scholarly journals Systematic Multiomics Analysis of Alterations in C1QBP mRNA Expression and Relevance for Clinical Outcomes in Cancers

2019 ◽  
Vol 8 (4) ◽  
pp. 513 ◽  
Author(s):  
Subbroto Saha ◽  
Kyung Kim ◽  
S.M. Islam ◽  
Ssang-Goo Cho ◽  
Minchan Gil
Keyword(s):  
Cancer Progression ◽  
Ribosome Biogenesis ◽  
Patient Survival ◽  
Protein A ◽  
The Cancer Genome Atlas ◽  
Therapeutic Modality ◽  
Relative Expression ◽  
Kaplan Meier ◽  
Infection Processes ◽  
The Relationship

C1QBP (Complement Component 1 Q Subcomponent-Binding Protein), a multicompartmental protein, participates in various cellular processes, including mRNA splicing, ribosome biogenesis, protein synthesis in mitochondria, apoptosis, transcriptional regulation, and infection processes of viruses. The correlation of C1QBP expression with patient survival and molecular function of C1QBP in relation to cancer progression has not been comprehensively studied. Therefore, we sought to systematically investigate the expression of C1QBP to evaluate the change of C1QBP expression and the relationship with patient survival and affected pathways in breast, lung, colon, and bladder cancers as well as lymphoma. Relative expression levels of C1QBP were analyzed using the Oncomine, Gene Expression Across Normal and Tumor Tissue (GENT), and The Cancer Genome Atlas (TCGA) databases. Mutations and copy number alterations in C1QBP were also analyzed using cBioPortal, and subsequently, the relationship between C1QBP expression and survival probability of cancer patients was explored using the PrognoScan database and the R2: Kaplan Meier Scanner. Additionally, the relative expression of C1QBP in other cancers, and correlation of C1QBP expression with patient survival were investigated. Gene ontology and pathway analysis of commonly differentially coexpressed genes with C1QBP in breast, lung, colon, and bladder cancers as well as lymphoma revealed the C1QBP-correlated pathways in these cancers. This data-driven study demonstrates the correlation of C1QBP expression with patient survival and identifies possible C1QBP-involved pathways, which may serve as targets of a novel therapeutic modality for various human cancers.

scholarly journals CYSTM1: A Novel Biomarker for Hepatocellular Carcinoma Prognosis

2021 ◽  
Author(s):  
Jun Du ◽  
Jinguo Wang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Poor Prognosis ◽  
Early Stage ◽  
Human Tumor ◽  
The Cancer Genome Atlas ◽  
Data Set ◽  
Kaplan Meier ◽  
Cancer Genome Atlas ◽  
Cox Proportional Hazard Regression ◽  
The Relationship

Abstract Background: The expression and molecular mechanism of cysteine rich transmembrane module containing 1 (CYSTM1) in human tumor cells remains unclear. The aim of this study was to determine whether CYSTM1 could be used as a potential prognostic biomarker for hepatocellular carcinoma (HCC).Methods: We first demonstrated the relationship between CYSTM1 expression and HCC in various public databases. Secondly, Kaplan–Meier analysis and Cox proportional hazard regression model were performed to evaluate the relationship between the expression of CYSTM1 and the survival of HCC patients which data was downloaded in the cancer genome atlas (TCGA) database. Finally, we used the expression data of CYSTM1 in TCGA database to predict CYSTM1-related signaling pathways through bioinformatics analysis.Results: The expression level of CYSTM1 in HCC tissues was significantly correlated with T stage (p = 0.039). In addition, Kaplan–Meier analysis showed that the expression of CYSTM1 was significantly associated with poor prognosis in patients with early-stage HCC (p = 0.003). Multivariate analysis indicated that CYSTM1 is a potential predictor of poor prognosis in HCC patients (p = 0.036). The results of biosynthesis analysis demonstrated that the data set of CYSTM1 high expression was mainly enriched in neurodegeneration and oxidative phosphorylation pathways.Conclusion: CYSTM1 is an effective biomarker for the prognosis of patients with early-stage HCC and may play a key role in the occurrence and progression of HCC.

scholarly journals Prognostic Significance of NBEAL2 in Liver hepatocellular carcinoma

