scholarly journals Expression of Pu.1, C/Ebp? and Bach1 Transcription Factors in Immune Cells in Patients with Cancer

2021 ◽  
Vol 3 (4) ◽  
Keyword(s):  
Transcription Factors ◽  
Immune Cells ◽  
Patients With Cancer

scholarly journals High copy number variations, particular transcription factors, and low immunity contribute to the stemness of prostate cancer cells

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Zao Dai ◽  
Ping Liu
Keyword(s):  
Prostate Cancer ◽  
Transcription Factors ◽  
Copy Number Variation ◽  
Cancer Cells ◽  
Immune Cells ◽  
Copy Number ◽  
Tumor Metastasis ◽  
Prostate Cancer Cells ◽  
Immune Microenvironment ◽  
Number Variation

Abstract Background Tumor metastasis is the main cause of death of cancer patients, and cancer stem cells (CSCs) is the basis of tumor metastasis. However, systematic analysis of the stemness of prostate cancer cells is still not abundant. In this study, we explore the effective factors related to the stemness of prostate cancer cells by comprehensively mining the multi-omics data from TCGA database. Methods Based on the prostate cancer transcriptome data in TCGA, gene expression modules that strongly relate to the stemness of prostate cancer cells are obtained with WGCNA and stemness scores. Copy number variation of stemness genes of prostate cancer is calculated and the difference of transcription factors between prostate cancer and normal tissues is evaluated by using CNV (copy number variation) data and ATAC-seq data. The protein interaction network of stemness genes in prostate cancer is constructed using the STRING database. Meanwhile, the correlation between stemness genes of prostate cancer and immune cells is analyzed. Results Prostate cancer with higher Gleason grade possesses higher cell stemness. The gene set highly related to prostate cancer stemness has higher CNV in prostate cancer samples than that in normal samples. Although the transcription factors of stemness genes have similar expressions, they have different contributions between normal and prostate cancer tissues; and particular transcription factors enhance the stemness of prostate cancer, such as PUM1, CLOCK, SP1, TCF12, and so on. In addition, the lower tumor immune microenvironment is conducive to the stemness of prostate cancer. CD8 + T cells and M1 macrophages may play more important role in the stemness of prostate cancer than other immune cells in the tumor microenvironment. Finally, EZH2 is found to play a central role in stemness genes and is negatively correlated with resting mast cells and positively correlated with activated memory CD4 + T cells. Conclusions Based on the systematic and combined analysis of multi-omics data, we find that high copy number variation, specific transcription factors, and low immune microenvironment jointly contribute to the stemness of prostate cancer cells. These findings may provide us new clues and directions for the future research on stemness of prostate cancer.

scholarly journals APOC1 is a Potential Prognostic Biomarker and Correlated With Immune Infiltration in ESCC

2020 ◽  
Author(s):  
Jia-yi XIE ◽  
Ming Liu ◽  
Yaxin Luo ◽  
Zhen Wang ◽  
Zhenghong Lu ◽  
...  
Keyword(s):  
T Cells ◽  
Transcription Factors ◽  
Cd8 T Cells ◽  
Immune Cells ◽  
Poor Prognosis ◽  
Killer Cell ◽  
Gene Set Enrichment Analysis ◽  
Immune Infiltration ◽  
Kaplan Meier ◽  
Kaplan Meier Plotter

