scholarly journals A pan-cancer analysis revealed the role of the SLC16 family in cancer

Channels ◽  
2021 ◽  
Vol 15 (1) ◽  
pp. 528-540 ◽  
Author(s):  
Jun Li ◽  
Jiaheng Xie ◽  
Dan Wu ◽  
Liang Chen ◽  
Zetian Gong ◽  
...  
Keyword(s):  
Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 4828-4840
Author(s):  
Guoliang Cui ◽  
Can Wang ◽  
Zhenyan Lin ◽  
Xiaoke Feng ◽  
Muxin Wei ◽  
...  
Keyword(s):  

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Linbang Wang ◽  
Tao He ◽  
Jingkun Liu ◽  
Jiaojiao Tai ◽  
Bing Wang ◽  
...  

Abstract Background Tumor-associated macrophages (TAMs) are abundant in the tumor microenvironment (TME). However, their contribution to the immunosuppressive status of the TME remains unclear. Methods We integrated single-cell sequencing and transcriptome data from different tumor types to uncover the molecular features of TAMs. In vitro experiments and prospective clinical tests confirmed the results of these analysis. Results We first detected intra- and inter-tumoral heterogeneities between TAM subpopulations and their functions, with CD86+ TAMs playing a crucial role in tumor progression. Next, we focused on the ligand-receptor interactions between TAMs and tumor cells in different TME phenotypes and discovered that aberrant expressions of six hub genes, including FLI1, are involved in this process. A TAM-tumor cell co-culture experiment proved that FLI1 was involved in tumor cell invasion, and FLI1 also showed a unique pattern in patients. Finally, TAMs were discovered to communicate with immune and stromal cells. Conclusion We determined the role of TAMs in the TME by focusing on their communication pattern with other TME components. Additionally, the screening of hub genes revealed potential therapeutic targets.


2020 ◽  
Vol 89 ◽  
pp. 107080
Author(s):  
Yandong Miao ◽  
Jiangtao Wang ◽  
Qiutian Li ◽  
Wuxia Quan ◽  
Yingying Wang ◽  
...  
Keyword(s):  

2021 ◽  
Author(s):  
S. M. Riazul Islam ◽  
Subbroto Kumar Saha ◽  
Shaker El-Sappagh ◽  
Faisal Tariq ◽  
Joydeep Das ◽  
...  

GRINA is an emerging target for cancer therapy. However, the role of GRINA expression and its correlation with cancer patient survival has not been comprehensively studied. Here, we found that mRNA and protein expression of GRINA was upregulated in breast, colon, gastric, and prostate cancers and negatively correlated with patient survival. Also, the upregulation of GRINA expression is associated with hypomethylation of its promoter region. Our GRINA-miRNAs network analysis revealed potential regulatory miRNAs regulating the GRINA expression and its downstream pathways. Next, functional enrichment and pathway analysis of genes commonly co-express with GRINA in breast, colon, gastric, and prostate cancers revealed GRINA regulatory pathways. Concurrently, our upstream regulator analysis revealed possible kinases, transcription factors, and proteins that may potentially regulate GRINA . Overall, this study demonstrates the prognostic significance of GRINA expression and identifies potential regulatory mechanisms, which might have significant implications in targeted therapies for human cancers.


2021 ◽  
Author(s):  
Yong Jiang ◽  
Yaodan Chang ◽  
Jiahui Sun ◽  
Yanping Sun ◽  
Chunjuan Yang ◽  
...  

Abstract Despite there are many cellular or animal experiments that support a link between NRF1 and cancer, there is currently no pan-cancer analysis available. Therefore, the source of data is TCGA and GEO, we explored the potential role of NRF1 in 33 kinds of tumors. The expression of NRF1 is significantly increased in most tumors, and the expression of NRF1 is correlated to the prognosis of tumor patients. We discovered that the expression level of NRF1 in PAAD was correlated to immune infiltration. The methylation of NRF1 increased significantly in KIRC, PAAD, ACC. In addition, RNA metabolic pathway or cell biology-related functions participate in the functional mechanism of NRF1.Our research provides a comprehensive explanation of the pathogenic effects of NRF1 in related tumors.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Neng Tang ◽  
Xiaolin Dou ◽  
Xing You ◽  
Qiman Shi ◽  
Mujing Ke ◽  
...  

