scholarly journals CTHRC1 expression is a novel shared diagnostic and prognostic biomarker of survival in six different human cancer subtypes

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nuzhat Sial ◽  
Mukhtiar Ahmad ◽  
Muhammad Safdar Hussain ◽  
Muhammad Junaid Iqbal ◽  
Yasir Hameed ◽  
...  
Keyword(s):  
Cell Carcinoma ◽  
Prognostic Biomarker ◽  
Human Cancer ◽  
Enrichment Analysis ◽  
Genetic Alterations ◽  
Renal Clear Cell Carcinoma ◽  
Clinicopathological Features ◽  
Cancer Subtypes ◽  
Normal Tissues ◽  
Collagen Triple Helix

AbstractAccording to the previous reports, the collagen triple helix repeat containing 1 (CTHRC1) causes tumorigenesis by modulating the tumor microenvironment, however, the evidence is limited to a few human cancer subtypes. In the current study, we analyzed and validated the CTHRC1 expression variations in 24 different human cancer tissues paired with normal tissues using publically available databases. We observed that CTHRC1 was overexpressed in all the 24 major subtypes of human cancers and its overexpression was significantly associated with the reduced overall survival (OS) duration of head and neck squamous cell carcinoma (HNSC), kidney renal clear cell carcinoma (KIRC), liver hepatocellular carcinoma (LIHC), Lung adenocarcinoma (LUAD), stomach adenocarcinoma (STAD), and Uterine corpus endometrial carcinoma (UCEC). This implies that CTHRC1 plays a significant role in the development and progression of these cancers. We further noticed that CTHRC1 was also overexpressed in HNSC, KIRC, LIHC, LUAD, STAD, and UCEC patients of different clinicopathological features. Pathways enrichment analysis revealed the involvement of CTHRC1 associated genes in seven diverse pathways. We also explored few interesting correlations between CTHRC1 expression and promoter methylation, genetic alterations, CNVs, CD8+ T immune cells infiltration, and tumor purity. In conclusion, CTHRC1 can serve as a shared diagnostic and prognostic biomarker in HNSC, KIRC, LIHC, LUAD, STAD, and UCEC patients of different clinicopathological features.

Up-regulation of GINS1 highlighted a good diagnostic and prognostic potential of survival in three different subtypes of human cancer

2024 ◽  
Vol 84 ◽  
Author(s):  
M. Ahmad ◽  
Y. Hameed ◽  
M. Khan ◽  
M Usman ◽  
A. Rehman ◽  
...  
Keyword(s):  
Immune Cells ◽  
Promoter Methylation ◽  
Prognostic Biomarker ◽  
Human Cancer ◽  
Interaction Network ◽  
Enrichment Analysis ◽  
Copy Number Variations ◽  
Pathway Enrichment Analysis ◽  
Poor Overall Survival ◽  
Cancer Subtypes

Abstract Cancer is a fatal malignancy and its increasing worldwide prevalence demands the discovery of more sensitive and reliable molecular biomarkers. To investigate the GINS1 expression level and its prognostic value in distinct human cancers using a series of multi-layered in silico approach may help to establish it as a potential shared diagnostic and prognostic biomarker of different cancer subtypes. The GINS1 mRNA, protein expression, and promoter methylation were analyzed using UALCAN and Human Protein Atlas (HPA), while mRNA expression was further validated via GENT2. The potential prognostic values of GINS1 were evaluated through KM plotter. Then, cBioPortal was utilized to examine the GINS1-related genetic mutations and copy number variations (CNVs), while pathway enrichment analysis was performed using DAVID. Moreover, a correlational analysis between GINS1 expression and CD8+ T immune cells and a the construction of gene-drug interaction network was performed using TIMER, CDT, and Cytoscape. The GINS1 was found down-regulated in a single subtypes of human cancer while commonly up-regulated in 23 different other subtypes. The up-regulation of GINS1 was significantly correlated with the poor overall survival (OS) of Liver Hepatocellular Carcinoma (LIHC), Lung Adenocarcinoma (LUAD), and Kidney renal clear cell carcinoma (KIRC). The GINS1 was also found up-regulated in LIHC, LUAD, and KIRC patients of different clinicopathological features. Pathways enrichment analysis revealed the involvement of GINS1 in two diverse pathways, while few interesting correlations were also documented between GINS1 expression and its promoter methylation level, CD8+ T immune cells level, and CNVs. Moreover, we also predicted few drugs that could be used in the treatment of LIHC, LUAD, and KIRC by regulating the GINS1 expression. The expression profiling of GINS1 in the current study has suggested it a novel shared diagnostic and prognostic biomarker of LIHC, LUAD, and KIRC.