Abstract PurposeEsophageal cancer (EC) is the sixth leading cause of cancer death worldwide. Esophageal squamous cell carcinoma (ESCC) is a predominant subtype of EC. Identifying diagnostic biomarkers for ESCC is necessary for cancer practice. Increasing evidence illustrates that apolipoprotein C-1 (APOC1) participates in the carcinogenesis. However, the biological function of APOC1 in ESCC remains unclear. Patients and methodsWe investigated the expression level of APOC1 using TIMER2.0 and GEO databases, the prognostic value of APOC1 in ESCC using Kaplan-Meier plotter and TCGA databases. We used LinkedOmics to identify co-expressed genes with APOC1 and perform GO and KEGG pathway analysis. The target networks of kinases, miRNAs and transcription factors were predicted by gene set enrichment analysis (GSEA). The correlations between APOC1 and immune infiltration were calculated using TIMER2.0 and CIBERSORT databases. We further performed the prognostic analysis based on APOC1 expression levels in related immune cells subgroups via Kaplan-Meier plotter database. ResultsAPOC1 was found overexpressed in tumor tissues in multiple ESCC cohorts and high APOC1 expression was related to a dismal prognosis. Multivariate analysis confirmed that APOC1 overexpression was an independent indicator of poor OS. Functional network analysis indicated that APOC1 might regulate the natural killer cell mediated cytotoxicity, phagosome, AMPK and hippo signaling through pathways involving some cancer-related kinases, miRNA and transcription factors. Immune infiltration analysis showed that APOC1 was significantly positively correlated with M0 macrophages cells, M1 macrophages cells and activated NK cells, negatively correlated with regulatory T cells, CD8 T cells, neutrophils and monocytes. High APOC1 expression had a poor prognosis in server immune cells subgroups in ESCC, including decreased CD8+ T cells subgroups. ConclusionThese findings suggest that increased expression of APOC1 is related to poor prognosis and immune infiltration in ESCC. APOC1 holds promise for serving as a valuable diagnostic and prognostic marker in ESCC.

scholarly journals The fibrotic and immune microenvironments as targetable drivers of metastasis

2020 ◽  
Vol 124 (1) ◽  
pp. 27-36
Author(s):  
Luke Boulter ◽  
Esme Bullock ◽  
Zeanap Mabruk ◽  
Valerie G. Brunton
Keyword(s):  
Metastatic Disease ◽  
Immune Cells ◽  
Stromal Cell ◽  
Primary Tumour ◽  
Tumour Microenvironment ◽  
Paracrine Signalling ◽  
Patients With Cancer ◽  
New Therapeutic Approaches ◽  
Substantial Progress ◽  
Metastatic Sites

AbstractAlthough substantial progress has been made over the past 40 years in treating patients with cancer, effective therapies for those who are diagnosed with advanced metastatic disease are still few and far between. Cancer cells do not exist in isolation: rather, they exist within a complex microenvironment composed of stromal cells and extracellular matrix. Within this tumour microenvironment exists an interplay between the two main stromal cell subtypes, cancer-associated fibroblasts (CAFs) and immune cells, that are important in controlling metastasis. A complex network of paracrine signalling pathways between CAFs, immune cells and tumour cells are involved at multiple stages of the metastatic process, from invasion and intravasation at the primary tumour site to extravasation and colonisation in the metastatic site. Heterogeneity and plasticity within stromal cell populations also contribute to the complexity. Although many of these processes are likely to be common to a number of metastatic sites, we will describe in detail the interplay within the liver, a preferred site of metastasis for many tumours. A greater understanding of these networks provides opportunities for the design of new therapeutic approaches for targeting the metastatic disease.

Breaking the cycle: the role of omega-3 polyunsaturated fatty acids in inflammation-driven cancers

2014 ◽  
Vol 92 (5) ◽  
pp. 321-328 ◽  
Author(s):  
William L. Patterson ◽  
Philippe T. Georgel
Keyword(s):  
Fatty Acids ◽  
Transcription Factors ◽  
Polyunsaturated Fatty Acids ◽  
Chronic Inflammation ◽  
Cancer Progression ◽  
Immune Cells ◽  
Signaling Molecules ◽  
Inflammatory Signaling ◽  
Vast Number ◽  
Anti Inflammatory

Chronic inflammation is a cyclical, self-stimulating process. Immune cells called to sites of inflammation release pro-inflammatory signaling molecules that stimulate activation of inducible enzymes and transcription factors. These enzymes and transcription factors then stimulate production of signaling molecules that attract more immune cells and induce more enzymatic and transcriptional activity, creating a perpetual loop of inflammation. This self-renewing pool of inflammatory stimuli makes for an ideal tumor microenvironment, and chronic inflammation has been linked to oncogenesis, tumor growth, tumor cell survival, and metastasis. Three protein pathways in particular, nuclear factor kappa B (NF-kB), cyclooxygenase (COX), and lipoxygenase (LOX), provide excellent examples of the cyclical, self-renewing nature of chronic inflammation-driven cancers. NF-kB is an inducible transcription factor responsible for the expression of a vast number of inflammation and cancer related genes. COX and LOX convert omega-6 (n-6) and omga-3 (n-3) polyunsaturated fatty acids (PUFA) into pro- and anti-inflammatory signaling molecules. These signaling molecules stimulate or repress activity of all three of these pathways. In this review, we will discuss the pro- and anti-inflammatory functions of these fatty acids and their role in chronic inflammation and cancer progression.