2021 ◽  
Author(s):  
Yanghui Wen ◽  
Hui Su ◽  
Wuke Wang ◽  
Feng Ren ◽  
Haitao Jiang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Expression Profiles ◽  
Prognostic Significance ◽  
The Cancer Genome Atlas ◽  
Clinicopathological Parameters ◽  
Chi Square ◽  
Kaplan Meier ◽  
Chi Square Test ◽  
Liver Hepatocellular Carcinoma ◽  
The Relationship

Abstract Background: NBEAL2 is a member of the BEACH domain–containing protein (BDCP) family and little is known about the relationship between NBEAL2 and malignancy.Methods: We downloaded the Gene expression profiles and clinical data of Liver hepatocellular carcinoma(LIHC) form the Cancer Genome Atlas (TCGA) dataset. The expression difference of NBEAL2 in LIHC tissues and adjacent nontumor tissues was analyzed by R software. The relationship between NBEAL2 expression and clinicopathological parameters was evaluate by Chi-square test. The effect of NBEAL2 expression on survival were assessed by Kaplan–Meier survival analysis and Cox proportional hazards regression model. GSEA was used to explore the potential molecular mechanism of NBEAL2 in LIHC.Results: Up-regulation of NBEAL2 expression was detected in the LIHC tissue compared with adjacent nontumor tissues(P < 0.001). The chi-square test showed that no significant correlation between the expression level of NBEAL2 and various clinicopathological parameters (including T, N and M classifications) were detected. The Kaplan–Meier curves suggested that lower NBEAL2 expression was related with poor prognosis. The results of Multivariate analysis revealed that a lower expression of NBEAL2 in LIHC was an independent risk of poor overall survival (HR, 8.873; 95% CI, 1.159-67.936; P = 0.035). GSEA suggested that multiple tumor-related metabolic pathways were evidently enriched in samples with the low-NBEAL2 expression phenotype. Conlusion: NBEAL2 might act as an tumor suppressor gene in the progression of LIHC but the precise role of NBELA2 in LIHC needs further vertification.

scholarly journals CEND1 and GJB6 co-expression as a prognostic factor in colorectal cancer

2021 ◽  
Author(s):  
Rui Chen ◽  
Zhan Wang ◽  
Dong Ma ◽  
Yijiang Han ◽  
Junsong Liu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Perineural Invasion ◽  
Patient Survival ◽  
Colorectal Cancer Patient ◽  
Cell Communication ◽  
Tumor Location ◽  
Protein Levels ◽  
Kaplan Meier ◽  
Clinicopathological Findings

Abstract Background: Perineural invasion is an important mechanism of cancer progression that is not well understood at present. The present study explored the relationship between GJB6, CEND1, and cell-cell communication as regulators of colorectal cancer patient survival and clinicopathological findings.Method: Immunohistochemical staining was performed to assess CEND1 and GJB6 expression levels in CRC patient samples, while survival outcomes were assessed using Kaplan-Meier curves and log-rank tests.Results: Elevated CEND1 expression was associated with tumor location, poor differentiation, and perineural invasion, while GJB6 expression was positively correlated with TNM stage, distant metastasis, and perineural invasion. In addition, GJB6 and CEND1 protein levels were correlated with one another in CRC patient tissues, and high expression of both of these proteins was associated with a higher risk of perineural invasion. CEND1+/GJB6+ status was also associated with poorer patient survival, highlighting both of these proteins as prognostic biomarkers in CRC patients.Conclusion: Elevated levels of CEND1 and GJB6 are independent predictors of poorer CRC patient prognosis.

scholarly journals CPXM1: a novel biomarker for gastric cancer prognosis

2021 ◽  
Author(s):  
Jun Du ◽  
Mengxiang Zhu ◽  
Wenwu Yan ◽  
Changsheng Yao ◽  
Qingyi Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Poor Prognosis ◽  
The Cancer Genome Atlas ◽  
Cancer Prognosis ◽  
Signal Pathways ◽  
Data Set ◽  
Kaplan Meier ◽  
Cancer Genome Atlas ◽  
Cox Proportional Hazard Regression ◽  
The Relationship

