scholarly journals Serine Metabolism Regulates YAP Activity Through USP7 in Colon Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Xiaoya Zhao ◽  
Jianfei Fu ◽  
Bin Hu ◽  
Lin Chen ◽  
Jing Wang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Size Control ◽  
Metabolic Reprogramming ◽  
Tumor Tissues ◽  
Significant Enrichment ◽  
Phosphoglycerate Dehydrogenase ◽  
New Treatment ◽  
The Relationship ◽  
Serine Metabolism

Metabolic reprogramming is a vital factor in the development of many types of cancer, including colon cancer. Serine metabolic reprogramming is a major feature of tumor metabolism. Yes-associated protein (YAP) participates in organ size control and tumorigenesis. However, the relationship between YAP and serine metabolism in colon cancer is unclear. In this study, RNA sequencing and metabolomics analyses indicated significant enrichment of the glycine, serine, and threonine metabolism pathways in serine starvation–resistant cells. Short-term serine deficiency inhibited YAP activation, whereas a prolonged response dephosphorylated YAP and promoted its activity. Mechanistically, USP7 increases YAP stability under increased serine conditions by regulating deubiquitination. Verteporfin (VP) effectively inhibited the proliferation of colon cancer cells and organoids and could even modulate serine metabolism by inhibiting USP7 expression. Clinically, YAP was significantly activated in colon tumor tissues and positively correlated with the expression of phosphoglycerate dehydrogenase (PHGDH) and USP7. Generally, our study uncovered the mechanism by which serine metabolism regulates YAP via USP7 and identified the crucial role of YAP in the regulation of cell proliferation and tumor growth; thus, VP may be a new treatment for colon cancer.

scholarly journals High Expression of PRMT6 Associated With Prognosis and Immune Infiltration in Glioma

2020 ◽  
Author(s):  
Yi Yang ◽  
Zhenshuang Wang ◽  
Shengrong Long ◽  
Jinhai Huang ◽  
Chengran Xu ◽  
...  
Keyword(s):  
Enrichment Analysis ◽  
Clinical Work ◽  
High Expression ◽  
Clinical Indicators ◽  
Immune Infiltration ◽  
Tumor Tissues ◽  
Potential Biomarker ◽  
Patient Prognosis ◽  
The Relationship

Abstract Background: Gliomas are characterised by easy invasion of surrounding tissues, high mortality and poor prognosis. Moreover, with the increase of grade, the prognosis of glioma is increasingly poor and not optimistic. Therefore, biological markers for glioma are needed in clinical work, which can be utilized to detect and evaluate the situation and prognosis of glioma patients. Many studies have found that the protein arginine methyltransferase 6 (PRMT6) expression is elevated in various tumors and is associated with patient prognosis. However, the role of PRMT6 in glioma has not been reported or analyzed. Methods: In this study, we used a variety of tumor related databases to analyze the mechanism of PRMT6 in tumors, especially gliomas, from the perspective of bioinformatics, and carried out relevant experimental verification with tumor tissues extracted from patients during surgery. In addition, we analyzed the relationship between PRMT6 expression and immune infiltration and immune-related cells, and discussed the possible mechanisms. We also discussed the role of PRMT6 expression in glioma from the perspectives of mutation, clinical indicators, enrichment analysis, and immunohistochemical results. Results: PRMT6 is significantly differentially expressed in a variety of tumors and is associated with survival and prognosis. Especially in gliomas, the expression of PRMT6 gradually increased with the increase of grade. In addition, PRMT6 can be used as an independent prognostic risk factor in the nomogram and has been verified in a variety of databases. Conclusions: Our results indicate that high expression of PRMT6 is a potential biomarker for predicting glioma prognosis and progression.

scholarly journals Identification and Validation of a Glycolysis Related Metabolic Reprogramming Gene Signature for Predicting Survival in Colon Cancer Patients

2021 ◽  
Author(s):  
Gang Liu ◽  
Xiaowang WU ◽  
Jian Chen
Keyword(s):  
Colon Cancer ◽  
Prediction Model ◽  
Cox Regression ◽  
Malignant Tumors ◽  
Gene Signature ◽  
Metabolic Reprogramming ◽  
Risk Scores ◽  
Cox Regression Analysis ◽  
Prognosis Model ◽  
The Relationship

