scholarly journals Comprehensive analysis of the transcriptional profile of the Mediator complex across human cancer types

Oncotarget ◽  
2016 ◽  
Vol 7 (17) ◽  
pp. 23043-23055 ◽  
Author(s):  
Isabella Syring ◽  
Niklas Klümper ◽  
Anne Offermann ◽  
Martin Braun ◽  
Mario Deng ◽  
...  
2021 ◽  
Vol 9 (1) ◽  
pp. 29
Author(s):  
Jamila Sameer Daraghmeh ◽  
Bayan Mustafa Mansour ◽  
Asmaa Yousef Kmail ◽  
Iqab Ghalib Daraghmeh

Studies over the last years revealed significant insights into the β-Catenin & TGF β signal transduction pathways and that such pathways are abnormal activated in abundant cancer types. According to the straight forward effect of these pathways in various tumor types, both pathways are currently considered targets for innovative cancer therapies. This view study emphasizes 13 proteins that are implicated in these two pathways. As there has been widespread research into the proteins that involved in these pathways, we have utilized data existing in the Human Protein Atlas database in this paper to examine the expression of 53 crucial proteins that are recognized to be involved in the activation of these pathways in a distinct group of 45 cancer types. Our findings revealed notably that the proteins (SKIL, SHC, ERK1/2, RAS, PI3K (PIK3CA), SMAD8, ACVR2A/1B SNON, AKT, and SMAD3, from TGF β and (RNF43, SNAIL1 and DVl) for β catenin show high expression in most caner tissues. Our results strongly suggest that these proteins might have the ability to act as potential objects for remedies and provide perception into the molecular basis of cancer.


2018 ◽  
Author(s):  
Yuwei Zhang ◽  
Yang Tao ◽  
Huihui Ji ◽  
Wei Li ◽  
Xingli Guo ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 433
Author(s):  
Bijesh George ◽  
P. Mukundan Pillai ◽  
Aswathy Mary Paul ◽  
Revikumar Amjesh ◽  
Kim Leitzel ◽  
...  

To define the growing significance of cellular targets and/or effectors of cancer drugs, we examined the fitness dependency of cellular targets and effectors of cancer drug targets across human cancer cells from 19 cancer types. We observed that the deletion of 35 out of 47 cellular effectors and/or targets of oncology drugs did not result in the expected loss of cell fitness in appropriate cancer types for which drugs targeting or utilizing these molecules for their actions were approved. Additionally, our analysis recognized 43 cellular molecules as fitness genes in several cancer types in which these drugs were not approved, and thus, providing clues for repurposing certain approved oncology drugs in such cancer types. For example, we found a widespread upregulation and fitness dependency of several components of the mevalonate and purine biosynthesis pathways (currently targeted by bisphosphonates, statins, and pemetrexed in certain cancers) and an association between the overexpression of these molecules and reduction in the overall survival duration of patients with breast and other hard-to-treat cancers, for which such drugs are not approved. In brief, the present analysis raised cautions about off-target and undesirable effects of certain oncology drugs in a subset of cancers where the intended cellular effectors of drug might not be good fitness genes and that this study offers a potential rationale for repurposing certain approved oncology drugs for targeted therapeutics in additional cancer types.


Author(s):  
Anika Tabassum ◽  
Md. Nazmus Samdani ◽  
Tarak Chandra Dhali ◽  
Rahat Alam ◽  
Foysal Ahammad ◽  
...  

Abstract Transporter associated with antigen processing 1 (TAP1) is a transporter protein that represent tumor antigen in the MHC I or HLA complex. Any defect in the TAP1 gene resulting in inadequate tumor tracking. TAP1 influences multidrug resistance (MDR) in human cancer cell lines and hinders the treatment during chemotherapeutic. The association of TAP1 in cancer progression remains mostly unknown and further study of the gene in relation with cancer need to conduct. Thus, the study has designed to analyze the association between the TAP1 with cancer by computationally. The expression pattern of the gene has determined by using ONCOMINE, GENT2, and GEPIA2 online platforms. The protein level of TAP1 was examined by the help of Human Protein Atlas. Samples with different clinical outcomes were investigated to evaluate the expression and promoter methylation in cancer vs. normal tissues by using UALCAN server. The copy number alteration, mutation frequency, and expression level of the gene in different cancer were analyzed by using cBioPortal server. The PrognoScan and KM plotter platforms were used to perform the survival analysis and represented graphically. Additionally, pathway and gene ontology (GO) features correlated to the TAP1 gene were analyzed and presented by bar charts. After arranging the data in a single panel like correlating expression to prognosis, mutational and alterations characteristic, and pathways analysis, we observed some interesting insights that emphasized the importance of the gene in cancer progression. The study found the relationship between the TAP1 expression pattern and prognosis in different cancer tissues and shows how TAP1 affects the clinical characteristics. The analytical data presented in the study is vital to learn about the effect of TAP1 in tumor tissue, where previously studies showing contradicting expression of TAP1 in cancer tissue. The analyzed data can also be utilized further to evade the threats against chemotherapy. Overall, the study provided a new aspect to consider the role of TAP1 gene in cancer progression and survival status. Key messages • This study demonstrated, for the first time, a correlation between the TAP1 gene and tumor progression. • An upregulation of TAP1 mRNA was demonstrated in various cancer types. • This study reported a significant negative correlation for TAP1 gene expression and the survival rate in different cancer types.


2009 ◽  
Author(s):  
A. El-Hussein ◽  
H. Ismail ◽  
A. K. Kasem ◽  
M. A. Harith ◽  
Mohamed Abdel Harith
Keyword(s):  

Cell ◽  
2017 ◽  
Vol 171 (5) ◽  
pp. 1042-1056.e10 ◽  
Author(s):  
Brittany B. Campbell ◽  
Nicholas Light ◽  
David Fabrizio ◽  
Matthew Zatzman ◽  
Fabio Fuligni ◽  
...  

2016 ◽  
Vol 44 (5) ◽  
pp. 1305-1312 ◽  
Author(s):  
Teresa Rubio ◽  
Maja Köhn

The phosphatase of regenerating liver (PRL)-3 is overexpressed in many human cancer types and tumor metastases when compared with healthy tissues. Different pathways and mechanisms have been suggested to modulate PRL-3 expression levels and activity, giving some valuable insights but still leaving an incomplete picture. Investigating these mechanisms could provide new targets for therapeutic drug development. Here, we present an updated overview and summarize recent findings concerning the different PRL-3 expression regulatory mechanisms and posttranslational modifications suggested to modulate the activity, localization, or stability of this phosphatase.


2020 ◽  
Vol 16 (35) ◽  
pp. 2981-2995
Author(s):  
Ning Lou ◽  
Guohong Liu ◽  
Yunbao Pan

The long noncoding RNA ANRIL, located in the human chromosome 9p21 region, has been reported to be involved in tumor progression. ANRIL regulates gene expression via recruiting PRC2 or titrating miRNA; it also participates in signaling pathways. Evidence has indicated that ANRIL is overexpressed in many cancer types and is capable of enhancing cell proliferation and cell cycle progression and inhibiting apoptosis and senescence. ANRIL has the potential to serve as a biomarker for diagnosis and prognosis in cancer. In this article we focus on recent advances in studies of the oncogenic role of ANRIL and its potential role in cancer medicine.


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