scholarly journals AFP-Inhibiting Fragments for Drug Delivery: The Promise and Challenges of Targeting Therapeutics to Cancers

2021 ◽  
Vol 9 ◽  
Author(s):  
Bo Lin ◽  
Xu Dong ◽  
Qiujiao Wang ◽  
Wei Li ◽  
Mingyue Zhu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Drug Delivery ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Immune Cells ◽  
Targeted Chemotherapy ◽  
Patients With Cancer ◽  
Important Target ◽  
Intracellular Proteins ◽  
New Strategy

Alpha fetoprotein (AFP) plays a key role in stimulating the growth, metastasis and drug resistance of hepatocellular carcinoma (HCC). AFP is an important target molecule in the treatment of HCC. The application of AFP-derived peptides, AFP fragments and recombinant AFP (AFP-inhibiting fragments, AIFs) to inhibit the binding of AFP to intracellular proteins or its receptors is the basis of a new strategy for the treatment of HCC and other cancers. In addition, AIFs can be combined with drugs and delivery agents to target treatments to cancer. AIFs conjugated to anticancer drugs not only destroy cancer cells with these drugs but also activate immune cells to kill cancer cells. Furthermore, AIF delivery of drugs relieves immunosuppression and enhances chemotherapy effects. The synergism of immunotherapy and targeted chemotherapy is expected to play an important role in enhancing the treatment effect of patients with cancer. AIF delivery of drugs will be an available strategy for the targeted treatment of cancer in the future.

scholarly journals Neutrophils in cancer carcinogenesis and metastasis

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Shumin Xiong ◽  
Liaoliao Dong ◽  
Lin Cheng
Keyword(s):  
Immune Cells ◽  
Prognostic Indicator ◽  
Pathological Process ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Patients With Cancer ◽  
Single Function ◽  
Cancer Initiation ◽  
Potential Strategy ◽  
New Perspective

AbstractIn recent years, neutrophils have attracted increasing attention because of their cancer-promoting effects. An elevated neutrophil-to-lymphocyte ratio is considered a prognostic indicator for patients with cancer. Neutrophils are no longer regarded as innate immune cells with a single function, let alone bystanders in the pathological process of cancer. Their diversity and plasticity are being increasingly recognized. This review summarizes previous studies assessing the roles and mechanisms of neutrophils in cancer initiation, progression, metastasis and relapse. Although the findings are controversial, the fact that neutrophils play a dual role in promoting and suppressing cancer is undeniable. The plasticity of neutrophils allows them to adapt to different cancer microenvironments and exert different effects on cancer. Given the findings from our own research, we propose a reasonable hypothesis that neutrophils may be reprogrammed into a cancer-promoting state in the cancer microenvironment. This new perspective indicates that neutrophil reprogramming in the course of cancer treatment is a problem worthy of attention. Preventing or reversing the reprogramming of neutrophils may be a potential strategy for adjuvant cancer therapy.

scholarly journals Identification of Prognostic Biomarkers and Immunotherapeutic Targets with CXC Chemokines in Glioblastoma Multiforme Using Integrated Bioinformatic Analysis

2020 ◽  
Author(s):  
Hailing Liu ◽  
Jinguang Zhu ◽  
Guangwen Wang
Keyword(s):  
Transcription Factors ◽  
Glioblastoma Multiforme ◽  
Signaling Pathway ◽  
Immune Cells ◽  
Disease Free Survival ◽  
Bioinformatic Analysis ◽  
Differentially Expressed ◽  
Prognostic Biomarkers ◽  
Receptor Interaction ◽  
Dismal Prognosis