scholarly journals Integrative Analysis Reveals Methylenetetrahydrofolate Dehydrogenase 1-Like as an Independent Shared  Diagnostic and Prognostic Biomarker in Five Different Human Cancers

2021 ◽  
Author(s):  
Nuzhat Sial ◽  
Jalil Ur Rehman ◽  
Saba Saeed ◽  
Mukhtiar Ahmad ◽  
Yasir Hameed ◽  
...  
Keyword(s):  
Urothelial Cancer ◽  
Prognostic Biomarker ◽  
Enrichment Analysis ◽  
Genetic Alterations ◽  
Clinicopathological Features ◽  
Human Cancers ◽  
Kaplan Meier ◽  
Online Databases ◽  
Methylenetetrahydrofolate Dehydrogenase ◽  
Normal Controls

Background: Defects in MTHFD1L expression have earlier been examined in only a few human cancers. Objectives: Multi-omics profiling of MTHFD1L as a shared biomarker in distinct subtypes of human cancers. Methods: In the current study, for the multi-omics analysis of MTHFD1L in 24 major subtypes of human cancers, a comprehensive in silico approach was adopted to mine different open access online databases including UALCAN, Kaplan Meier (KM) plotter, LOGpc, GEPIA, HPA, GENT2, MEXPRESS, cBioportal, STRING, DAVID, TIMER., and CTD database. Results: We noticed that the expression of MTHFD1L was significantly higher in all the analyzed 24 subtypes of human cancers as compared to the normal controls. Moreover, MTHDF1L overexpression was also found to be significantly associated with the reduced overall survival (OS) duration of Bladder urothelial cancer (BLCA), Head and Neck Cancer (HNSC), Kidney Renal papillary Cell Carcinoma (KIRP), Lung adenocarcinoma (LUAD), and Uterine corpus endometrial carcinoma (UCEC). This implies that MTHFD1L plays a significant role in the development and progression of these cancers. We further noticed that MTHFD1L was also overexpressed in BLCA, HNSC, KIRP, LUAD, and UCEC patients of different clinicopathological features. Pathways enrichment analysis revealed the involvement of MTHFD1L associated genes in 5 diverse pathways. We also explored few interesting correlations between MTHFD1L expression and its promoter methylation, genetic alterations, CNVs, and between CD8+ T immune cells level. Conclusion: In conclusion, our results elucidated that MTHFD1L can serve as a shared diagnostic and prognostic biomarker in BLCA, HNSC, KIRP, LUAD, and UCEC patients of different clinicopathological features.

scholarly journals Identification of Tumor Microenvironment-Related Genes in Kidney Renal Clear Cell Carcinoma Patients via Bioinformatic Analysis

2021 ◽  
Author(s):  
Rongjiong Zheng ◽  
Yaosen SHao ◽  
Mingming Wang ◽  
Yeli Tang ◽  
Meiling Hu
Keyword(s):  
Tumor Microenvironment ◽  
Cell Carcinoma ◽  
Clear Cell ◽  
Clear Cell Carcinoma ◽  
Expression Profiles ◽  
Prognostic Significance ◽  
Enrichment Analysis ◽  
Renal Clear Cell Carcinoma ◽  
The Cancer Genome Atlas ◽  
Functional Enrichment

Abstract BackgroundTumor microenvironment has been implicated in the development and progression of cancers. However, the prognostic significance of tumor microenvironment-related genes in kidney renal clear cell carcinoma (KIRC) remains unclear. MethodsIn this study, we obtained and analyzed gene expression profiles from The Cancer Genome Atlas database. Stromal and immune scores were calculated based on the ESTIMATE algorithm. ResultsIn the discovery series of 537 patients, we identified a list of differentially expressed genes which was significantly associated with prognosis in KIRC patients. Protein-protein interaction networks and functional enrichment analysis were both performed, indicating that these identified genes were related to the immune response. ConclusionsThe tumor microenvironment-related genes could serve as the potential biomarkers for KIRC.

