Hsp27 Modulates p53 Signaling and Suppresses Cellular Senescence

O'Callaghan-Sunol, Cornelia; Gabai, Vladimir L.; Sherman, Michael Y.

doi:10.1158/0008-5472.can-07-2441

Cited by 121 publications

(116 citation statements)

References 29 publications

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“…Restricted tumor analysis suggested that cell cycle was blocked due to the upregulation of the tumor suppressor protein p21-waf1. This is in agreement with O'Callaghan observation in HCT116 colon carcinomas cells after Hsp27 depletion (O'Callaghan-Sunol et al, 2007). Interestingly, this upregulation was restricted to the in vivo model and probably due to the tumor environment.…”

Section: Discussionsupporting

confidence: 91%

Inhibition of heat shock protein 27 (HspB1) tumorigenic functions by peptide aptamers

et al. 2011

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Section: Discussionsupporting

confidence: 91%

Inhibition of heat shock protein 27 (HspB1) tumorigenic functions by peptide aptamers

et al. 2011

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“…By comparing their peptide mass fingerprints to the IPI human database, eleven known proteins were identified and found to be a series of proteins related to proliferation, differentiation, apoptosis and cell survival (34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47). The SSX proteins are thought to act as transcriptional repressors through transcription repression domain (48).…”

Section: Discussionmentioning

confidence: 99%

Cancer/testis antigen SSX2 enhances invasiveness in MCF-7 cells by repressing ERα signaling

et al. 2012

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Abstract. Cancer/testis antigen (CTA) SSX2, which is silent in most normal adult tissues and expressed in various malignant tumors, has been identified for decades. Expression of SSX in tumors has been associated with advanced stages and worse patient prognosis. However, little is known about its role in breast cancer. The SSX2 expression plasmid constructed was stably transfected into the breast cancer cell line MCF-7. The influence of SSX2 on MCF-7 cells was assessed using MTT assay, flow cytometry, transwell invasion assay and in vivo tumorigenicity assay. A comparative proteomic approach was performed to identify and clarify the underlying molecular mechanisms. SSX2 expression was more pronounced in ERα-negative breast cancer cells compared with the positive ones. Overexpression of SSX2 induced cell growth and prompted cell invasion. Both ERα and E-cadherin expression were suppressed in the SSX2 overexpressing MCF-7 cells. Eleven known proteins were identified with significant differential expression. Among these, five were decreased, while other six were increased in the SSX2 overexpressing MCF-7 cells. These results suggested SSX2 may enhance invasiveness in MCF-7 cells both in vivo and in vitro. The regulation of ERα signaling by target proteins of SSX2 may explain the metastatic potential of breast cancer cells.

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“…A recent study reported that elevated levels of hsp27 protected human mammary epithelial cells from doxorubicin. This protection was associated with suppression of doxorubicin-induced senescence, whereby Hsp27 inhibited p53-mediated induction of p21, the major regulator of the senescence program (O'Callaghan-Sunol et al 2007). In other words, the common characteristic of cells treated with HA or NMH may be that senescence-like phenotypes are induced by Hsp27 downregulation associated with the activation of the p53 pathway and the induction of p21.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the effects of 40% oxygen and two atmospheric absolute air pressure conditions on stress-induced premature senescence of normal human diploid fibroblasts

Oh¹,

Lee²,

Lee³

et al. 2008

Cell Stress and Chaperones

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The pressure during hyperbaric oxygen treatment may increase oxygen toxicity via an augmented oxygen pressure in the gas. Nevertheless, only a few reports have been published on the effect of cells grown under 2 atmospheric absolute (ATA) pressure. To evaluate the effect of pressure on oxygen toxicity and to study effects in addition to oxygen toxicity, we designed an experiment to compare the effects of normobaric mild hyperoxia (NMH, 40% oxygen) and hyperbaric air condition (HA, air with 2 ATA) on human diploid fibroblasts (HDF) in a hyperbaric incubator. HDFs in both the NMH and the HA condition had a similar oxidative stress response and exhibited premature senescence. To investigate differences in gene profiling in cells grown in the NMH and HA conditions, samples from cells exposed to each condition were applied to microarrays. We found no expression difference in genes related to aging and deoxyribonucleic acid damage, but the expression of genes including cell adhesion, stress response, and transcription were significantly increased in fibroblasts that were responsive to pressure. Among 26 statistically reliable genes, the expression of apoptosis related genes such as ADAM22, Bax, BCL2L14, and UBD, as well as tumor suppressor-related genes like Axin2 and ATF, and also mitogen-activated protein kinase-related genes like mitogen-activated protein kinase kinase kinase 1, histamine receptor, and RAB24, were significantly changed in cells responsive to pressureinduced oxidative stress.

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Hsp27 Modulates p53 Signaling and Suppresses Cellular Senescence

Abstract: The small heat shock protein Hsp27 is expressed at high levels in many tumors and provides protection against anticancer drugs. Here, we show that expression of

Cited by 121 publications

References 29 publications

Inhibition of heat shock protein 27 (HspB1) tumorigenic functions by peptide aptamers

Inhibition of heat shock protein 27 (HspB1) tumorigenic functions by peptide aptamers

Cancer/testis antigen SSX2 enhances invasiveness in MCF-7 cells by repressing ERα signaling

Comparison of the effects of 40% oxygen and two atmospheric absolute air pressure conditions on stress-induced premature senescence of normal human diploid fibroblasts

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