Abstract Background Colon cancer (CC) is one of the most common gastrointestinal malignant tumors with high mortality rate. Because of malignancy and easily metastasis feather, and limited treatments, the prognosis of CC remains poor. Glycolysis is a metabolic process of glucose in anoxic environments which is an important way to provide energy for tumor. The role of glycolysis in CC largely remains unknown and is necessary to be explored. Method In our study, we analyzed glycolysis related genes expression in CC, patients gene expression and corresponding clinical data were downloaded from GEO dataset, glycolysis related genes sets were collected from Msigdb. Through COX regression analysis, prognosis model based on glycolysis-related genes was established. The efficacy of gene model was tested by Survival analysis, ROC analysis and PCA analysis. Furthermore, the relationship between risk scores and clinical characteristic was researched. Results Our findings identified 13 glycolysis related genes (NUP107, SEC13, ALDH7A1, ALG1, CHPF, FAM162A, FBP2, GALK1, IDH1, TGFA, VLDLR, XYLT2 and OGDHL) consisted prognostic prediction model with relative high accuracy. The relationship between prediction model and clinical feathers were specifically studied, results showed age > 65years, TNM III-IV, T3-4, N1-3, M1 and high-risk score were independent prognostic risk factors with poorer prognosis. Finally, model genes were significantly expressed and EMT were activated in CC patients. Conclusion This study provided a new aspect to advance our understanding in the potential mechanism of glycolysis in CC.

scholarly journals The Role of Tumor-Infiltrating B Cells in Tumor Immunity

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Fei Fei Guo ◽  
Jiu Wei Cui
Keyword(s):  
T Cells ◽  
B Cells ◽  
Tumor Immunity ◽  
Therapeutic Target ◽  
Tumor Biomarker ◽  
Potential Therapeutic Target ◽  
Tumor Inhibition ◽  
Tumor Tissues ◽  
The Relationship

Earlier studies on elucidating the role of lymphocytes in tumor immunity predominantly focused on T cells. However, the role of B cells in tumor immunity has increasingly received better attention in recent studies. The B cells that infiltrate tumor tissues are called tumor-infiltrating B cells (TIBs). It is found that TIBs play a multifaceted dual role in regulating tumor immunity rather than just tumor inhibition or promotion. In this article, latest research advances focusing on the relationship between TIBs and tumor complexity are reviewed, and light is shed on some novel ideas for exploiting TIBs as a possible tumor biomarker and potential therapeutic target against tumors.

scholarly journals THE ROLE OF ADIPOCYTOKINES IN COLON CANCER AND ADENOMAS / ULOGA ADIPOCITOKINA U KANCERU I ADENOMIMA DEBELOG CREVA

2013 ◽  
Vol 33 (2) ◽  
pp. 135-142 ◽  
Author(s):  
Feti Tulubas ◽  
Rafet Mete ◽  
Meltem Oznur ◽  
Birol Topcu
Keyword(s):  
Colon Cancer ◽  
Pearson Correlation ◽  
Continuous Variables ◽  
Colon Adenoma ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
And Control ◽  
The Relationship ◽  
Insulin Insensitivity

Summary Metabolic changes resulting from obesity, insulin insensitivity, and imbalances in hormones such as adiponectin, leptin, resistin, apelin and visfatin, which are derived from white adipose tissue-derived hormone, are directly linked to both colon cancer (CC) and inflammatory bowel diseases increasing tissue-derived risk. We conducted this study to evaluate the relationship between the circulating concentrations of adiponectin, leptin, resistin, apelin and visfatin and colon adenoma and CC. Our study included 90 participants aged >18 years who were divided into three groups: colon cancer, adenoma and control. The serum concentrations of the investigated adipohormones were measured with ELISA in 30 patients with colon adenoma, 30 with CC and 30 controls with no colon pathology. Demographic, anthropometric, metabolic and hormonal parameters were also recorded. The group means were compared by using one-way analysis of variance (ANOVA). Dual comparisons between groups were analyzed with the Tukey test. Pearson correlation coefficient was used to determine the relation between continuous variables. Adiponectin and leptin levels in patients with adenomas (p<0.000; p<0.000, respectively) and CC (p<0.000; p<0.000, respectively) were lower than in controls. Apelin level in patients with CC (p<0.000; p<0.000, respectively) was lower than in patients with adenomas and in controls. Resistin and visfatin levels in patients with CC (p<0.000; p<0.000, respectively) were higher than in patients with adenomas and in controls.