Abstract Background The molecular role of carboxypeptidase X, M14 family member (CPXM1) in oncogenesis or tumor progression remains unclear. The aim of this study was to determine whether CPXM1 can be used as a potential prognostic biomarker for gastric cancer (GC). Methods We first demonstrated the relationship between CPXM1 expression and GC in various public databases. Secondly, the expression of CPXM1 in GC tissues was further verified by immunohistochemical staining using tissue microarray containing 96 cases of GC patients. Kaplan–Meier analysis and a Cox proportional hazard regression model were performed to evaluate the relationship between the expression of CPXM1 and the survival of GC patients. Finally, we used the expression data of CPXM1 in The Cancer Genome Atlas database to predict CPXM1-related signaling pathways through bioinformatics analysis. Results The expression level of CPXM1 in GC tissues was significantly correlated with tumor size (p = 0.041) and lymph node metastasis (p = 0.014). In addition, Kaplan–Meier analysis showed that the expression of CPXM1 in GC tissues was significantly associated with poor prognosis (p = 0.011). Multivariate analysis indicated that CPXM1 is a potential predictor of poor prognosis in GC patients (p = 0.026). The results of biosynthesis analysis demonstrated that the data set of CPXM1 high expression was mainly enriched in cancer-related signal pathways. Conclusion CPXM1 is an effective biomarker for the prognosis of GC patients and may play a key role in the occurrence and progression of GC.

scholarly journals Identification of Key Genes Associated with Progression and Prognosis of Bladder Cancer through Integrated Bioinformatics Analysis

Cancers ◽  
2021 ◽  
Vol 13 (23) ◽  
pp. 5931
Author(s):  
Shiv Verma ◽  
Eswar Shankar ◽  
Spencer Lin ◽  
Vaibhav Singh ◽  
E. Ricky Chan ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Progression ◽  
Univariate Analysis ◽  
Gene Expression Omnibus ◽  
The Cancer Genome Atlas ◽  
Cancer Prognosis ◽  
Kaplan Meier ◽  
Human Protein Atlas ◽  
Validation Set ◽  
Muscle Invasive

Bladder cancer prognosis remains dismal due to lack of appropriate biomarkers that can predict its progression. The study aims to identify novel prognostic biomarkers associated with the progression of bladder cancer by utilizing three Gene Expression Omnibus (GEO) datasets to screen differentially expressed genes (DEGs). A total of 1516 DEGs were identified between non-muscle invasive and muscle invasive bladder cancer specimens. To identify genes of prognostic value, we performed gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. A total of seven genes, including CDKN2A, CDC20, CTSV, FOXM1, MAGEA6, KRT23, and S100A9 were confirmed with strong prognostic values in bladder cancer and validated by qRT-PCR conducted in various human bladder cancer cells representing stage-specific disease progression. ULCAN, human protein atlas and The Cancer Genome Atlas datasets were used to confirm the predictive value of these genes in bladder cancer progression. Moreover, Kaplan–Meier analysis and Cox hazard ratio analysis were performed to determine the prognostic role of these genes. Univariate analysis performed on a validation set identified a 3-panel gene set viz. CDKN2A, CTSV and FOXM1 with 95.5% sensitivity and 100% specificity in predicting bladder cancer progression. In summary, our study screened and confirmed a 3-panel biomarker that could accurately predict the progression and prognosis of bladder cancer.

scholarly journals ATG101 as a Novel Prognostic Biomarker Related to Immunotherapy in Pan-cancer

2021 ◽  
Author(s):  
Zijian Zhang ◽  
Jinggang Mo ◽  
Chong Jin ◽  
Hao Jiang ◽  
Zhongtao Liu ◽  
...  
Keyword(s):  
Critical Role ◽  
Tissue Expression ◽  
The Cancer Genome Atlas ◽  
Immune Checkpoints ◽  
Integrated Analysis ◽  
Tumour Immunity ◽  
Kaplan Meier ◽  
Cancer Genome Atlas ◽  
The Relationship ◽  
Pan Cancer