scholarly journals Overexpression of NEIL3 associated with altered genome and poor survival in selected types of human cancer

Tumor Biology ◽  
2020 ◽  
Vol 42 (5) ◽  
pp. 101042832091840
Author(s):  
Oanh TN Tran ◽  
Serkalem Tadesse ◽  
Christopher Chu ◽  
Dawit Kidane
Keyword(s):  
Cell Carcinoma ◽  
Base Excision Repair ◽  
Cancer Genomics ◽  
Excision Repair ◽  
Human Cancer ◽  
Renal Clear Cell Carcinoma ◽  
Lower Grade ◽  
Cancer Phenotypes ◽  
Base Excision ◽  
Repair Genes

Base excision repair, which is initiated by the DNA N-glycosylase proteins, is the frontline for repairing potentially mutagenic DNA base damage. Several base excision repair genes are deregulated in cancer and affect cellular outcomes to chemotherapy and carcinogenesis. Endonuclease VIII-like 3 (NEIL3) is a DNA glycosylase protein that is involved in oxidative and interstrand crosslink DNA damage repair. Our previous work has showed that NEIL3 is required to maintain replication fork integrity. It is unknown whether NEIL3 overexpression could contribute to cancer phenotypes, and its prognostic value and use as potential drug target remain unexplored. Our analysis of cancer genomics data sets reveals that NEIL3 frequently undergoes overexpression in several cancers. Furthermore, patients who exhibited NEIL3 overexpression with pancreatic adenocarcinoma, lung adenocarcinoma, lower grade glioma, kidney renal clear cell carcinoma, and kidney papillary cell carcinoma had worse overall survival. Importantly, NEIL3 overexpressed tumors accumulate mutation and chromosomal variations. Furthermore, NEIL3 overexpressed tumors exhibit simultaneous overexpression of homologous recombination genes (BRCA1/2) and mismatch repair genes ( MSH2/MSH6). However, NEIL3 overexpression is negatively correlated with tumor overexpressing nucleotide excision repair genes ( XPA, XPC, ERCC1/ 2). Our results suggest that NEIL3 might be a potential prognosis marker for high-risk patients, and/or an attractive therapeutic target for selected cancers.

scholarly journals H2A Histone Family Member X (H2AX) Is Upregulated in Ovarian Cancer and Demonstrates Utility as a Prognostic Biomarker in Terms of Overall Survival

2020 ◽  
Vol 9 (9) ◽  
pp. 2844
Author(s):  
Sayeh Saravi ◽  
Eriko Katsuta ◽  
Jeyarooban Jeyaneethi ◽  
Hasnat A. Amin ◽  
Matthias Kaspar ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Overall Survival ◽  
Prognostic Biomarker ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Nucleotide Polymorphisms ◽  
Gene Set Enrichment ◽  
Gene Set ◽  
Normal Tissues

Background: H2AX can be of prognostic value in breast cancer, since in advanced stage patients with high levels, there was an association with worse overall survival (OS). However, the clinical relevance of H2AX in ovarian cancer (OC) remains to be elucidated. Methods: OC H2AX expression studied using the TCGA/GTEX datasets. Subsequently, patients were classified as either high or low in terms of H2AX expression to compare OS and perform gene set enrichment. qRT-PCR validated in-silico H2AX findings followed by immunohistochemistry on a tissue microarray. The association between single nucleotide polymorphisms in the area of H2AX; prevalence and five-year OC survival was tested in samples from the UK Biobank. Results: H2AX was significantly overexpressed in OCs compared to normal tissues, with higher expression associated with better OS (p = 0.010). Gene Set Enrichment Analysis demonstrated gene sets involved in G2/M checkpoint, DNA repair mTORC1 signalling were enriched in the H2AX highly expressing OCs. Polymorphisms in the area around the gene were associated with both OC prevalence (rs72997349-C, p = 0.005) and worse OS (rs10790282-G, p = 0.011). Finally, we demonstrated that H2AX gene expression correlated with γ-H2AX staining in vitro. Conclusions: Our findings suggest that H2AX can be a novel prognostic biomarker for OC.

