The expression of HSP60 and HSP10 in large bowel carcinomas with lymph node metastase

Cappello, Francesco; David, Sabrina; Rappa, Francesca; Bucchieri, Fabio; Marasà, L; Bartolotta, T; Farina, Felicia; Zummo, Giovanni

doi:10.1186/1471-2407-5-139

Cited by 122 publications

(114 citation statements)

References 54 publications

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“…They provided data that are in agreement with our previous results [1]. More recently, we also showed that the expression of HSP60 in primary tumor and lymph node metastasis is correlated with tumor grade [3], confirming independently the results of Mori et al…”

supporting

confidence: 93%

HSP60 expression during carcinogenesis: Where is the pilot?

Cappello

Zummo

2006

Pathology - Research and Practice

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supporting

confidence: 93%

HSP60 expression during carcinogenesis: Where is the pilot?

Cappello

Zummo

2006

Pathology - Research and Practice

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“…Indeed, higher levels of HSPs 10 and 60 were found in the cytoplasm of lymphocytes in lymph nodes with metastatic colon cancer than in non-metastatic lymph nodes. 23 The presence of HSP10 was also detected in the serum and ascites from ovarian cancer patients and it was found that HSP10 in the serum may play a role in T lymphocyte inhibition, allowing cancer cells to escape immunitary surveillance. 24 However, the prognostic significance of HSPs is not clear.…”

Section: Discussionmentioning

confidence: 98%

Immunohistochemical analysis of possible chemoresistance markers identified by micro-arrays on serous ovarian carcinomas

et al. 2008

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Using the DNA microarray technology, we have identified genes that are differentially expressed in chemosensitive and chemoresistant ovarian serous papillary carcinomas and could potentially distinguish ovarian cancer patients based on their response to chemotherapy. The present study aims to evaluate the clinical usefulness of overexpression of selected genes by immunohistochemistry. Our cohort included 158 women who were operated on and received chemotherapy for an advanced serous papillary ovarian carcinoma (FIGO stages III and IV). The end point used in this study was progression-free survival. Immunohistochemistry was performed on microarray blocks containing all 158 cases. Twelve commercially available antibodies were selected. Of them, 10 corresponded to differentially expressed genes in our micro-array study and p53 and Ki67 were included. Antibodies were obtained for the following selected genes: GSTA1, MMP1, FOSB, CTSL2, HSP10, CD36, CXCL2, RBBP7, Siva, and PTGDS. Cox proportional hazards models, adjusted for standard risk factors, were used to estimate the associations between the markers and progression-free survival. No association was found between mRNA level and protein expression by immunohistochemistry. In multivariate analyses, patients whose tumors overexpressed HSP10 had a lower risk of progression than those with low expression (HR: 0.6; CI: 0.42-0.87; P ¼ 0.007). High level of proliferation (Ki67) tended to be associated with a lower risk of progression (HR: 0.72; CI: 0.51-1.03; P ¼ 0.07) whereas MMP1 overexpression tended to be associated with a higher risk of progression (HR: 1.61; CI: 0.94-2.79; P ¼ 0.08). Our study shows that gene expression analysis coupled with immunohistochemistry allowed the identification of HSP10 as an independent factor of progression-free survival. Modern Pathology (2008Pathology ( ) 21, 1002Pathology ( -1010 doi:10.1038/modpathol.2008 published online 23 May 2008 Keywords: serous ovarian carcinoma; chemoresistance; HSP10; DNA microarray; immunohistochemistry Ovarian cancer is responsible for more cancer deaths among women in the Western world than any other gynecologic malignancy. 1 An initial surgical approach is essential for aggressive cytoreduction and proper staging of the disease, since minimal residual tumor after surgery is a major factor of better response to chemotherapy and survival. 2 Intravenous combinated chemotherapy with taxol plus carboplatin is the current regimen of choice for the treatment of advanced ovarian cancer and is followed by a 50% complete pathologic remission rate. 3 Resistance to chemotherapy is, however, a major concern. Indeed, although significant proportions of women respond to chemotherapy, the majority of responders (approximately 60-75%) eventually relapses and dies from recurrent disease while 20-30% of patients never experience a clinical remission. 4 Chemotherapy resistance in ovarian

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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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The expression of HSP60 and HSP10 in large bowel carcinomas with lymph node metastase

Cited by 122 publications

References 54 publications

HSP60 expression during carcinogenesis: Where is the pilot?

HSP60 expression during carcinogenesis: Where is the pilot?

Immunohistochemical analysis of possible chemoresistance markers identified by micro-arrays on serous ovarian carcinomas

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

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