scholarly journals TRIM14 is a Putative Tumor Suppressor and Regulator of Innate Immune Response in Non-Small Cell Lung Cancer

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Josephine Hai ◽  
Chang-Qi Zhu ◽  
Tao Wang ◽  
Shawna L. Organ ◽  
Frances A. Shepherd ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Immune Response ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Innate Immune Response ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Innate Immune ◽  
Small Cell Lung ◽  
Putative Tumor Suppressor

scholarly journals Splenectomy inhibits non-small cell lung cancer growth by modulating anti-tumor adaptive and innate immune response

2015 ◽  
Vol 4 (4) ◽  
pp. e998469 ◽  
Author(s):  
Liran Levy ◽  
Inbal Mishalian ◽  
Rachel Bayuch ◽  
Lida Zolotarov ◽  
Janna Michaeli ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Immune Response ◽  
Small Cell Lung Cancer ◽  
Innate Immune Response ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Innate Immune ◽  
Cancer Growth ◽  
Small Cell Lung

scholarly journals Functional and Clinical Characterization of the Putative Tumor Suppressor WWOX in Non-small Cell Lung Cancer

2011 ◽  
Vol 6 (12) ◽  
pp. 1976-1983 ◽  
Author(s):  
Silvan Becker ◽  
Boyka Markova ◽  
Rainer Wiewrodt ◽  
Sandra Hoffarth ◽  
Patricia S. Hähnel ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Putative Tumor Suppressor

scholarly journals Use tumor suppressor genes as biomarkers for diagnosis of non-small cell lung cancer

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Chuantao Zhang ◽  
Man Jiang ◽  
Na Zhou ◽  
Helei Hou ◽  
Tianjun Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Mortality Rate ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Network Effects ◽  
Small Cell ◽  
The Other ◽  
Small Cell Lung ◽  
High Efficient

AbstractLung cancer is the leading cause of death worldwide. Especially, non-small cell lung cancer (NSCLC) has higher mortality rate than the other cancers. The high mortality rate is partially due to lack of efficient biomarkers for detection, diagnosis and prognosis. To find high efficient biomarkers for clinical diagnosis of NSCLC patients, we used gene differential expression and gene ontology (GO) to define a set of 26 tumor suppressor (TS) genes. The 26 TS genes were down-expressed in tumor samples in cohorts GSE18842, GSE40419, and GSE21933 and at stages 2 and 3 in GSE19804, and 15 TS genes were significantly down-expressed in tumor samples of stage 1. We used S-scores and N-scores defined in correlation networks to evaluate positive and negative influences of these 26 TS genes on expression of other functional genes in the four independent cohorts and found that SASH1, STARD13, CBFA2T3 and RECK were strong TS genes that have strong accordant/discordant effects and network effects globally impacting the other genes in expression and hence can be used as specific biomarkers for diagnosis of NSCLC cancer. Weak TS genes EXT1, PTCH1, KLK10 and APC that are associated with a few genes in function or work in a special pathway were not detected to be differentially expressed and had very small S-scores and N-scores in all collected datasets and can be used as sensitive biomarkers for diagnosis of early cancer. Our findings are well consistent with functions of these TS genes. GSEA analysis found that these 26 TS genes as a gene set had high enrichment scores at stages 1, 2, 3 and all stages.

scholarly journals An Immune Response Enriched 72-Gene Prognostic Profile for Early-Stage Non–Small-Cell Lung Cancer

2008 ◽  
Vol 15 (1) ◽  
pp. 284-290 ◽  
Author(s):  
Paul Roepman ◽  
Jacek Jassem ◽  
Egbert F. Smit ◽  
Thomas Muley ◽  
Jacek Niklinski ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Immune Response ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Early Stage ◽  
Small Cell ◽  
Small Cell Lung ◽  
Prognostic Profile

scholarly journals Interferon Consensus Sequence-Binding Protein 8, a Tumor Suppressor, Suppresses Tumor Growth and Invasion of Non-Small Cell Lung Cancer by Interacting with the Wnt/β-Catenin Pathway

2018 ◽  
Vol 51 (2) ◽  
pp. 961-978 ◽  
Author(s):  
Lin Ye ◽  
Tingxiu Xiang ◽  
Jing Zhu ◽  
Dairong Li ◽  
Qin Shao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Consensus Sequence ◽  
Three Dimensional ◽  
Small Cell ◽  
Immunofluorescence Staining ◽  
Small Cell Lung

Background/Aims: Interferon consensus sequence-binding protein 8 (IRF8) belongs to a family of interferon (IFN) regulatory factors that modulates various important physiological processes including carcinogenesis. As reported by others and our group, IRF8 expression is silenced by DNA methylation in both human solid tumors and hematological malignancies. However, the role of IRF8 in lung carcinoma remains elusive. In this study, we determined IRF8 epigenetic regulation, biological functions, and the signaling pathway involved in non-small cell lung cancer (NSCLC). Methods: IRF8 expression were determined by Q- PCR. MSP and A+T determined promotor methylation. MTS, clonogenic, Transwell assay, Flow cytometry, three-dimensional culture and AO/EB stain verified cell function. In vivo tumorigenesis examed the in vivo effects. By Chip-QPCR, RT-PCR, Western blot and Immunofluorescence staining, the mechanisms were studied. Results: IRF8 was significantly downregulated in lung tumor tissues compared with adjacent non-cancerous tissues. Furthermore, methylation-specific PCR analyses revealed that IRF8 methylation in NSCLC was a common event, and demethylation reagent treatment proved that downregulation of IRF8 was due to its promoter CpG hypermethylation. Clinical data showed that the IRF8 methylation was associated with tumor stage, lymph node metastasis status, patient outcome, and tumor histology. Exogenous expression of IRF8 in the silenced or downregulated lung cancer cell lines A549 and H1299 at least partially restored the sensitivity of lung cancer cells to apoptosis, and arrested cells at the G0/G1 phase. Cell viability, clonogenicity, and cell migration and invasive abilities were strongly inhibited by restored expression of IRF8. A three-dimensional culture system demonstrated that IRF8 changed the cells to a more spherical phenotype. Moreover, ectopic expression of IRF8 enhanced NSCLC chemosensitivity to cisplatin. Furthermore, as verified by Chip-qPCR, immunofluorescence staining, and western blotting, IRF8 bound to the T-cell factor/lymphoid enhancer factor (TCF /LEF) promoter, thus repressing β-catenin nuclear translocation and its activation. IRF8 significantly disrupted the effects of Wnt agonist, bml284, further suggesting its involvement in the Wnt/β-catenin pathway. Conclusion: IRF8 acted as a tumor suppressor gene through the transcriptional repression of β-catenin-TCF/LEF in NSCLC. IRF8 methylation may serve as a potential biomarker in NSCLC prognosis.

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