Abstract 2008: Proteomic analysis of SIAH2 E3 ligase complex in oncogenic K-Ras-driven cell transformation in human cancer

2015 ◽  
Author(s):  
Monicah M. Njogu ◽  
Ming Lei Bian ◽  
Jamie Eisner ◽  
Amy H. Tang
Keyword(s):  
Proteomic Analysis ◽  
Cell Transformation ◽  
Human Cancer ◽  
E3 Ligase

scholarly journals Simian virus 40 and cancer

2011 ◽  
pp. 131-140
Author(s):  
Sandra Eliasz ◽  
Michele Carbone ◽  
Maurizio Bocchetta
Keyword(s):  
Molecular Biology ◽  
Human Population ◽  
Animal Studies ◽  
Cell Transformation ◽  
Human Cancer ◽  
Mesothelial Cell ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Oncogenic Virus ◽  
Experimental Approaches

Since its discovery in 1960 as a contaminant of poliovaccines, Simian Virus 40 (SV40) has been the object of extensive studies to assess whether this oncogenic virus plays a role in human carcinogenesis. Over the last two decades, this question has met with broad scepticism. However, there is increasing evidence linking SV40 to specific types of human cancer, especially malignant mesothelioma. Recently, two laboratories using different experimental approaches independently confirmed that SV40 acts synergistically with environmental fibers to promote mesothelial cell transformation and mesothelioma. Most of the scepticism concerning SV40 and cancer was due to the lack of clear epidemiologic data. However, it is still not clear how SV40 circulates in the human population, making the identification of SV40-exposed versus non-exposed cohorts problematic. Consequently, the most helpful insights into SV40-mediated carcinogenesis have come from molecular pathology, cell and molecular biology, and from animal studies.

scholarly journals Integrated Proteomic Analysis of Human Cancer Cells and Plasma from Tumor Bearing Mice for Ovarian Cancer Biomarker Discovery

PLoS ONE ◽  
2009 ◽  
Vol 4 (11) ◽  
pp. e7916 ◽  
Author(s):  
Sharon J. Pitteri ◽  
Lellean JeBailey ◽  
Vitor M. Faça ◽  
Jason D. Thorpe ◽  
Melissa A. Silva ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Proteomic Analysis ◽  
Biomarker Discovery ◽  
Human Cancer ◽  
Cancer Biomarker ◽  
Human Cancer Cells ◽  
Tumor Bearing

scholarly journals FXR1 regulates transcription and is required for growth of human cancer cells with TP53/FXR2 homozygous deletion

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Yichao Fan ◽  
Jiao Yue ◽  
Mengtao Xiao ◽  
Han Han-Zhang ◽  
Yao Vickie Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cells ◽  
Rna Binding ◽  
Cell Transformation ◽  
Human Cancer ◽  
Homozygous Deletion ◽  
Gene Promoters ◽  
Neighboring Gene ◽  
Human Cancer Cells ◽  
Human Cancers

Tumor suppressor p53 prevents cell transformation by inducing apoptosis and other responses. Homozygous TP53 deletion occurs in various types of human cancers for which no therapeutic strategies have yet been reported. TCGA database analysis shows that the TP53 homozygous deletion locus mostly exhibits co-deletion of the neighboring gene FXR2, which belongs to the Fragile X gene family. Here, we demonstrate that inhibition of the remaining family member FXR1 selectively blocks cell proliferation in human cancer cells containing homozygous deletion of both TP53 and FXR2 in a collateral lethality manner. Mechanistically, in addition to its RNA-binding function, FXR1 recruits transcription factor STAT1 or STAT3 to gene promoters at the chromatin interface and regulates transcription thus, at least partially, mediating cell proliferation. Our study anticipates that inhibition of FXR1 is a potential therapeutic approach to targeting human cancers harboring TP53 homozygous deletion.