Abstract Background In recent years, there have been many studies on the relationship between DLGAP5 and different types of cancers, yet there is no pan-cancer analysis of DLGAP5. Therefore, this study aims to analyze the roles of DLGAP5 in human tumors. Methods Firstly, we evaluated the expression level of DLGAP5 in 33 types of tumors throughout the datasets of TCGA (Cancer Genome Atlas) and GEO (Gene Expression Synthesis). Secondly, we used the GEPIA2 and Kaplan-Meier plotter to conduct Survival prognosis analysis. Additionally, cBioPortal web was utilized to analyze the genetic alteration of DLGAP5, after which we selected hepatocellular carcinoma (HCC) cell lines to define the function of DLGAP5. Last but not least, we performed immune infiltration analysis and DLGAP5-related gene enrichment analysis. Results DLGAP5 is highly expressed in most type of cancers, and there is a significant correlation between the expression of DLGAP5 and the prognosis of cancer patients. We have observed that DLGAP5 promotes the proliferation and invasion of hepatocellular carcinoma (HCC) cell lines. We also found that DLGAP5 expression was related with the CD8+ T-cell infiltration status in kidney renal clear cell carcinoma, uveal melanoma, and thymoma, and cancer-associated fibroblast infiltration was observed in breast invasive carcinoma, kidney renal papillary cell carcinoma and testicular germ cell tumors. In addition, enrichment analysis revealed that cell cycle- and oocyte meiosis-associated functions were involved in the functional mechanism of DLGAP5. Conclusions Taken together, our unpresented pan-cancer analysis of DLGAP5 provides a relatively integrative understanding of the oncogenic role of DLGAP5 in various tumors. DLGAP5 may prompt HCC cellular proliferation, invasion and metastasis. All of these provides solid basement and will promote more advanced understanding the role of DLGAP5 in tumorigenesis and development from the perspective of clinical tumor samples and cells.


2021 ◽  
Vol 11 ◽  
Author(s):  
Zhiyong Zhang ◽  
Xin Zhang ◽  
Aimin Huang

BackgroundHistone deacetylase 6 (HDAC6) regulates cytoplasmic signaling networks through the deacetylation of various cytoplasmic substrates. Recent studies have identified the role of HDAC6 in tumor development and immune metabolism, but its specific function remains unclear.MethodsThe current study determined the role of HDAC6 in tumor metabolism and tumor immunity through a multi-database pan-cancer analysis. The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and Cancer Cell Line Encyclopedia (CCLE) datasets were used to determine the expression levels, prognosis, tumor progression, immune checkpoints, and immune metabolism of HDAC6 in 33 tumors. Pathways, immune checkpoints, immune neoantigens, immune microenvironment, tumor mutational burden (TMB), microsatellite instability (MSI), DNA mismatch repair (MMR), and the value of methyltransferases. The R package was used for quantitative analysis and panoramic description.ResultsIn the present study, we determined that HDAC6 is differentially expressed in pan carcinomas, and by survival, we found that HDAC6 was generally associated with the prognosis of pancreatic adenocarcinoma, Thymoma, and uveal melanoma, where low expression of HDAC6 had a significantly worse prognosis. Secondly, through this experiment, we confirmed that HDAC6 expression level was associated with tumor immune infiltration and tumor microenvironment, especially in PAAD. Finally, HDAC6 was associated with immune neoantigen and immune checkpoint gene expression profiles in all cancers in addition to TMB and MSI in pan-cancers.ConclusionHDAC6 is differentially expressed in pan-cancers and plays an essential role in tumor metabolism and immunity. HDAC6 holds promise as a tumor potential prognostic marker, especially in colon cancer.


2019 ◽  
Author(s):  
Burcu Aykac Fas ◽  
Mukesh Kumar ◽  
Valentina Sora ◽  
Maliha Mashkoor ◽  
Matteo Lambrughi ◽  
...  

AbstractAutophagy is a cellular process to recycle damaged cellular components and its modulation can be exploited for disease treatments. A key autophagy player is a ubiquitin-like protein, LC3B. Compelling evidence attests the role of autophagy and LC3B in different cancer types. Many LC3B structures have been solved, but a comprehensive study, including dynamics, has not been yet undertaken. To address this knowledge gap, we assessed ten physical models for molecular dynamics for their capabilities to describe the structural ensemble of LC3B in solution using different metrics and comparison with NMR data. With the resulting LC3B ensembles, we characterized the impact of 26 missense mutations from Pan-Cancer studies with different approaches. Our findings shed light on driver or neutral mutations in LC3B, providing an atlas of its modifications in cancer. Our framework could be used to assess the pathogenicity of mutations by accounting for the different aspects of protein structure and function altered by mutational events.


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