insight into the mechanistic basis for ccRCC, potentially helping to identify novel therapeutic targets for the treatment of this deadly disease.

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“…In addition, it predicts response to immune checkpoint blockade in human melanoma [33]. Together with genetic alterations, the inflammatory tumor environment leads to progression and metastasis of tumors eventually [34]. A3G in SKCM regulates a range of inflammation-related signaling pathways such as TNF-α signaling via the NF-κB pathway, IL2-STAT5 signaling, IL6/JAK-STAT3 signaling.…”

Section: Discussionmentioning

confidence: 99%

Prognostic implication and functional annotations of APOBEC3G expression in patients with Melanoma

Han¹,

Xu²,

Shen³

2020

J. Cancer

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Aim: Skin cutaneous melanoma (SKCM) is one of the most life-threatening malignancies damaging human health. APOBEC3G (A3G) has been found in several cancers; however, the role of A3G in SKCM is rarely studied. This study aimed to investigate the expression of A3G in tumor tissue and its prognostic value in SKCM patients. Method: A total of 512 SKCM patients from the First Affiliated Hospital of Soochow University (FAHSU) and the Cancer Genome Atlas (TCGA) database were consecutively recruited in analyses. Differential transcriptional and proteome expression profiles were obtained from multiple datasets. GEPIA was used to assess the survival analysis between distinguished groups. Both univariate and multivariate Cox regression analysis was performed to address the influence of independent factors on disease-free survival (RFS) and overall survival (OS). In addition, 31 SKCM and 31 nevus tissues were collected for immunohistochemical (IHC) staining and evaluation. STRING, DAVID and Gene Set Enrichment Analysis (GSEA) was utilized to conduct a network of related genes and significant pathways. Furthermore, we investigated the relationship of A3G with tumor-infiltrating immune cells (TIICs) by TIMER and TISIDB. Result: We found both transcriptional and proteomics expressions of A3G were elevated in SKCM. Survival analysis and ROC curves showed significant diagnostic and prognostic ability of A3G. IHC results showed increased expression of A3G in SKCM compared to nevus tissues. Importantly, A3G expression was closely associated with the immune-infiltrating levels of B cells, CD4+ T, CD8+ T, neutrophils, macrophages and dendritic cells. Conclusion: In summary, our study first reveals that elevated A3G expression is significantly correlated with better prognosis in SKCM patients. The role of A3G in SKCM demonstrated that it might be a prognostic and immunotherapeutic biomarker for SKCM.

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Inflammation, Immunity, and Cancer

Cited by 159 publications

References 0 publications

FPR1 mediates the tumorigenicity of human cervical cancer cells

FPR1 mediates the tumorigenicity of human cervical cancer cells

Identification of potential novel differentially-expressed genes and their role in invasion and migration in renal cell carcinoma

Prognostic implication and functional annotations of APOBEC3G expression in patients with Melanoma

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