Abstract 4442: Inhibition of SIAH E3 ligase function leads to increased cell death in metastatic human cancer cells

2014 ◽  
Author(s):  
Zena M. Urban ◽  
Lauren van Reesema ◽  
Minglei Bian ◽  
Thomas C. Smyrk ◽  
Gloria Peterson ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Human Cancer ◽  
E3 Ligase ◽  
Human Cancer Cells ◽  
Ligase Function

scholarly journals Wnt regulation: exploring Axin-Disheveled interactions and defining mechanisms by which the SCF E3 ubiquitin ligase is recruited to the destruction complex

2020 ◽  
Vol 31 (10) ◽  
pp. 992-1014 ◽  
Author(s):  
Kristina N. Schaefer ◽  
Mira I. Pronobis ◽  
Clara E. Williams ◽  
Shiping Zhang ◽  
Lauren Bauer ◽  
...  
Keyword(s):  
Stem Cell ◽  
Embryonic Development ◽  
Wnt Signaling ◽  
Ubiquitin Ligase ◽  
Human Cancer ◽  
E3 Ubiquitin Ligase ◽  
E3 Ligase ◽  
Adult Stem Cell ◽  
Cell Homeostasis ◽  
Test Models

Wnt signaling plays key roles in embryonic development and adult stem cell homeostasis and is altered in human cancer. We explore β-catenin transfer from the destruction complex to the E3 ligase, and test models suggesting Dishevelled and APC2 compete for association with Axin.

scholarly journals Fbxl8 suppresses lymphoma growth and hematopoietic transformation through degradation of cyclin D3

Oncogene ◽  
2020 ◽  
Author(s):  
Akihiro Yoshida ◽  
Jaewoo Choi ◽  
Hong Ri Jin ◽  
Yan Li ◽  
Sagar Bajpai ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
E3 Ligase ◽  
Protein Stabilization ◽  
Cyclin D3 ◽  
Deficient Mutant ◽  
Cycle Progression ◽  
Functional Investigation

Abstract Overexpression of D-type cyclins in human cancer frequently occurs as a result of protein stabilization, emphasizing the importance of identification of the machinery that regulates their ubiqutin-dependent degradation. Cyclin D3 is overexpressed in ~50% of Burkitt’s lymphoma correlating with a mutation of Thr-283. However, the E3 ligase that regulates phosphorylated cyclin D3 and whether a stabilized, phosphorylation deficient mutant of cyclin D3, has oncogenic activity are undefined. We describe the identification of SCF-Fbxl8 as the E3 ligase for Thr-283 phosphorylated cyclin D3. SCF-Fbxl8 poly-ubiquitylates p-Thr-283 cyclin D3 targeting it to the proteasome. Functional investigation demonstrates that Fbxl8 antagonizes cell cycle progression, hematopoietic cell proliferation, and oncogene-induced transformation through degradation of cyclin D3, which is abolished by expression of cyclin D3T283A, a non-phosphorylatable mutant. Clinically, the expression of cyclin D3 is inversely correlated with the expression of Fbxl8 in lymphomas from human patients implicating Fbxl8 functions as a tumor suppressor.

scholarly journals Hsp70 acts as a fine-switch that controls E3 ligase CHIP-mediated TAp63 and ΔNp63 ubiquitination and degradation

2021 ◽  
Author(s):  
H Helena Wu ◽  
Benfan Wang ◽  
Stephen R Armstrong ◽  
Yasser Abuetabh ◽  
Sarah Leng ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Human Cancer ◽  
E3 Ligase ◽  
Clinical Problem ◽  
Dominant Negative ◽  
Migration And Invasion ◽  
E3 Ligases ◽  
Dominant Negative Inhibitor ◽  
Major Clinical Problem ◽  
P63 Isoforms

Abstract The major clinical problem in human cancer is metastasis. Metastases are the cause of 90% of human cancer deaths. TAp63 is a critical suppressor of tumorigenesis and metastasis. ΔNp63 acts as a dominant-negative inhibitor to block the function of p53 and TAp63. Although several ubiquitin E3 ligases have been reported to regulate p63 stability, the mechanism of p63 regulation remains partially understood. Herein, we show that CHIP, an E3 ligase with a U-box domain, physically interacts with p63 and promotes p63 degradation. Notably, Hsp70 depletion by siRNA stabilizes TAp63 in H1299 cells and destabilizes ΔNp63 in SCC9 cells. Loss of Hsp70 results in a reduction in the TAp63-CHIP interaction in H1299 cells and an increase in the interaction between ΔNp63 and CHIP in SCC9 cells. Our results reveal that Hsp70 acts as a molecular switch to control CHIP-mediated ubiquitination and degradation of p63 isoforms. Furthermore, regulation of p63 by the Hsp70-CHIP axis contributes to the migration and invasion of tumor cells. Hence, our findings demonstrate that Hsp70 is a crucial regulator of CHIP-mediated ubiquitination and degradation of p63 isoforms and identify a new pathway for maintaining TAp63 or ΔNp63 stability in cancers.

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