PROMO: an interactive tool for analyzing clinically-labeled multi-omic cancer datasets

Netanely, Dvir; Stern, Neta; Laufer, Itay; Shamir, Ron

doi:10.1186/s12859-019-3142-5

Cited by 23 publications

(12 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The expression profiles of 474 samples from TCGA’s melanoma RNA-Seq dataset [ 12 ] were downloaded from UCSC XENA’s web site in April 2018 ( http://xena.ucsc.edu/ ), together with their associated clinical information (213 labels). We used the PROMO software suite (release 2019.5) [ 43 , 44 ] for importing, preprocessing, analyzing, and visualizing the data. The downloaded RNA-Seq dataset (Illumina HiSeq platform, gene-level RSEM-normalized, log2 transformed) included 104 primary and 365 metastasis samples.…”

Section: Methodsmentioning

confidence: 99%

Classification of node-positive melanomas into prognostic subgroups using keratin, immune, and melanogenesis expression patterns

et al. 2021

Self Cite

View full text Add to dashboard Cite

Cutaneous melanoma tumors are heterogeneous and show diverse responses to treatment. Identification of robust molecular biomarkers for classifying melanoma tumors into clinically distinct and homogenous subtypes is crucial for improving the diagnosis and treatment of the disease. In this study, we present a classification of melanoma tumors into four subtypes with different survival profiles based on three distinct gene expression signatures: keratin, immune, and melanogenesis. The melanogenesis expression pattern includes several genes that are characteristic of the melanosome organelle and correlates with worse survival, suggesting the involvement of melanosomes in melanoma aggression. We experimentally validated the secretion of melanosomes into surrounding tissues by melanoma tumors, which potentially affects the lethality of metastasis. We propose a simple molecular decision tree classifier for predicting a tumor’s subtype based on representative genes from the three identified signatures. Key predictor genes were experimentally validated on melanoma samples taken from patients with varying survival outcomes. Our three-pattern approach for classifying melanoma tumors can contribute to advancing the understanding of melanoma variability and promote accurate diagnosis, prognostication, and treatment.

show abstract

Section: Methodsmentioning

confidence: 99%

Classification of node-positive melanomas into prognostic subgroups using keratin, immune, and melanogenesis expression patterns

et al. 2021

Self Cite

View full text Add to dashboard Cite

show abstract

“…Clinical Proteomic Tumor Analysis Consortium database (CPTAC) ( https://proteomics.cancer.gov/data-portal ) and The Human Protein Atlas database ( https://www.proteinatlas.org/ ) were used to examine the protein expression of MRPL42 in LUAD tissue samples 20 , 21 . The YY1 binding motif in the promoter region of MRPL42 was predicted by JASPAR database ( http://jaspar.genereg.net/ ) and PROMO database ( http://alggen.lsi.upc.es/cgibin/promo_v3/promo/promoinit.cgi?dirDB=TF_8.3 ) 22 , 23 .…”

Section: Methodsmentioning

confidence: 99%

MRPL42 is activated by YY1 to promote lung adenocarcinoma progression

Jiang¹,

Zhang²,

Kang³

et al. 2021

J. Cancer

View full text Add to dashboard Cite

Mammalian mitochondrial ribosomal proteins are a group of protein factors encoded by nuclear genes, responsible for the synthesis of proteins in mitochondria. As a member of mitochondrial ribosomal proteins, MRPL42 (mitochondrial ribosomal protein L42) belongs to 28S and 39S subunits. The current literature showed that its role in lung adenocarcinoma (LUAD) was not clear. We found that MRPL42 was highly expressed in early-stage LUAD tissues and cell lines, and remarkably related to the prognosis of patients. Knockdown of MRPL42 could reduce the proliferation and colonization, promote cell cycle arrest in G1/S phase, and weaken the migration and invasion ability of LUAD cells in vitro. Moreover, depletion of MRPL42 also inhibited tumor growth in vivo. Bioinformatics analysis found that YY1 may bind to the promoter region upstream of the MRPL42 gene to promote the transcription of MRPL42, which was verified by the ChIP and Dual luciferase reporter assay. QRT-PCR confirmed that knocking down YY1 could attenuate the expression of MRPL42. In summary, MRPL42 acts as an oncogene in LUAD, and its expression level is regulated by YY1.

show abstract

“…Transcription factors (TFs) had been widely reported to play roles in activating lncRNAs aberrantly high expression 16 . Hence, we next employed “JASPAR” and “PROMO algorithms” to discover the potential TFs that may bind to LINC00466 promoters 17,18 . The results showed that there are seven common TFs in both prediction results (Figure 2A).…”

Section: Resultsmentioning

confidence: 99%

YY1‐mediated up‐regulation of lncRNA LINC00466 facilitates glioma progression via miR‐508/CHEK1

Shen

Xiao

et al. 2020

The Journal of Gene Medicine

View full text Add to dashboard Cite

BackgroundThe abnormal expression of lncRNA LINC00466 (LINC00466) has been demonstrated in several tumor types. However, the expression pattern and functions of LINC00466 in glioma remain uninvestigated.MethodsA reverse transcriptase‐polymerase chain reaction (RT‐PCR) was utilized to analyze LINC00466 in human glioma tissues and cell lines. Luciferase reporter assays were performed to explore whether YY1 could bind to the promoter region of LINC00466. Cell counting kit‐8, flow cytometry, colony‐formation, transwell migration and invasion assays were carried out to determine the involvement of INC00466 in glioma. Luciferase assays and pulldown assays were conducted to verify the binding sites.ResultsWe report that LINC00466 expression is increased in glioma cells and tissues. YY1 transcription factor (YY1) can bind directly to the LINC00466 promoter region. Clinical studies revealed that the elevated expression of LINC00466 is closely correlated with an advanced World Health Organization grade (p = 0.008), Karnofsky Performance Status score (p = 0.004) and a short overall survival (p = 0.0035) of glioma patients. Functional assays revealed that LINC00466 knockdown distinctly suppresses glioma cell proliferation, migration, invasion and epithelial–mesenchymal progress, and also promotes apoptosis. Moreover, dual‐luciferase reporter assays indicated that LINC00466 acts as an endogenous sponge via binding to miR‐508 and decreasing its expression. Luciferase assays and RT‐PCR assays demonstrated that checkpoint kinase 1 (CHEK1) is a target of miR‐508, and LINC00466 modulates CHEK1 levels by competing for miR‐508. LINC00466 may exhibit its anti‐oncogenic roles through targeting the miR‐508/CHEK1 axis.ConclusionsOur findings identified a novel glioma‐related long non‐coding RNA, LINC00466, which may provide a potential novel prognostic and therapeutic target for glioma.

show abstract

PROMO: an interactive tool for analyzing clinically-labeled multi-omic cancer datasets

Cited by 23 publications

References 43 publications

Classification of node-positive melanomas into prognostic subgroups using keratin, immune, and melanogenesis expression patterns

Classification of node-positive melanomas into prognostic subgroups using keratin, immune, and melanogenesis expression patterns

MRPL42 is activated by YY1 to promote lung adenocarcinoma progression

YY1‐mediated up‐regulation of lncRNA LINC00466 facilitates glioma progression via miR‐508/CHEK1

Contact Info

Product

Resources

About