GENT2: an updated gene expression database for normal and tumor tissues

Park, Seung Jin; Yoon, Byoung-Ha; Kim, Seon‐Kyu; Kim, Seon‐Young

doi:10.1186/s12920-019-0514-7

Cited by 294 publications

(304 citation statements)

References 22 publications

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“…METABRIC dataset [30] on breast cancer (METABRIC, Nature 2012) acquired from cBioPortal (http://www.cbioportal.org/) were utilized for this study (access date: Feb 01, 2020). CCT2 expression data in GSE15852, GSE54002, GSE45827 and GSE42568 datasets were collected from GENT2 database [31] (http://gent2.appex.kr/gent2/), a newly updated platform for exploring gene expression patterns across tumor and normal tissues. Gene expression patterns of CCT2 across tumor and normal tissues were assessed using GENT2 database.…”

Section: Data Acquisitionmentioning

confidence: 99%

Molecular and clinical characterization of CCT2 expression at transcriptional level via 2994 samples of breast cancer

Liu¹,

Qi²,

Wang³

et al. 2020

Preprint

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BackgroundMolecular chaperones play important roles in regulating various cellular processes and malignant transformation. Expression of some subunits of molecular chaperonen CCT/TRiC complex have been reported to be correlated with cancer development and patient survival. However, little is known about the expression and prognostic significance of Chaperonin Containing TCP1 Subunit 2 (CCT2), a gene encoding a molecular chaperone that is a member of the chaperonin containing TCP1 complex (CCT), also known as the TCP1 ring complex (TRiC).MethodThrough the Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) databases, we systematically reviewed a total of 2994 cases with transcriptome data and analyzed the functional annotation of CCT2 by Gene ontology (GO) and KEGG analysis. Univariate and multivariate survival analysis were performed to investigate the prognostic value of CCT2 in breast cancer.ResultsWe found CCT2 was significantly upregulated in various tumors. In breast cancer, CCT2 expression was significantly upregulated in HER2-positive (HER2+) group, and more malignant group. In addition, we investigated correlations between CCT2 and other CCT members. Interestingly, almost all CCTs expression were positively correlated with each other, but not CCT6B. Survival analysis suggested that CCT2 overexpression was independently associated with worse prognosis of patients with breast cancer, especially in luminal A subtype.ConclusionIn summary, our results revealed that CCT2 might be involved in regulating cell cycle pathway, and independently predicted worse prognosis in breast cancer patients. These findings may expand understanding of potential anti-CCT2 treatments. To our knowledge, this is the largest and most comprehensive study characterizing the expression pattern of CCT2 together with its prognostic values in breast cancer.

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Section: Data Acquisitionmentioning

confidence: 99%

Molecular and clinical characterization of CCT2 expression at transcriptional level via 2994 samples of breast cancer

Liu¹,

Qi²,

Wang³

et al. 2020

Preprint

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“…Other members of the kallikrein family have also been linked to cancer disease and poor patient prognosis. Examples include kallikrein 2 (prostate cancer) and kallikreins 6, 10, 11, and 15 (ovarian, prostate, and pancreatic cancers) . In addition to cancer, kallikreins are also involved in other diseases, such as hypertension and inflammation .…”

Section: Proteases In Health and Diseasementioning

confidence: 99%

“…The dysregulation of this enzyme has been implicated in numerous cancers, such as breast, prostate, colon, cervical, and ovarian cancers . Other examples of TTSPs in the context of their role in cancer progression include hepsin (prostate cancer) , TMPRSS2 (pancreatic, kidney, and colon cancer) , and TMPRSS4 (multiple cancer types) . The roles of TTSPs are not limited only to cancer.…”

Section: Proteases In Health and Diseasementioning

confidence: 99%

“…Recently, one of its analogs, tumor‐homing cyclic peptide with CRGDKGPDC sequence (iRGD; a nine amino acid cyclic peptide), has gained substantial research attention. This peptide (developed by the Ruoslahti laboratory ) can specifically guide cargo into tumors that express integrins and neuropilin proteins through a two‐step mechanism (called the C‐end rule rule), making it suitable for the treatment of neuropilin‐positive cancers, that is, breast, pancreatic, or neuroblastoma . Although iRGD appears to be a very promising tumor‐homing peptide (clinical trials are ongoing), to date, no cyclic iRGD‐equipped protease‐labile PDCs have been developed.…”