scholarly journals NCF1/2/4 Are Prognostic Biomarkers Related to the Immune Infiltration of Kidney Renal Clear Cell Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-31
Author(s):  
Yifei Chen ◽  
Fei He ◽  
Ruhua Wang ◽  
Menglin Yao ◽  
Yarui Li ◽  
...  
Keyword(s):  
Cell Carcinoma ◽  
Clear Cell ◽  
Clear Cell Carcinoma ◽  
Genetic Alterations ◽  
Renal Clear Cell Carcinoma ◽  
Prognostic Biomarkers ◽  
Mrna Levels ◽  
Poor Overall Survival ◽  
Cytoplasmic Factor ◽  
Value Analysis

Neutrophil cytoplasmic factor 1/2/4 (NCF1/2/4) belongs to the NADPH oxidase complex, which is a cytoplasmic component, and its polymorphism is the main factor related to autoimmune diseases, which is probably caused by the regulation of peroxide. They also play a role in tumor growth and metastasis. This research is aimed at evaluating the biological function and prognostic role of NCF1, NCF2, and NCF4 genes in kidney renal clear cell carcinoma (KIRC) by using multiple online bioinformatics website, including Oncomine, GEPIA, UALCAN, Kaplan–Meier Plotter, TIMER, TISIDB, cBioPortal, LinkedOmics, GeneMANIA, and DAVID databases. The mRNA levels of NCFs were higher in KIRC tissues than in normal tissues. The overexpression of NCFs was significantly correlated with advanced pathological grades and individual cancer stages in KIRC. Meanwhile, the expressions of NCFs played an important role in the tumorigenesis and progression of KIRC. Prognostic value analysis suggested that high transcription levels of NCF1/4 were associated with poor overall survival in KIRC patients. In addition, results from the LinkedOmics database showed that the KEGG pathway related to NCFs mainly focused on immune activation and immune regulation function. NCF genetic alterations, including copy number amplification, missense mutation, and deep deletion, could be found through the cBioPortal database. Further, NCF expression was significantly correlated with infiltration levels of various immune cells as well as immune signatures. Protein-protein interaction network and enrichment analysis of NCF1/2/4 in KIRC showed that NCF coexpressed genes mainly associated with diverse immune marker sets showed significance. Overall, these results indicated that NCFs could be prognostic biomarkers as well as effective targets for diagnosis in KIRC.

scholarly journals Identification of lysine acetylome of oral squamous cell carcinoma by label-free quantitative proteomics

2021 ◽  
Author(s):  
Jingjing Dong ◽  
Jingquan He ◽  
Zeyu Zhang ◽  
Wei Zhang ◽  
Yixi Li ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Cellular Response ◽  
Enrichment Analysis ◽  
Lysine Acetylation ◽  
Label Free ◽  
Normal Tissues

Abstract Background Lysine acetylation (Kac) favors gene transcription and activates various genes involved in the regulation of oncogenesis, whereas the acetylation profiling of oral squamous cell carcinoma (OSCC) is unknown. We performed lysine acetylation analyses to achieve a comprehensive profile and revealed the specific pathogenesis in patients with OSCC. Methods Liquid chromatography − tandem mass spectrometry (LC-MS/MS) was utilized to investigate lysine acetylation features of tumor tissues and adjacent normal tissues from 9 patients with OCSS. Results Among the upregulated different acetylation proteins (DAPs), the biological process of GO analysis was closely related to cellular response to regulation of apoptotic process, and regulation of programmed cell death. KEGG enrichment analysis was associated with HIF-1 signaling pathway, ferroptosis, and JAK-STAT signaling pathway. In PPI network, seven differently Kac proteins (SRSF1, HNPNPM, PRPF8, DHX9, DHX15, RBMX, SNRPG) in MCODE1 and the top 30 hub gene involved in mRNA splicing process and spliceosome pathway. Six differently Kac modified proteins of RPS15A, RPL11, RPS11, RPS3, RPL24, RPL19 in MCODE1 was enriched in ribosome pathway, particular lower expression of RPS3, RPL24 and RPL19 were related to the overall survival of OSCC. Conclusion This study contributes a foundation for understanding the functions of Kac modification in OSCC and investigates lysine acetylation on proteins involved in ribosome pathway, particularly the ones that acted as hub genes and related to the OSCC survival, which may be a potential therapeutic direction of OSCC in the future.

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