scholarly journals In silico assessment of EpCAM transcriptional expression and determination of the prognostic biomarker for human lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC)

2021 ◽  
Vol 27 ◽  
pp. 101074
Author(s):  
Abu Tayab Moin ◽  
Bishajit Sarkar ◽  
Md Asad Ullah ◽  
Yusha Araf ◽  
Nafisa Ahmed ◽  
...  
2021 ◽  
Author(s):  
Yan Gao ◽  
Yi-Jia Chen ◽  
Fuyan Li ◽  
Ruimin Wu ◽  
Daobing Zeng ◽  
...  

Abstract Background Overexpression of vesicular nucleotide transporter (SLC17A9) has been found in different types of cancers. Nonetheless, little is known about its influence on lung cancers including human lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Methods Integrative analysis of SLC17A9 and other solute carrier family 17 genes (SLC17A1-8) was performed in patients with LUAD and LUSC based on The Cancer Genome Atlas database. Real-time PCR, western blots, MTS assay, EdU assay, ATP production assays and cell cycle analysis were applied to determine the effect and mechanism of SLC17A9 knockdown in LUAD cells. Results Compared with normal tissue, two SLC17 genes (SLC17A5 and SLC17A9) exhibited a distinctly different expression pattern in LUAD and LUSC. The expression of SLC17A3/7/8/9 expression was significantly correlated with worse overall survival (p < 0.05) in LUAD. Conversely, SLC17A1/2/4/6/9 expression was correlated with poorer OS (p < 0.05) in LUSC. ROC analysis suggested that the area under the curve of most SLC17 family genes was higher than 0.5. Meanwhile, multiple types of genetic alterations in SLC17 family genes were observed in tumor samples. Gene set enrichment analysis GSEA and protein-protein interaction results revealed that oncogenic signaling pathways and biological regulation, metabolic process, hallmark of myc targets, DNA repair, coagulation and complement were linked to SLC17A9 upregulation. Moreover, SLC17A9 knockdown significantly inhibited cell proliferation and ATP levels by affecting Myc, MFN2, STAT3, Cytochrome C and P2X1 expression in A549 cells. Specifically, SLC17A9 expression correlated negatively with overall survival and positively with most LUSC immune cells. SLC17A9 expression has correlations with infiltrating levels of B cells, CD4 + T cells, M1 macrophages, natural killer cells, Th1, Th2, Tfh, Th17 and Treg cells, as well as PD-1, CTLA4, and LAG3 of T cell exhaustion in LUAD. Conclusions Together, SLC17A9 could potentially serve as a prognostic biomarker correlated with immune infiltrates in LUAD and LUSC.


2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Liyan Hou ◽  
Yingbo Li ◽  
Ying Wang ◽  
Dongqiang Xu ◽  
Hailing Cui ◽  
...  

In this study, we investigated the potential prognostic value of ubiquitin-conjugating enzyme E2D1 (UBE2D1) RNA expression in different histological subtypes of non-small-cell lung cancer (NSCLC). A retrospective study was performed by using molecular, clinicopathological, and survival data in the Cancer Genome Atlas (TCGA)—Lung Cancer. Results showed that both lung adenocarcinoma (LUAD) (N=514) and lung squamous cell carcinoma (LUSC) (N=502) tissues had significantly elevated UBE2D1 RNA expression compared to the normal tissues (p<0.001 and p=0.036, respectively). UBE2D1 RNA expression was significantly higher in LUAD than in LUSC tissues. Increased UBE2D1 RNA expression was independently associated with shorter OS (HR: 1.359, 95% CI: 1.031–1.791, p=0.029) and RFS (HR: 1.842, 95% CI: 1.353–2.508, p<0.001) in LUAD patients, but not in LUSC patients. DNA amplification was common in LUAD patients (88/551, 16.0%) and was associated with significantly upregulated UBE2D1 RNA expression. Based on these findings, we infer that UBE2D1 RNA expression might only serve as an independent prognostic indicator of unfavorable OS and RFS in LUAD, but not in LUSC.


2021 ◽  
Author(s):  
Jun Yang ◽  
Xiaohui Chen ◽  
Mingqiang Lin ◽  
Mengyan Zhang ◽  
Zhiping Wang ◽  
...  

Abstract Background: Lung cancer has become the leading cause of cancer-related deaths worldwide with a rising trend of incidence and mortality. Lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) account for the major numbers, which should be paid enough attention. Advanced glycation end products receptor (AGER) is a multi-ligand receptor that interacts with a wide range of ligands. Previous studies have shown that abnormal AGER expression is closely related to immune infiltration and tumorigenesis. Nevertheless, the AGER DNA methylation relationship between prognosis and infiltrating immune cells in LUAD and LUSC is still unclear. Results: Compared with the normal lung tissues, the expression level of AGER was significantly reduced in LUAD and LUSC. Low expression of AGER was markedly correlated with histology, stage, lymph node metastasis and Tumor protein 53 (TP53) mutation and could be used as a potential indicator of poor prognosis of LUAD and LUSC. Further analysis showed that copy number variation (CNV), mutation and DNA methylation involved in the low level of AGER. Additionally, we found that AGER DNA hypermethylation meant a worse prognosis in LUAD and LUSC. In addition, we also found that hypermethylated AGER was significantly correlated with tumor infiltrating lymphocytes. Conclusion: AGER may be a candidate for the prognostic biomarker of LUAD and LUSC related with tumor immune microenvironment.


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