CSB ablation induced apoptosis is mediated by increased endoplasmic reticulum stress response.
The DNA repair protein Cockayne syndrome group B (CSB) has been recently identified as a promising anticancer target. Suppression, by antisense technology, of this protein causes devastating effects on tumor cells viability, through a massive induction of apoptosis, while being non-toxic to non-tran...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2017-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC5333825?pdf=render |
| _version_ | 1828928915731644416 |
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| author | Manuela Caputo Alessio Balzerano Ivan Arisi Mara D'Onofrio Rossella Brandi Silvia Bongiorni Stefano Brancorsini Mattia Frontini Luca Proietti-De-Santis |
| author_facet | Manuela Caputo Alessio Balzerano Ivan Arisi Mara D'Onofrio Rossella Brandi Silvia Bongiorni Stefano Brancorsini Mattia Frontini Luca Proietti-De-Santis |
| author_sort | Manuela Caputo |
| collection | DOAJ |
| description | The DNA repair protein Cockayne syndrome group B (CSB) has been recently identified as a promising anticancer target. Suppression, by antisense technology, of this protein causes devastating effects on tumor cells viability, through a massive induction of apoptosis, while being non-toxic to non-transformed cells. To gain insights into the mechanisms underlying the pro-apoptotic effects observed after CSB ablation, global gene expression patterns were determined, to identify genes that were significantly differentially regulated as a function of CSB expression. Our findings revealed that response to endoplasmic reticulum stress and response to unfolded proteins were ranked top amongst the cellular processes affected by CSB suppression. The major components of the endoplasmic reticulum stress-mediated apoptosis pathway, including pro-apoptotic factors downstream of the ATF3-CHOP cascade, were dramatically up-regulated. Altogether our findings add new pieces to the understanding of CSB mechanisms of action and to the molecular basis of CS syndrome. |
| first_indexed | 2024-12-14T00:11:16Z |
| format | Article |
| id | doaj.art-5ada6a63f88243899d7d00ad3620186f |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-14T00:11:16Z |
| publishDate | 2017-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-5ada6a63f88243899d7d00ad3620186f2022-12-21T23:25:44ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01123e017239910.1371/journal.pone.0172399CSB ablation induced apoptosis is mediated by increased endoplasmic reticulum stress response.Manuela CaputoAlessio BalzeranoIvan ArisiMara D'OnofrioRossella BrandiSilvia BongiorniStefano BrancorsiniMattia FrontiniLuca Proietti-De-SantisThe DNA repair protein Cockayne syndrome group B (CSB) has been recently identified as a promising anticancer target. Suppression, by antisense technology, of this protein causes devastating effects on tumor cells viability, through a massive induction of apoptosis, while being non-toxic to non-transformed cells. To gain insights into the mechanisms underlying the pro-apoptotic effects observed after CSB ablation, global gene expression patterns were determined, to identify genes that were significantly differentially regulated as a function of CSB expression. Our findings revealed that response to endoplasmic reticulum stress and response to unfolded proteins were ranked top amongst the cellular processes affected by CSB suppression. The major components of the endoplasmic reticulum stress-mediated apoptosis pathway, including pro-apoptotic factors downstream of the ATF3-CHOP cascade, were dramatically up-regulated. Altogether our findings add new pieces to the understanding of CSB mechanisms of action and to the molecular basis of CS syndrome.http://europepmc.org/articles/PMC5333825?pdf=render |
| spellingShingle | Manuela Caputo Alessio Balzerano Ivan Arisi Mara D'Onofrio Rossella Brandi Silvia Bongiorni Stefano Brancorsini Mattia Frontini Luca Proietti-De-Santis CSB ablation induced apoptosis is mediated by increased endoplasmic reticulum stress response. PLoS ONE |
| title | CSB ablation induced apoptosis is mediated by increased endoplasmic reticulum stress response. |
| title_full | CSB ablation induced apoptosis is mediated by increased endoplasmic reticulum stress response. |
| title_fullStr | CSB ablation induced apoptosis is mediated by increased endoplasmic reticulum stress response. |
| title_full_unstemmed | CSB ablation induced apoptosis is mediated by increased endoplasmic reticulum stress response. |
| title_short | CSB ablation induced apoptosis is mediated by increased endoplasmic reticulum stress response. |
| title_sort | csb ablation induced apoptosis is mediated by increased endoplasmic reticulum stress response |
| url | http://europepmc.org/articles/PMC5333825?pdf=render |
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