Abstract Background: ATG101 plays a significant role in the occurrence and development of tumours by regulating autophagy. Our study aimed to research the correlation between the expression of ATG101 and tumour prognosis and its role in tumour immunity. Methods: First, integrated analysis of The Cancer Genome Atlas and Genotype-Tissue Expression portals were used to analyse the expression of ATG101. Then, we used Kaplan–Meier curves for survival analysis. Next, we analysed the relationship between ATG101 expression and six immune cells, the immune microenvironment and immune checkpoints. Besides, we analysed the relationship between the expression of ATG101 and methyltransferase. Finally, we used GSEA to study the function of ATG101 in COAD and LIHC. Results: Integrated analysis showed that ATG101 was overexpressed in different tumours. Kaplan–Meier curves found that ATG101 was associated with poor prognosis in most tumours. We found that that ATG101 can be used as a target and prognostic marker of tumour immunotherapy for different tumours. We also found that ATG101 regulates DNA methylation. GSEA analysis showed that ATG101 may play a critical role in COAD and LIHC.Conclusions: Our study highlights the significance of ATG101 in the study of tumour immunity from a pan-cancer perspective.

scholarly journals A Targeted Bioinformatics Assessment of Adrenocortical Carcinoma Reveals Prognostic Implications of GABA System Gene Expression

2020 ◽  
Vol 21 (22) ◽  
pp. 8485
Author(s):  
Erika L. Knott ◽  
Nancy J. Leidenheimer
Keyword(s):  
Cell Line ◽  
Cancer Progression ◽  
Adrenocortical Carcinoma ◽  
Patient Survival ◽  
Gabab Receptor ◽  
The Cancer Genome Atlas ◽  
Functional Studies ◽  
Gaba Transporters ◽  
Gaba System ◽  
Metabolic Heterogeneity

Adrenocortical carcinoma (ACC) is a rare but deadly cancer for which few treatments exist. Here, we have undertaken a targeted bioinformatics study of The Cancer Genome Atlas (TCGA) ACC dataset focusing on the 30 genes encoding the γ-aminobutyric acid (GABA) system—an under-studied, evolutionarily-conserved system that is an emerging potential player in cancer progression. Our analysis identified a subset of ACC patients whose tumors expressed a distinct GABA system transcriptome. Transcript levels of ABAT (encoding a key GABA shunt enzyme), were upregulated in over 40% of tumors, and this correlated with several favorable clinical outcomes including patient survival; while enrichment and ontology analysis implicated two cancer-related biological pathways involved in metastasis and immune response. The phenotype associated with ABAT upregulation revealed a potential metabolic heterogeneity among ACC tumors associated with enhanced mitochondrial metabolism. Furthermore, many GABAA receptor subunit-encoding transcripts were expressed, including two (GABRB2 and GABRD) prognostic for patient survival. Transcripts encoding GABAB receptor subunits and GABA transporters were also ubiquitously expressed. The GABA system transcriptome of ACC tumors is largely mirrored in the ACC NCI-H295R cell line, suggesting that this cell line may be appropriate for future functional studies investigating the role of the GABA system in ACC cell growth phenotypes and metabolism.

ARRB2 promotes colorectal cancer growth through triggering WTAP

2020 ◽  
Author(s):  
Hongguang Liang ◽  
Zelong Lin ◽  
Youqiong Ye ◽  
Rongcheng Luo ◽  
Lixian Zeng
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Wilms Tumor ◽  
The Cancer Genome Atlas ◽  
Cancer Pathways ◽  
Normal Tissues ◽  
Kaplan Meier ◽  
Cancer Genome Atlas ◽  
And Migration ◽  
Proliferation And Migration

Abstract Colorectal cancer (CRC) is one of the most lethal cancers worldwide. The expression of β-arrestin2 (β-Arr2, ARRB2) in CRC has been well investigated; however, its exact mechanism causing the cancer progression remains unclear. In this study, we discovered that the expression level of ARRB2 was significantly upregulated in CRC as compared to the normal tissues by employing the Cancer Genome Atlas (TCGA) data, western blot analysis, and immunohistochemistry. Furthermore, the level of ARRB2 was correlated with the patients’ overall survival by Kaplan–Meier analysis. The higher expression of ARRB2 promoted CRC cell growth, enhanced the cell motility, and blocked cell apoptosis, which is crucial for tumor growth. Lastly, the suppression of ARRB2 expression was enough to attenuate the progression of CRC induced by azoxymethane/dextran sodium sulfate. Interestingly, we also found that the knockdown of ARRB2 decreased several cancer pathways mediated by the expression of Wilms tumor 1 associated protein (WTAP), which led to the inhibition of cell proliferation and migration. Altogether, our results demonstrated that ARRB2 promoted the growth and migration of CRC cells by regulating the WTAP expression.

