Identification of Prognostic Biomarkers and Molecular Targets Among JAK Family in Breast Cancer

Liu, Fang-Teng; Wu, Hengyu

doi:10.2147/jir.s284889

Cited by 13 publications

(8 citation statements)

References 87 publications

(76 reference statements)

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“…This is in line with the results of univariate analysis in the current study, confirming metastasis formation, lymph nodular status, and TYK2 expression to be predictors of survival. This was similar in other malignancies, including breast cancer ([ 26 ]) and lung adenocarcinoma ([ 28 ]), while other studies found TYK2 overexpression to be related to worse survival, e.g., in stomach adenocarcinoma ([ 29 ]). TYK2 has different potentially relevant functions in cancer and metastasis formation; stimulation of proliferation and protection from cell death, promotion of migration and invasion, and metastasis formation could be important factors regarding survival in different cancer entities ([ 30 ]).…”

Section: Discussionsupporting

confidence: 77%

“…Survival is a critical outcome parameter of HNSC; thereby, majority of recurrence or disease-specific deaths take place within 2-3 years since diagnosis ([ 25 ]). TYK2 has previously been found to be related to autoimmunity ([ 15 – 17 ]) and various cancers ([ 24 , 26 , 27 ]). A previous study on laryngeal squamous cell carcinoma found that lower TYK2 would be significantly associated to worse overall survival ([ 24 ]), which is in line with the current analysis.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Identification of Gene-Tyrosine Kinase 2 (TYK2) in Head and Neck Squamous Cell Carcinoma Patients—An Integrated Bioinformatics Approach

Gong

Ren

2022

Disease Markers

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Background. The human tyrosine kinase 2 (TYK2) has been found to be associated with at least 20 autoimmune diseases; however, its tumor-regulating role in head and neck squamous cell carcinoma (HNSC) has not been researched by using an integrative bioinformatics approach, yet. Objective. To investigate the regulating mechanisms of the TYK2 gene in HNSC in terms of its expression pattern, prognostic values, involved biological functions, and implication of tumor immunity. Methods. The TYK2 gene expression pattern and regulatory involvement in HNSC were investigated using publically accessible data from TCGA database. R software tools and public web servers were utilized to conduct statistical analysis on cancer and noncancerous samples. Results. TYK2 was found to be significantly upregulated in HNSC samples compared with healthy control samples. The expression of TYK2 gene was shown to be associated with the prognosis of HNSC by showing its upregulation represented better survival outcome. The regulating role of TYK2 in HNSC was found mainly in several pathways including DNA replication, base excision repair, apoptosis, p53 signaling pathway, and NF-kappa B signaling pathway. The gene set enrichment analysis (GSEA) results showed that TYK2-significantly correlated genes were mainly enriched in several biological functional terms including cell cycle, DNA replication, PLK1 pathway, ATR pathway, and Rho GTPase pathway. In addition, TYK2 was found to be involved in tumor immunity, showing positive correlation with the majority of tumor infiltrating immune cells, immune checkpoint genes, and significant representative components of tumor microenvironment, according to the ESTIMATE-Stromal-Immune score. Conclusions. Given the dysregulation, prognostic values, regulating tumor progression-related pathways, and the tumor immune-modulatory role of TYK2 in HNSC, the TYK2 gene should be regarded as a potential therapeutic target in treating head and neck cancer.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Identification of Gene-Tyrosine Kinase 2 (TYK2) in Head and Neck Squamous Cell Carcinoma Patients—An Integrated Bioinformatics Approach

Gong

Ren

2022

Disease Markers

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“…Importantly, these hub genes (CXCL1, DDX58 and JAK3) have been reported to be targets of DNA methylated modification in schizophrenia, 38 hand, foot and mouth disease (HFMD), 39 and breast cancer. 40 The present results further suggested functional DNA methylation modification in these hub genes might play a crucial role in CS-induced airway inflammation in COPD.…”

Section: Discussionsupporting

confidence: 67%

DNA Methylation Profiling in a Cigarette Smoke-Exposed Mouse Model of Airway Inflammation

