scholarly journals Integrative analysis of prognostic long non-coding RNAs with copy number variation in bladder cancer

2021 ◽  
Vol 22 (8) ◽  
pp. 664-681
Author(s):  
Wenwen Zhong ◽  
Dejuan Wang ◽  
Bing Yao ◽  
Xiaoxia Chen ◽  
Zhongyang Wang ◽  
...  
2021 ◽  
Vol 12 ◽  
Author(s):  
Jinfeng Ning ◽  
Fengjiao Wang ◽  
Kaibin Zhu ◽  
Binxi Li ◽  
Qing Shu ◽  
...  

Lung squamous cell carcinoma (LUSC) has a poor clinical prognosis and a lack of available targeted therapies. Therefore, there is an urgent need to identify novel prognostic markers and therapeutic targets to assist in the diagnosis and treatment of LUSC. With the development of high-throughput sequencing technology, integrated analysis of multi-omics data will provide annotation of pathogenic non-coding variants and the role of non-coding sequence variants in cancers. Here, we integrated RNA-seq profiles and copy number variation (CNV) data to study the effects of non-coding variations on gene regulatory network. Furthermore, the 372 long non-coding RNAs (lncRNA) regulated by CNV were used as candidate genes, which could be used as biomarkers for clinical application. Nine lncRNAs including LINC00896, MCM8-AS1, LINC01251, LNX1-AS1, GPRC5D-AS1, CTD-2350J17.1, LINC01133, LINC01121, and AC073130.1 were recognized as prognostic markers for LUSC. By exploring the association of the prognosis-related lncRNAs (pr-lncRNAs) with immune cell infiltration, GPRC5D-AS1 and LINC01133 were highlighted as markers of the immunosuppressive microenvironment. Additionally, the cascade response of pr-lncRNA-CNV-mRNA-physiological functions was revealed. Taken together, the identification of prognostic markers and carcinogenic regulatory mechanisms will contribute to the individualized treatment for LUSC and promote the development of precision medicine.


2021 ◽  
Vol 22 (2) ◽  
Author(s):  
Victoria Spasova ◽  
Boris Mladenov ◽  
Simeon Rangelov ◽  
Zora Hammoudeh ◽  
Desislava Nesheva ◽  
...  

2011 ◽  
Vol 32 (2) ◽  
pp. 240-248 ◽  
Author(s):  
Gaëlle Marenne ◽  
Benjamín Rodríguez-Santiago ◽  
Montserrat García Closas ◽  
Luis Pérez-Jurado ◽  
Nathaniel Rothman ◽  
...  

2020 ◽  
Author(s):  
Xin Zhou ◽  
Fangyuan Zhang ◽  
Yan Liu ◽  
Dongxin Wei

Abstract Background: Belonging to the protein disulfide isomerase (PDI) family, anterior gradient 2 (AGR2) is overexpressed in mucus-secreting cells and endocrine organs such as breast, lung, and ovarian, but its exact function and regulation remain unclear. We aimed to perform integrative analysis of AGR2 in breast cancer.Methods: In our study, a serious of bioinformatic online databases were used to analyze the expression, regulation, prognostic value, and function of AGR2 in breast cancer.Results: The results suggested that AGR2 mRNA was overexpressed in non-basal-like or non-triple-negative breast cancer, but underexpressed in basal-like/ triple-negative breast cancer. AGR2 mRNA expression was correlated with its protein expression. Moreover, the expression of AGR2 was lower in more malignant breast cancer. Furthermore, we also found that DNA methylation, rather than copy number variation, led to AGR2 mRNA overexpression. Prognosis analysis showed no significant correlation between AGR2 level and survival, but in subtype investigation, patients with higher AGR2 level had a significantly better outcome in patients with basal-like / triple-negative breast cancer. Enrichment analysis for co-expression genes of AGR2 revealed that gene sets enriched for chromosome segregation, DNA conformation change, chromosomal region, and GABA receptor activity may play important roles in breast cancer, and that the most significant pathway was “ribosome biogenesis in eukaryotes”, in which negative co-expression genes of AGR2 were enriched.Conclusions: Overexpression of AGR2 was found in less malignant breast cancer, for the first time, our results propose that DNA methylation rather than copy number variation leads to AGR2 overexpression, which can predict favorable prognosis in basal-like/ triple-negative breast cancer, and AGR2 could be a possible regulator of ribosome biogenesis in patients with breast cancer.


Author(s):  
Huihui Hu ◽  
Hangdi Xu ◽  
Fen Lu ◽  
Jisong Zhang ◽  
Li Xu ◽  
...  

Lung cancer is the first cause of cancer death, and gene copy number variation (CNV) is a vital cause of lung cancer progression. Prognosis prediction of patients followed by medication guidance by detecting CNV of lung cancer is emerging as a promising precise treatment in the future. In this paper, the differences in CNV and gene expression between cancer tissue and normal tissue of lung adenocarcinoma (LUAD) from The Cancer Genome Atlas Lung Adenocarcinoma data set were firstly analyzed, and greater differences were observed. Furthermore, CNV-driven differentially expressed long non-coding RNAs (lncRNAs) were screened out, and then, a competing endogenous RNA (ceRNA) regulatory network related to the gene CNV was established, which involved 9 lncRNAs, seven microRNAs, and 178 downstream messenger RNAs (mRNAs). Pathway enrichment analyses sequentially performed revealed that the downstream mRNAs were mainly enriched in biological pathways related to cell division, DNA repair, and so on, indicating that these mRNAs mainly affected the replication and growth of tumor cells. Besides, the relationship between lncRNAs and drug effects was explored based on previous studies, and it was found that LINC00511 and LINC00942 in the CNV-associated ceRNA network could be used to determine tumor response to drug treatment. As examined, the drugs affected by these two lncRNAs mainly targeted metabolism, target of rapamycin signaling pathway, phosphatidylinositol-3-kinase signaling pathway, epidermal growth factor receptor signaling pathway, and cell cycle. In summary, the present research was devoted to analyzing CNV, lncRNA, mRNA, and microRNA of lung cancer, and nine lncRNAs that could affect the CNV-associated ceRNA network we constructed were identified, two of which are promising in determining tumor response to drug treatment.


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