Immunohistochemical analysis of P57(kip2), p53 and hsp60 expressions in premalignant and malignant oral tissues

Fan, Guo-Kang; Chen, Jun; Ping, Fei-yun; Geng, Yichao

doi:10.1016/j.oraloncology.2005.06.017

Cited by 50 publications

(40 citation statements)

References 15 publications

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“…Fan and colleagues (128) investigated p57 Kip2 expression in premalignant and malignant oral and laryngeal tissues. In particular, an immunohistochemistry analysis of 79 cases of leukoplakia and 67 cases of squamous cell carcinoma (SCC) showed a p57 Kip2 decrease in leukoplakia and, more severely, in SCC (128). This study also showed a correlation between the worst 5-year survival rate and absence of p57 Kip2 .…”

Section: P57 Kip2 Content In Human Malignanciesmentioning

confidence: 60%

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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Section: P57 Kip2 Content In Human Malignanciesmentioning

confidence: 60%

p57Kip2 and Cancer: Time for a Critical Appraisal

Borriello

Caldarelli

Bencivenga

et al. 2011

Molecular Cancer Research

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“…Hsp60 is a chaperonin localized to the inner mitochondrial membrane and C. Campanella et al matrix and, less frequently, to extramitochondrial sites (Soltys and Gupta, 1996, 1997Cappello et al, 2008). Hsp60 is constitutively expressed under normal conditions, but its levels can increase (as determined by immunohistochemical methods for example) in pre-neoplastic lesions (Cappello et al, 2002(Cappello et al, , 2003a(Cappello et al, , 2003bFan et al, 2006) and in many advanced cancers (Schneider et al, 1999;Cappello et al, 2005;Urushibara et al, 2007). The main function of the mitochondrial Hsp60 is considered to be assistance in the folding and degradation of mitochondrial proteins (Garrido et al, 2001;Levy-Rimler et al, 2002;Fersht and Daggett, 2002;Parcellier et al, 2003).The involvement of Hsp60 in the process of apoptosis and tumorigenesis is still under debate.…”

Section: Discussionmentioning

confidence: 99%

Upon oxidative stress, the antiapoptotic Hsp60/procaspase-3 complex persists in mucoepidermoid carcinoma cells

Campanella¹,

Bucchieri²,

Ardizzone³

et al. 2009

Eur J Histochem

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Hsp60, a mitochondrial chaperonin highly conserved during evolution, has been found elevated in the cytosol of cancer cells, both in vivo and in vitro, but its role in determining apoptosis during oxidative stress (OS) has not yet been fully elucidated. The aim of the present work was to study the effects of OS on Hsp60 levels and its interactions with procaspase- 3 (p-C3) and p53 in tumor cells. NCI-H292 (mucoepidermoid carcinoma) cells were exposed to various concentrations of hydrogen peroxide (H2O2) for 24 hours. Cell viability was determined by Trypan blue and MTT assays. DNA damage was assessed by the Comet assay, and apoptosis was measured by the AnnexinV cytofluorimetric test. Exposure to increasing concentrations of H2O2 resulted in a reduction of cell viability, DNA damage, and early apoptotic phenomena. Hsp60, p-C3, p53, and p21 were assessed by Western blotting and immunocytochemistry before and after OS. Hsp60 and p-C3 were present before and after OS induction. Immunoprecipitation experiments showed an Hsp60/p-C3 complex before OS that persisted after it, while an Hsp60/p53 complex was not detected in either condition. The presence of wild type (wt) p53 was confirmed by RT-PCR, and p21 detection suggested p53 activation after OS. We postulate that, although OS may induce early apoptosis in NCI-H292 cells, Hsp60 exerts an anti-apoptotic effect in these cells and, by extension, it may do so in other cancer cells

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“…Downregulation of p57 KIP2 is inversely correlated with proliferation in non-small cell lung carcinoma (59), in pancreatic adenocarcinoma (230), in hepatocellular carcinoma (234), in extrahepatic bile duct carcinoma, and intrahepatic cholangiocellular carcinoma (237). Diminished expression of p57 KIP2 predicts poor prognosis in oral squamous cell carcinoma (225), in laryngeal squamous cell carcinoma (226), in hepatocellular carcinoma (234,235), and in malignant ovarian tumors (242). Recently, Yang and colleagues (88) provided evidence that decreased p57 KIP2 expression is related with poor outcome in breast cancer.…”

Section: P57mentioning

confidence: 99%