Loss of p57KIP2 is associated with colorectal carcinogenesis

Li, Jiaqing; Wu, Fei; Usuki, Hisashi; Kubo, Akihito; Masaki, Tsutomu; Fujita, Jiro; Bandoh, Shuji; Saoo, Kousuke; Takeuchi, Hijiri; Kuriyama, Shigeki; Ishida, Toshihiko; Imaida, Katsumi

doi:10.3892/ijo.23.6.1537

Cited by 30 publications

(41 citation statements)

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“…As expected, both the 'replicative' DNA polymerase/primase POLA, which is the only DNA polymerase involved in DNA replication and not in DNA repair synthesis, and the proliferative marker PCNA were overexpressed. Conversely, the DNA replication-independent p57 gene that is known to be downregulated in colon cancer (Li et al, 2003), was mostly underexpressed (Table 1).…”

Section: Subsets Of Dna Replication Genes Are Deregulated In Colorectmentioning

confidence: 99%

A ‘DNA replication’ signature of progression and negative outcome in colorectal cancer

et al. 2009

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Colorectal cancer is one of the most frequent cancers worldwide. As the tumor-node-metastasis (TNM) staging classification does not allow to predict the survival of patients in many cases, additional prognostic factors are needed to better forecast their outcome. Genes involved in DNA replication may represent an underexplored source of such prognostic markers. Indeed, accidents during DNA replication can trigger 'replicative stress', one of the main features of cancer from earlier stages onward. In this study, we assessed the expression of 47 'DNA replication' genes in primary tumors and adjacent normal tissues from a homogeneous series of 74 patients. We found that genes coding for translesional (TLS) DNA polymerases, initiation of DNA replication, S-phase signaling and protection of replication forks were significantly deregulated in tumors. We also observed that the overexpression of either the MCM7 helicase or the TLS DNA polymerase POLQ (if also associated with a concomitant overexpression of firing genes) was significantly related to poor patient survival. Our data suggest the existence of a 'DNA replication signature' that might represent a source of new prognostic markers. Such a signature could help in understanding the molecular mechanisms underlying tumor progression in colorectal cancer patients.

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Section: Subsets Of Dna Replication Genes Are Deregulated In Colorectmentioning

confidence: 99%

A ‘DNA replication’ signature of progression and negative outcome in colorectal cancer

et al. 2009

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“…7 Taken together, these observations suggest that that p57 Kip2 exerts tissue-specific effects during development. Interestingly during adulthood, it has also been reported that p57 Kip2 expression is reduced in various tumors, [8][9][10][11][12][20][21][22][23][24] suggesting a possible function for this protein in tumorigenesis. Importantly, decreased p57 Kip2 expression may provide an important prognostic implication for patients with ovarian, hepatocellular and colorectal cancers, and acute lymphoblastic leukemia.…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, decreased p57 Kip2 expression may provide an important prognostic implication for patients with ovarian, hepatocellular and colorectal cancers, and acute lymphoblastic leukemia. [8][9][10]23 In spite of frequent low/absence of p57 Kip2 expression in various tumors, rare/no somatic mutations of p57 Kip2 gene are found in these tumors. [8][9][10][11][12] These observations suggest that inactivation of p57 Kip2 gene expression, rather than mutations in the p57 Kip2 gene, accounts for the involvement of p57 Kip2 in other types of cancer.…”

Section: Discussionmentioning

confidence: 99%

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The cell cycle inhibitor p57Kip2 promotes cell death via the mitochondrial apoptotic pathway

Vlachos

Nyman

et al. 2007

Cell Death Differ

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“…Two major investigations focused on p57 Kip2 levels in colorectal carcinomas (116,117). Both of these analyses employed an immunohistochemical technique.…”

Section: P57 Kip2 Content In Human Malignanciesmentioning

confidence: 99%

p57Kip2 and Cancer: Time for a Critical Appraisal

Borriello

Caldarelli

Bencivenga

et al. 2011

Molecular Cancer Research

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p57Kip2 is a cyclin-dependent kinase inhibitor belonging to the Cip/Kip family, which also includes p21Cip1 and p27Kip1. So far, p57Kip2 is the least-studied Cip/Kip protein, and for a long time its relevance has been related mainly to its unique role in embryogenesis. Moreover, genetic and molecular studies on animal models and patients with Beckwith-Wiedemann syndrome have shown that alterations in CDKN1C (the p57Kip2 encoding gene) have functional relevance in the pathogenesis of this disease. Recently, a number of investigations have identified and characterized heretofore unexpected roles for p57Kip2. The protein appears to be critically involved in initial steps of cell and tissue differentiation, and particularly in neuronal development and erythropoiesis. Intriguingly, p27Kip1, the Cip/Kip member that is most homologous to p57Kip2, is primarily involved in the process of cell cycle exit. p57Kip2 also plays a critical role in controlling cytoskeletal organization and cell migration through its interaction with LIMK-1. Furthermore, p57Kip2 appears to modulate genome expression. Finally, accumulating evidence indicates that p57Kip2 protein is frequently downregulated in different types of human epithelial and nonepithelial cancers as a consequence of genetic and epigenetic events. In summary, the emerging picture is that several aspects of p57Kip2's functions are only poorly clarified. This review represents an appraisal of the data available on the p57Kip2 gene and protein structure, and its role in human physiology and pathology. We particularly focus our attention on p57Kip2 changes in cancers and pharmacological approaches for modulating p57Kip2 levels. Mol Cancer Res; 9(10); 1269–84. ©2011 AACR.

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Loss of p57KIP2 is associated with colorectal carcinogenesis

Cited by 30 publications

References 0 publications

A ‘DNA replication’ signature of progression and negative outcome in colorectal cancer

A ‘DNA replication’ signature of progression and negative outcome in colorectal cancer

The cell cycle inhibitor p57Kip2 promotes cell death via the mitochondrial apoptotic pathway

p57Kip2 and Cancer: Time for a Critical Appraisal

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