Abstract Background Glioblastoma multiforme (GBM) is the most malignant central nervous system tumour bearing a dismal prognosis. The study aimed to explore the potential biomarkers and therapeutic targets with CXC chemokines in GBM by integrated bioinformatics analysis.Methods Differentially expressed CXC Chemokines were identified in GBM using GEPIA and UALCAN databases,and Kaplan–Meier analyses were performed by GEPIA subsequently. Protein -protein interaction (PPI) network was established in STRING database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways analysis were utilized to analyze differentially expressed CXC Chemokines and their similar genes gained from GEPIA. Then, we conducted transcription factors, kinase targets, and immune cells infiltration using TRRUST, LinkedOmics, and TIMER, respectively.Results The mRNA expression levels of CXCL3/5/6/9/10/11/12/13/16 in GMB were significantly elevated compared to normal tissues. GBM patients with higher transcriptional levels of CXCL5/6 were significantly associated with worse disease-free survival, while higher transcriptional levels of CXCL3/5/8 were significantly related to worse overall survival. The functions of CXC chemokines were enriched in Chemokine signaling pathway, Cytokine-cytokine receptor interaction, IL-17 signaling pathway, et.al. RELA and NFKB1were key transcription factors of CXC chemokines. The kinase targets of CXC chemokine contained CDK1, CDK2, PRKCD, MAPK14, ATM, LCK, MTOR, and GRK3, which are involved in oncogenesis, migration, and survival. Moreover, we revealed significant correlations between the expression of CXC chemokines and the infiltration immune cells, especially for dendritic cells.Conclusion The significant CXC chemokines and related pathways may provide a novel possibility for prognostic biomarkers and immunotherapeutic treatment in GMB.Short title: CXC Chemokines with prognosis in GBM

scholarly journals Targeting STAT3 and STAT5 in Tumor-Associated Immune Cells to Improve Immunotherapy

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1832 ◽  
Author(s):  
Grégory Verdeil ◽  
Toby Lawrence ◽  
Anne-Marie Schmitt-Verhulst ◽  
Nathalie Auphan-Anezin
Keyword(s):  
T Cells ◽  
Transcription Factors ◽  
T Cell ◽  
Immune Suppression ◽  
Immune Cells ◽  
Nuclear Translocation ◽  
Effector Memory ◽  
Negative Effects ◽  
Tumor Associated Macrophages ◽  
Term Survival

Oncogene-induced STAT3-activation is central to tumor progression by promoting cancer cell expression of pro-angiogenic and immunosuppressive factors. STAT3 is also activated in infiltrating immune cells including tumor-associated macrophages (TAM) amplifying immune suppression. Consequently, STAT3 is considered as a target for cancer therapy. However, its interplay with other STAT-family members or transcription factors such as NF-κB has to be considered in light of their concerted regulation of immune-related genes. Here, we discuss new attempts at re-educating immune suppressive tumor-associated macrophages towards a CD8 T cell supporting profile, with an emphasis on the role of STAT transcription factors on TAM functional programs. Recent clinical trials using JAK/STAT inhibitors highlighted the negative effects of these molecules on the maintenance and function of effector/memory T cells. Concerted regulation of STAT3 and STAT5 activation in CD8 T effector and memory cells has been shown to impact their tumor-specific responses including intra-tumor accumulation, long-term survival, cytotoxic activity and resistance toward tumor-derived immune suppression. Interestingly, as an escape mechanism, melanoma cells were reported to impede STAT5 nuclear translocation in both CD8 T cells and NK cells. Ours and others results will be discussed in the perspective of new developments in engineered T cell-based adoptive therapies to treat cancer patients.

scholarly journals Th17/Treg Imbalance and Atherosclerosis

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Xin He ◽  
Bo Liang ◽  
Ning Gu
Keyword(s):  
T Cells ◽  
Transcription Factors ◽  
Regulatory T Cells ◽  
Immune Cells ◽  
Vulnerable Plaque ◽  
Plaque Rupture ◽  
Chronic Inflammatory Disease ◽  
T Helper Cell ◽  
Helper Cell ◽  
T Helper

Atherosclerosis is nowadays recognized as a chronic inflammatory disease of large arteries. In recent years, cellular and molecular biology studies on atherosclerosis confirmed that the occurrence and development are related to inflammation and autoimmunity. A variety of immune cells, cytokines, and transcription factors are involved in this process. Current studies found that T helper cell 17, regulatory T cells, and their cytokines play an important role in the development of atherosclerosis and vulnerable plaque rupture. Here, we provide a review of the up-to-date applications of T helper cell 17, regulatory T cells, cytokines, and their balance in the prognosis and therapy of atherosclerosis.

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