Li¹,

Peng²,

Chen³

et al. 2022

COPD

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Purpose DNA methylation, a major epigenetic modification, has been documented to play an important role in chronic obstructive pulmonary disease (COPD). In this study, we aimed to profile the DNA methylation patterns in a mouse model of airway inflammation induced by cigarette smoke (CS), a foremost risk factor of COPD. Material and Methods To establish a model of airway inflammation, wild-type mice were exposed to mainstream CS or room air for 2 hours twice daily, 6 days per week for consecutive 4 weeks. Lung tissues of the mice were collected for genome-wide DNA methylation analysis by liquid hybridization capture-based bisulfite sequencing, which were used for intersection analysis with gene expression by cDNA microarray to identify candidate methylated genes. Then, functional enrichment analyses with protein–protein interaction (PPI) network regarding these genes were conducted to explore the potential mechanisms. Results After 4-week CS exposure, the level of DNA methylation accompanied by a subacute airway inflammation was markedly enhanced, and 2002 differentially methylated genes (DMGs) were annotated, including 565 DMGs contained methylations in gene promoters, which were used for intersection with the differentially expressed genes. Then, 135 candidate methylated genes were further selected by the intersection, among which 58 genes with functional methylated modification were finally identified. Further analyses revealed candidate methylated genes were significantly enriched in a complicated network of signals and processes, including interleukins, toll-like receptors, T-cells differentiation, oxidative stress, mast cells activation, stem cells proliferation, etc., as well as the 58 functional methylated genes were partially located at key positions in PPI network, especially CXCL1, DDX58 and JAK3. Conclusion This study suggests CS exposure significantly enhances DNA methylated level, and the potential functional methylated genes are closely related to complicated inflammatory-immune responses, which may provide some new experimental evidence in understanding the epigenetic mechanisms of CS-induced airway inflammation in COPD.

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“…To approximate the abundance of TIIGs, the TIMER database uses TCGA data for 10,897 samples across 32 types of cancer. To assess the relative variations in gene expression amongst sets in the samples [ 11 , 12 ], we used a deconvolution algorithm based on gene expression called CIBERSORT ( http://cibersort.stanford.edu/ ). With CIBERSORT, we measured the immune response of 22 TIICs to evaluate their association with the risk grouping in lung cancer and to reveal correlations amongst TIICs.…”

Section: Methodsmentioning

confidence: 99%

Construction of a prognostic signature of autophagy-related lncRNAs in non-small-cell lung cancer

2021

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Background Autophagy inhibits tumorigenesis by limiting inflammation. LncRNAs regulate gene expression at various levels as RNAs; thus, both autophagy and lncRNAs are closely related to the occurrence and development of tumours. Methods A total of 232 autophagy-related genes were used to construct a coexpression network to extract autophagy-related lncRNAs. A prognostic signature was constructed by multivariate regression analysis. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was applied to analyse enrichment in cancer-related pathways. Immune infiltration analysis was used to analyse the relationship between the prognostic signature and the tumour microenvironment. Results Nine autophagy-related lncRNAs were used to construct a prognostic model for non-small-cell lung cancer. The median risk score was used to discriminate the high- and low-risk groups, and the low-risk group was found to have better survival. Because KEGG pathway analysis showed that the prognostic signature was enriched in some immune pathways, further analysis of immune infiltration was conducted, and it was found that the prognostic signature did play a unique role in the immune microenvironment. Additionally, the prognostic signature was associated with clinical factors. Conclusion We constructed a prognostic model of autophagy-related lncRNAs that can predict the prognosis of non-small-cell lung cancer.

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Identification of Prognostic Biomarkers and Molecular Targets Among JAK Family in Breast Cancer

Cited by 13 publications

References 87 publications

Identification of Gene-Tyrosine Kinase 2 (TYK2) in Head and Neck Squamous Cell Carcinoma Patients—An Integrated Bioinformatics Approach

Identification of Gene-Tyrosine Kinase 2 (TYK2) in Head and Neck Squamous Cell Carcinoma Patients—An Integrated Bioinformatics Approach

DNA Methylation Profiling in a Cigarette Smoke-Exposed Mouse Model of Airway Inflammation

Construction of a prognostic signature of autophagy-related lncRNAs in non-small-cell lung cancer

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