scholarly journals High PRMT6 expression Associated With Prognosis and Immune Infiltration in Glioma

2021 ◽  
Author(s):  
Yi Yang ◽  
Zhenshuang Wang ◽  
Shengrong Long ◽  
Jinhai Huang ◽  
Chengran Xu ◽  
...  
Keyword(s):  
Risk Factor ◽  
Poor Prognosis ◽  
Enrichment Analysis ◽  
Arginine Methyltransferase ◽  
Clinical Indicators ◽  
Immune Infiltration ◽  
Tumor Tissues ◽  
Potential Biomarker ◽  
The Relationship

Abstract Background Glioma is characterised by easy invasion of surrounding tissues, high mortality and poor prognosis. Moreover, the prognosis of glioma is getting worse and worse with the increase of grade, which is not optimistic. Therefore, biological markers for glioma are needed in clinical to detect and evaluate the situation and prognosis of patients with glioma. In many studies, we have found that the protein arginine methyltransferase 6 (PRMT6) expression is elevated in various tumors, which is associated with prognosis of patient. However, there has been no report or study on the role of PRMT6 in glioma. Methods In this study, we used various tumor-related databases to analyze the mechanism of PRMT6 in tumors, especially gliomas, from bioinformatics, and carried out relevant experimental verification with tumor tissues extracted from patients during surgery. Besides, we analyzed the relationship between PRMT6 expression and immune infiltration and immune-related cells, and discussed the possible mechanisms. We also discussed the role of PRMT6 expression in glioma from mutation, clinical indicators, enrichment analysis, and immunohistochemical results. Results PRMT6 is significantly differentially expressed in multiple tumors, which is associated with survival and prognosis. Especially in gliomas, the PRMT6 expression gradually increased with the grade increasing. Besides, PRMT6 can be used as an independent prognostic risk factor in the nomogram and has been verified in various databases. Conclusions Our results indicate that high PRMT6 expression is a potential biomarker for predicting prognosis and progression of glioma.

Cancer and metabolism

2016 ◽  
pp. 119-124
Author(s):  
Cameron Snell ◽  
Kevin C. Gatter ◽  
Adrian L. Harris ◽  
Francesco Pezzella
Keyword(s):  
Tumour Growth ◽  
Glycogen Synthesis ◽  
Metabolic Reprogramming ◽  
Suppressor Activity ◽  
Metabolic Switch ◽  
Metabolic Genes ◽  
Tumour Suppressor Activity ◽  
Metabolic Transformation ◽  
The Relationship

This chapter covers the relationship between cancer and metabolism. It discusses the role of angiogenesis and metabolic reprogramming in influencing tumour growth. The transcription factors that orchestrate the metabolic switch are discussed. The chapter presents an overview of the contribution of tumour suppressors to increased glycolysis. The metabolic changes that support uncontrolled proliferation such as lactate and pH levels, hypoxia, and reactive oxygen species are discussed. The chapter also covers the contribution of metabolic genes with oncogenic or tumour suppressor activity to metabolic transformation, the upregulation of lipid biosynthesis in cancer, and glycogen synthesis in cancer. The chapter concludes with a description of the potential strategies for targeting metabolic transformation.

scholarly journals The size-wise nucleus: nuclear volume control in eukaryotes

2007 ◽  
Vol 179 (4) ◽  
pp. 583-584 ◽  
Author(s):  
Michael D. Huber ◽  
Larry Gerace
Keyword(s):  
Fission Yeast ◽  
Cell Size ◽  
Size Control ◽  
Growth Conditions ◽  
Nuclear Size ◽  
Yeast Cells ◽  
Volume Control ◽  
Wide Range ◽  
The Relationship

Eukaryotic cells have an “awareness” of their volume and organellar volumes, and maintain a nuclear size that is proportional to the total cell size. New studies in budding and fission yeast have examined the relationship between cell and nuclear volumes. It was found that the size of the nucleus remains proportional to cell size in a wide range of genetic backgrounds and growth conditions that alter cell volume and DNA content. Moreover, in multinucleated fission yeast cells, Neumann and Nurse (see p. 593 of this issue) found that the sizes of individual nuclei are controlled by the relative amount of cytoplasm surrounding each nucleus. These results highlight a role of the cytoplasm in nuclear size control.

