Cables1is a tumor suppressor gene that regulates intestinal tumor progression inApcMinmice

Arnason, Thomas; Pino, Maria Simona; Yılmaz, Ömer H.; Kirley, Sandra D.; Rueda, Bo R.; Chung, Daniel C.; Zukerberg, Lawrence

doi:10.4161/cbt.25089

Cited by 22 publications

(22 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mouse embryonic fibroblasts isolated from Cables 2/2 mice show an increased rate of growth, delayed onset of senescence, and decreased serum dependence (Kirley et al, 2005b). In the Apc Min/1 mouse model, the loss of Cables1 promotes tumor progression and activates the Wnt/b-catenin signaling pathway (Arnason et al, 2013). Together, these pieces of evidence strongly indicate that Cables1 functions as a tumor suppressor.…”

Section: The Role Of Cables1 In Cancermentioning

confidence: 97%

The Emerging Role of Cables1 in Cancer and Other Diseases

Huang

Tan

et al. 2017

Mol Pharmacol

View full text Add to dashboard Cite

Cdk5 and Abl enzyme substrate 1 (Cables1) is an adaptor protein that links cyclin-dependent kinase (Cdks) with nonreceptor tyrosine kinases and regulates the activity of Cdks by enhancing their Y15 phosphorylation. Emerging evidence also shows that Cables1 can interact with, for example, p53 family proteins, 14-3-3, and -catenin, suggesting that Cables1 may be a signaling hub for the regulation of cell growth. Abnormal expression of Cables1 has been observed in multiple types of cancers and other diseases. In this review, we summarize the characteristics of Cables1 and highlight the molecular mechanisms through which Cables1 regulates the development of cancer and other diseases. Finally, we discuss future challenges in demonstrating the role and potential application of Cables1 in cancer and other diseases.

show abstract

Section: The Role Of Cables1 In Cancermentioning

confidence: 97%

The Emerging Role of Cables1 in Cancer and Other Diseases

Huang

Tan

et al. 2017

Mol Pharmacol

View full text Add to dashboard Cite

show abstract

“…Several of these activated targets have established roles as oncogenes in other cellular contexts. In contrast, genes directly repressed by EWS-FLI1 include the known tumor suppressors ERRFI1 (Duncan et al, 2010), CABLES1 (Arnason et al, 2013), IER3 (Sebens Muerkoster et al, 2008), and TGFBI (Wang et al, 2012), as well as mesenchymal lineage factors, such as SNAI2 (Cobaleda et al, 2007), TRPS1 (Zhang et al, 2012), and CD73 (Chamberlain et al, 2007) ( Table S3 , S4 ).…”

Section: Resultsmentioning

confidence: 99%

EWS-FLI1 Utilizes Divergent Chromatin Remodeling Mechanisms to Directly Activate or Repress Enhancer Elements in Ewing Sarcoma

et al. 2014

View full text Add to dashboard Cite

Summary The aberrant transcription factor EWS-FLI1 drives Ewing sarcoma yet its molecular function is incompletely understood. We find that EWS-FLI1 reprograms gene regulatory circuits in Ewing sarcoma by directly inducing or repressing enhancers. At GGAA repeat elements, which lack evolutionary conservation and regulatory potential in other cell types, EWS-FLI1 multimers induce chromatin opening and create de novo enhancers that physically interact with target promoters. Conversely, EWS-FLI1 inactivates conserved enhancers containing canonical ETS motifs by displacing wild type ETS transcription factors. These divergent chromatin-remodeling patterns repress tumor suppressors and mesenchymal lineage regulators, while activating oncogenes and new potential therapeutic targets, such as the kinase VRK1. Our findings demonstrate how EWS-FLI1 establishes an oncogenic regulatory program governing both tumor survival and differentiation.

show abstract

“…Early studies demonstrated that CABLES1 is located in chromosome 18q, which is commonly lost in colon cancer [39], suggesting that CABLES1 played an important role in this malignancy. Indeed, later studies demonstrated that loss of CABLES1 enhanced tumor progression in the Apc(Min/+) mouse model, which may be a consequence of increased activation of the Wnt/β-catenin pathway [40]. It was also shown that CABLES1 overexpression induced apoptosis and inhibited cell growth at least in part through p21 stabilization [41,42], further consolidating that CABLES1 acts as a tumor suppressor.…”

Section: Atypical Cyclins For Novel Functions?mentioning

confidence: 99%

Atypical cyclins: the extended family portrait

Quandt

Ribeiro

Clotet

2019

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Regulation of cell division is orchestrated by cyclins, which bind and activate their catalytic workmates, the cyclin-dependent kinases (CDKs). Cyclins have been traditionally defined by an oscillating (cyclic) pattern of expression and by the presence of a characteristic "cyclin box" that determines binding to the CDKs. Noteworthy, the Human Genome Sequence Project unveiled the existence of several other proteins containing the "cyclin box" domain. These potential "cyclins" have been named new, orphan or atypical, creating a conundrum in cyclins nomenclature. Moreover, although many years have passed after their discovery, the scarcity of information regarding these possible members of the family has hampered the establishment of criteria for systematization. Here, we discuss the criteria that define cyclins and we propose a classification and nomenclature update based on structural features, interactors, and phylogenetic information. The application of these criteria allows to systematically define, for the first time, the subfamily of atypical cyclins and enables the use of a common nomenclature for this extended family.

show abstract

Cables1is a tumor suppressor gene that regulates intestinal tumor progression inApc^Minmice

Cited by 22 publications

References 26 publications

The Emerging Role of Cables1 in Cancer and Other Diseases

The Emerging Role of Cables1 in Cancer and Other Diseases

EWS-FLI1 Utilizes Divergent Chromatin Remodeling Mechanisms to Directly Activate or Repress Enhancer Elements in Ewing Sarcoma

Atypical cyclins: the extended family portrait

Contact Info

Product

Resources

About