BioXpress: an integrated RNA-seq-derived gene expression database for pan-cancer analysis

Wan, Qing; Dingerdissen, Hayley; Yu, Fan; Gulzar, Naila; Pan, Yang; Wu, Tsung-Jung; Cheng, Yan; Zhang, Haichen; Mazumder, Raja

doi:10.1093/database/bav019

Cited by 85 publications

(66 citation statements)

References 86 publications

(82 reference statements)

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“…11). 44 NF-kB has been hailed as a therapeutic target for cancer treatment owing to its ability to modulate inflammatory responses apart from the other major hallmarks of cancer. 18,45,46 The modulation of IL-4 and IL-8 by GNL3L could promote NF-kB-mediated inflammation in addition to its anti-apoptotic function.…”

Section: Discussionmentioning

confidence: 99%

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Leucine Zipper Down-regulated in Cancer-1 (LDOC1) interacts with Guanine nucleotide binding protein-like 3-like (GNL3L) to modulate Nuclear Factor-kappa B (NF-κB) signaling during cell proliferation

et al. 2016

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Guanine nucleotide binding protein-like 3-like (GNL3L) is an evolutionarily conserved putative nucleolar GTPase belonging to the HSR1-MMR1 family. In the present study, using protein-protein interaction assays, we show that Leucine Zipper Down-regulated in Cancer-1 (LDOC1) is a novel interacting partner of GNL3L. Furthermore, our results reveal that ectopic expression of LDOC1 destabilizes endogenous GNL3L levels and down modulates GNL3L-induced cell proliferation, in contrast, the knockdown of LDOC1 potentiates cell proliferation upon GNL3L expression. Interestingly, GNL3L upregulates NF-kB dependent transcriptional activity by modulating the expression of NF-kB subunit p65, which is reversed upon coexpression of LDOC1 with GNL3L. GNL3L also potentiates TNF-a mediated NF-kB activity. In addition, antiapoptotic function of GNL3L is impaired upon p65 knockdown, suggesting its critical role in GNL3L mediated cell proliferation/survival. An inverse correlation of GNL3L and LDOC1 expression profiles in various tumor tissues from BioXpress database indicate their critical role in cancer. Collectively, our data provides evidence that GNL3L-LDOC1 interplay regulates cell proliferation through the modulation of NFkB pathway during tumorigenesis.

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Section: Discussionmentioning

confidence: 99%

“…RNA-Seq data of 920 pairs of tumor were compared with those of normal tissue samples, which are available in the BioXpress database 44 …”

Section: Gene Expression Profiling From Datasetmentioning

confidence: 99%

Leucine Zipper Down-regulated in Cancer-1 (LDOC1) interacts with Guanine nucleotide binding protein-like 3-like (GNL3L) to modulate Nuclear Factor-kappa B (NF-κB) signaling during cell proliferation

et al. 2016

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“…We found that the levels of miR-3127 in BCA samples were significantly lower than those in the normal samples ( Figure 1C). We also analyzed RNA-sequencing gene expression data of BCA samples and normal samples, which are available in the BioXpress database (Wan et al, 2015). The results suggested that miR-3127 expression was reduced in multiple cancer types including BCA ( Figure 1D).…”

Section: Mir-3127 Expression Is Downregulated In Human Bca Tissues Anmentioning

confidence: 99%

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

Wang

Meng

2020

Front. Genet.

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Recent studies suggested that microRNA-3127 (miR-3127) was dysregulated in multiple tumor types and has important roles in tumorigenesis and cancer progression. However, its biological roles and the mechanisms that regulate its expression in bladder cancer (BCA) remain to be determined. The expression level of miR-3127 was measured in BCA tissues and its cellular functions were examined using both in vitro and in vivo experiments. The interaction between miR-3127 and long non-coding RNA (lncRNA) LINC00319 was explored using RNA immunoprecipitation assay and luciferase reporter assays. We showed that miR-3127 expression was significantly downregulated in human BCA tissues and BCA cell lines. Lower miR-3127 levels were associated with worse survival in BCA patients. The overexpression of miR-3127 impaired BCA cell proliferation and invasion, and the knockdown of miR-3127 enhanced BCA cell proliferation and invasion in vitro. Importantly, miR-3127 was able to suppress cell growth in vivo. We demonstrated that miR-3127 repressed the proliferation and invasion of BCA cells though directly targeted the 3-UTR of RAP2A, which served as a novel oncogene in BCA cells. The suppression of cell proliferation and invasion caused by miR-3127 overexpression could be partially abrogated by ectopic expression of RAP2A. Furthermore, high expression of LINC00319 was correlated with adverse survival in BCA patients. LINC00319 could bind directly with miR-3127 and inhibited its expression, and the tumor-promoting effects of LINC00319 could be reversed by re-expression of miR-3127 in BCA cells. Our findings indicated that lncRNA LINC00319-mediated miR-3127 repression promotes BCA progression through the upregulation of RAP2A. The re-introduction of miR-3127 or inhibition of LINC00319 might represent a promising therapeutic strategy for BCA treatment.

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“…To facilitate research on abnormal gene expression in human diseases, a variety of databases and pipelines have been developed to combine RNA-seq from different studies [3][4][5][6][7][8][9][20]. However, these databases or pipelines either directly incorporated expression data from the literature, retaining unwanted batch effects in the data [7][8], or only combined and reanalyzed samples from smaller studies, hence, not taking advantage of the power provided by the recent large data sets [3][4][5][6][20]. A recently published pipeline, Toil [10], attempts to unify RNA-seq data from different sources by uniformly processing raw sequencing reads.…”

Section: Introductionmentioning

confidence: 99%

Enabling cross-study analysis of RNA-Sequencing data

Wang

Armenia

Zhang

et al. 2017

Preprint

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Driven by the recent advances of next generation sequencing (NGS) technologies and an urgent need to decode complex human diseases, a multitude of large-scale studies were conducted recently that have resulted in an unprecedented volume of whole transcriptome sequencing (RNA-seq) data. While these data offer new opportunities to identify the mechanisms underlying disease, the comparison of data from different sources poses a great challenge, due to differences in sample and data processing. Here, we present a pipeline that processes and unifies RNA-seq data from different studies, which includes uniform realignment and gene expression quantification as well as batch effect removal. We find that uniform alignment and quantification is not sufficient when combining RNA-seq data from different sources and that the removal of other batch effects is essential to facilitate data comparison.

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BioXpress: an integrated RNA-seq-derived gene expression database for pan-cancer analysis

Cited by 85 publications

References 86 publications

Leucine Zipper Down-regulated in Cancer-1 (LDOC1) interacts with Guanine nucleotide binding protein-like 3-like (GNL3L) to modulate Nuclear Factor-kappa B (NF-κB) signaling during cell proliferation

Leucine Zipper Down-regulated in Cancer-1 (LDOC1) interacts with Guanine nucleotide binding protein-like 3-like (GNL3L) to modulate Nuclear Factor-kappa B (NF-κB) signaling during cell proliferation

LINC00319-Mediated miR-3127 Repression Enhances Bladder Cancer Progression Through Upregulation of RAP2A

Enabling cross-study analysis of RNA-Sequencing data

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