scholarly journals Genome-wide analysis of the hypoxia-related DNA methylation-driven genes in lung adenocarcinoma progression

2020 ◽  
Vol 40 (2) ◽  
Author(s):  
Hongxia Li ◽  
Li Tong ◽  
Hong Tao ◽  
Zhe Liu
Keyword(s):  
Dna Methylation ◽  
Lung Adenocarcinoma ◽  
Cancer Progression ◽  
Smoking Status ◽  
Disease Free Survival ◽  
Poor Prognostic Factor ◽  
Protein Protein Interaction ◽  
Kaplan Meier ◽  
Key Genes ◽  
The Relationship

Abstract Lung adenocarcinoma (LUAD) is a common type of lung cancer with high incidence and poor prognosis. Hypoxia and DNA methylation play important regulatory roles in cancer progression. The purpose of the present study was to explore the relationship between hypoxia and DNA methylation, and to identify key genes for hypoxia-regulated LUAD progression. Hypoxia score (HS) was calculated using the GSVA algorithm. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment and protein–protein interaction (PPI) analysis were performed using clusterProfile package, STRING database and Cytoscape software. Kaplan–Meier curves of overall survival (OS) and disease-free survival (DFS) were drawn using R software. Smoking status and cancer stages were significantly associated with LUAD hypoxia, and hypoxia is a poor prognostic factor for LUAD. Compared with HS-low group, 1803 aberrantly methylated DEGs were identified in HS-high group. KEGG analysis showed that the 1803 genes were enriched in the metabolic pathways associated with hypoxia stress, angiogenesis and cancer progression. FAM20C, MYLIP and COL7A1 were identified as the hypoxia-related key genes in LUAD progression, which were regulated by DNA methylation. Hypoxia in LUAD tumor cells led to changes in DNA methylation patterns. In-depth study of the relationship between hypoxia and DNA methylation is helpful to elucidate the mechanism of tumorigenesis, and provides new ideas for LUAD treatment.

scholarly journals The overexpression of FKBP4 in patients with lung adenocarcinoma predicts poor prognosis and tumor progression

2021 ◽  
Author(s):  
Sha Tian ◽  
Shang qing Wang ◽  
Piao Zheng ◽  
Xu Zhu ◽  
Huan Han ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathways ◽  
Cancer Progression ◽  
Poor Prognosis ◽  
Cox Regression ◽  
Gene Set Enrichment Analysis ◽  
The Cancer Genome Atlas ◽  
Clinicopathological Parameters ◽  
Poor Overall Survival ◽  
Kaplan Meier

Abstract Background: The FK506-binding protein 4 ( FKBP4 ), a tumor-related gene, plays a vital role in tumorigenesis and cancer progression. The study is aimed to clarify the effect of FKBP4 in lung adenocarcinoma (LUAD). Methods: Relying on The Cancer Genome Atlas (TCGA) cohort, the FKBP4 expression difference between LUAD tissues and non-tumor tissues was first detected, and verified with public tissue microarrays (TMAs), clinical LUAD specimen cohort and Gene Expression Omnibus (GEO) cohort. Then, logistic regression analysis and chi-square test were applied to detect the correlation between FKBP4 expression and clinicopathological parameters. Kaplan-Meier survival analysis and Cox regression model were utilized to evaluate the effect of FKBP4 expression on survival. Signaling pathways related to LUAD were obtained via employing Gene Set Enrichment Analysis (GSEA). Results: The FKBP4 expression level in LUAD samples was dramatically higher than that in non-tumor samples. High FKBP4 expression in LUAD is associated with gender, pathological stage, T classification, lymph node metastasis and distant metastasis. The Kaplan-Meier curve indicated a poor prognosis for LUAD patients with high FKBP4 expression. Multivariate analysis suggested that the high FKBP4 expression was a vital independent predictor of poor overall survival (OS). GSEA showed that a total of 15 signaling pathways were enriched in samples with high FKBP4 expression phenotype. Conclusions: FKBP4 may be an oncogene in LUAD, and is promised to become a prognostic indicator and therapeutic target for LUAD.

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