Section: Peptide–drug Conjugatesmentioning

confidence: 99%

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Protease‐activated prodrugs: strategies, challenges, and future directions

Poręba

2020

The FEBS Journal

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Proteases play critical roles in virtually all biological processes, including proliferation, cell death and survival, protein turnover, and migration. However, when dysregulated, these enzymes contribute to the progression of multiple diseases, with cancer, neurodegenerative disorders, inflammation, and blood disorders being the most prominent examples. For a long time, disease-associated proteases have been used for the activation of various prodrugs due to their well-characterized catalytic activity and ability to selectively cleave only those substrates that strictly correspond with their active site architecture. To date, versatile peptide sequences that are cleaved by proteases in a site-specific manner have been utilized as bioactive linkers for the targeted delivery of multiple types of cargo, including fluorescent dyes, photosensitizers, cytotoxic drugs, antibiotics, and pro-antibodies. This platform is highly adaptive, as multiple protease-labile conjugates have already been developed, some of which are currently in clinical use for cancer treatment. In this review, recent advancements in the development of novel protease-cleavable linkers for selective drug delivery are described. Moreover, the current limitations regarding the selectivity of linkers are Abbreviations AAC, antibody-antibiotic conjugate; Ab, antibody; ACC, 7-amino-4-carbamoylmethylcoumarin; ADAM, a disintegrin and metalloproteinase; ADAMTS, a disintegrin and metalloproteinase with thrombospondin motifs; ADC, antibody-drug conjugate; aPSs, activatable photosensitizers; BHQ-3, black hole quencher 3; Boc, tert-butyloxycarbonyl group; BT20, a type of mammary gland carcinoma; Cas9, CRISPR-associated protein 9;

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“…The gene expression of TLR1-TLR10, BGN, HSPD1, HMGB1, S100A8, S100A9, TNC, SDC2 (HSPG1), HSPG2, HYAL1, HYAL2, HAS1, HAS2, and HAS3 in normal (n = 397) and colon cancer samples (n = 3775) was analyzed through the Gene Expression database of Normal and Tumor tissues (GENT2). Gene expression data was downloaded from the GEO public repository using the U133Plus2 (GPL570) platform [13]. The amounts of TLR1-TLR10 and TLR4 ligands in the colorectal cancer samples were compared to those of normal colon samples by Gene Expression Profiling Interactive Analysis (GEPIA2) [14].…”

Section: Bioinformatics Analysis Of Gene Expressionmentioning

confidence: 99%

BGN/TLR4/NF-κB Mediates Epigenetic Silencing of Immunosuppressive Siglec Ligands in Colon Cancer Cells

Huang

Cai

Suen

et al. 2020

Cells

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Human Toll-like receptor (TLR) signaling plays a vital role in intestinal inflammation by activating the NF-κB pathway. By querying GENT2 datasets, we identified the gene expression level of TLR2 and TLR4 as being substantially increased in colorectal cancer. Introduction of shRNAs for TLR4 but not TLR2 dramatically recovered disialyl Lewis a and sialyl 6-sulfo Lewis x glycans, which are preferentially expressed in non-malignant colonic epithelial cells and could serve as ligands for the immunosuppressive molecule Siglec-7. We screened several TLR4 ligands and found that among them BGN is highly expressed in cancers and is involved in the epigenetic silencing of Siglec-7 ligands. Suppression of BGN expression substantially downregulated NF-κB activity and the marker H3K27me3 in the promoter regions of the SLC26A2 and ST6GalNAc6 genes, which are involved in the synthesis of those glycans, and restored expression of normal glycans as well as Siglec-7 binding activities. We show that in the presence of TLR4, inflammatory stimuli initiate a positive loop involving NF-κB that activates BGN and further enhances TLR4 activity. Present findings indicate a putative mechanism for the promotion of carcinogenesis by loss of immunosuppressive ligands by the BGN/TLR4/ NF-κB pathway.

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GENT2: an updated gene expression database for normal and tumor tissues

Cited by 294 publications

References 22 publications

Molecular and clinical characterization of CCT2 expression at transcriptional level via 2994 samples of breast cancer

Molecular and clinical characterization of CCT2 expression at transcriptional level via 2994 samples of breast cancer

Protease‐activated prodrugs: strategies, challenges, and future directions

BGN/TLR4/NF-κB Mediates Epigenetic Silencing of Immunosuppressive Siglec Ligands in Colon Cancer Cells

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