p97 and Ubiquitin: A Complex Story

Briggs, Louise C.; Dreveny, Ingrid; Pye, V.E.; Beuron, Fabienne; McKeown, Ciarn F.; Zhang, Xiaodong; Freemont, Paul S.

doi:10.1002/9783527619320.ch7b

Cited by 1 publication

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References 162 publications

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“…In patients with metachronous metastases from colorectal cancer, p27 was found to be down-regulated in the metastatic tumor cells compared with the primary tumors, a phenomenon not seen in metastatic colorectal disease diagnosed at the same time (synchronous) with the primary tumors, where p27 expression was low in both primary and metastatic sites [86]. p27 down-regulation in metachronous colorectal metastases was due to spindle disassembly and post-mitotic membrane fusion [93][94][95][96][97]. In colorectal carcinoma patients whose tumors showed high p97 expression were found to have statistically significantly higher probability of distant metastases development and lower disease free and overall survival compared with patients whose tumors showed low p97 expression by immunohistochemistry [98].…”

Section: Accepted Manuscriptmentioning

confidence: 90%

The ubiquitin-proteasome system in colorectal cancer

Voutsadakis

2008

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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The proteasome is a multiprotein complex that regulates the stability of hundreds of cellular proteins and thus, it is implicated in virtually all cellular functions. Most of the time, to be recognized and processed by the proteasome, a protein has to be linked to a chain of ubiquitin molecules. Cell proliferation, apoptosis, angiogenesis and motility, processes with particular importance for carcinogenesis are regulated by the ubiquitin-proteasome system (UPS). In colorectal epithelium, UPS plays a role in the regulation of the Wnt/beta-catenin/APC/TCF4 signaling which regulates proliferation of colorectal epithelial cells in the bottom of the crypts and the inhibition of this proliferation as cells move towards colon villi tips. In most colorectal cancers APC (Adenomatous Polyposis Coli) disabling mutations interfere with the ability of the proteasome to degrade beta-catenin leading to uninhibited cell proliferation. Other key molecules in colorectal carcinogenesis such as p53, Smad4 and components of the k-ras pathways are also regulated by the UPS. In this review I discuss the role of UPS in colorectal carcinogenesis and colorectal cancer prognosis and aspects of its inhibition for therapeutic purposes.

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Section: Accepted Manuscriptmentioning

confidence: 90%

The ubiquitin-proteasome system in colorectal cancer

Voutsadakis

2008

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

View full text Add to dashboard Cite

show abstract

p97 and Ubiquitin: A Complex Story

Cited by 1 publication

References 162 publications

The ubiquitin-proteasome system in colorectal cancer

The ubiquitin-proteasome system in colorectal cancer

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