AKR1B10 accelerates the production of pro-inflammatory cytokines via NF-κB signaling pathway in colon cancer

2019 ◽  
Author(s):  
Cong Liu ◽  
Lei Shi ◽  
Wanyun Li ◽  
Zilan Huang ◽  
Shengyu Wang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Reductase Activity ◽  
Clinical Stage ◽  
Clinicopathological Characteristics ◽  
The Relationship ◽  
Pro Inflammatory Cytokines

Abstract Aldo-keto reductase family 1, member B10 (AKR1B10) has been reported to be involved in tumorigenesis of various cancer. In our studies, we evaluated the relationship between AKR1B10 expression and clinicopathological characteristics in colon cancer and showed that AKR1B10 expression was significantly correlated with TNM stage and clinical stage of colon cancer. It has been reported that colorectal cancer is closely associated with chronic inflammation and the underlying molecular mechanisms are still elusive. Here we found that knockdown of AKR1B10 significantly decreased the expression of the inflammatory cytokines, IL1α and IL6, induced by lipopolysaccharide (LPS) via inhibiting NF-κB signaling pathway. Furthermore, AKR1B10 depends on its reductase activity to affect the NF-κB signaling pathway and subsequently affect the production of inflammatory cytokines. In addition, knockdown of AKR1B10 effectively reduced cell proliferation and clonogenic growth, indicating the biologic role of AKR1B10 in colon cancer. Collectively, our findings provided important insights into a previously unrecognized role of AKR1B10 in colon cancer.

scholarly journals Interplay of Immunometabolism and Epithelial–Mesenchymal Transition in the Tumor Microenvironment

2021 ◽  
Vol 22 (18) ◽  
pp. 9878
Author(s):  
Ming-Yu Chou ◽  
Muh-Hwa Yang
Keyword(s):  
Tumor Microenvironment ◽  
Immune Cells ◽  
Tumor Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Immune Surveillance ◽  
Metabolic Reprogramming ◽  
Mesenchymal Transition ◽  
Regulatory Loop ◽  
The Relationship

Epithelial–mesenchymal transition (EMT) and metabolic reprogramming in cancer cells are the key hallmarks of tumor metastasis. Since the relationship between the two has been well studied, researchers have gained increasing interest in the interplay of cancer cell EMT and immune metabolic changes. Whether the mutual influences between them could provide novel explanations for immune surveillance during metastasis is worth understanding. Here, we review the role of immunometabolism in the regulatory loop between tumor-infiltrating immune cells and EMT. We also discuss the challenges and perspectives of targeting immunometabolism in cancer treatment.

scholarly journals Metabolic Reprogramming and Renal Fibrosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Xiaoyu Zhu ◽  
Lili Jiang ◽  
Mengtuan Long ◽  
Xuejiao Wei ◽  
Yue Hou ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Potential Role ◽  
Acid Metabolism ◽  
Metabolic Reprogramming ◽  
Novel Drugs ◽  
Future Challenges ◽  
And Function ◽  
Relationship Of ◽  
The Relationship

There are several causes of chronic kidney disease, but all of these patients have renal fibrosis. Although many studies have examined the pathogenesis of renal fibrosis, there are still no effective treatments. A healthy and balanced metabolism is necessary for normal cell growth, proliferation, and function, but metabolic abnormalities can lead to pathological changes. Normal energy metabolism is particularly important for maintaining the structure and function of the kidneys because they consume large amounts of energy. We describe the metabolic reprogramming that occurs during renal fibrosis, which includes changes in fatty acid metabolism and glucose metabolism, and the relationship of these changes with renal fibrosis. We also describe the potential role of novel drugs that disrupt this metabolic reprogramming and the development of fibrosis, and current and future challenges in the treatment of fibrosis.

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