ArticleThe Journal of biological chemistry2013
Regulation of Rad17 protein turnover unveils an impact of Rad17-APC cascade in breast carcinogenesis and treatment.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Emerging roles of i-motif in gene expression and disease treatment.Frontiers in pharmacology · 2023Review
- TOP1 inhibition induces bifurcated JNK/MYC signaling that dictates cancer cell sensitivity.International journal of biological sciences · 2022Article
- The noncoding function of NELFA mRNA promotes the development of oesophageal squamous cell carcinoma by regulating the Rad17-RFC2-5 complex.Molecular oncology · 2020Article
- Effect of ghost pepper on cell proliferation, apoptosis, senescence and global proteomic profile in human renal adenocarcinoma cells.PloS one · 2018Article
- Regulation of XIAP Turnover Reveals a Role for USP11 in Promotion of Tumorigenesis.EBioMedicine · 2017Article
- Insights into APC/C: from cellular function to diseases and therapeutics.Cell division · 2016Review
- Role of AMP-activated protein kinase in cross-talk between apoptosis and autophagy in human colon cancer.Cell death & disease · 2014Article
- DNA damage response genes and the development of cancer metastasis.Radiation research · 2014Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Aberrant regulation of DNA damage checkpoint function leads to genome instability that in turn can predispose cellular tissues to become cancerous. Previous works from us and others demonstrated the role of Rad17 in either activation or termination of DNA damage checkpoint function. In the current study, we have revealed the unexpected accumulation of Rad17 in various types of breast cancer cell lines as well as human breast cancer tissues. We observed that Rad17 protein turnover rate in breast epithelial cells is much faster than in breast cancer cells, where the turnover of Rad17 is regulated by the Cdh1/APC pathway. We further observed that Rad17-mediated checkpoint function is modulated by proteolysis. Stabilization of Rad17 disrupts cellular response to chemotherapeutic drug-induced DNA damage and enhances cellular transformation. In addition, manipulation of Rad17 by RNA interference or stabilization of Rad17 significantly sensitize breast cancer cell to various chemotherapeutic drugs. Our present results indicate the manipulation of Rad17 proteolysis could be a valuable approach to sensitize breast cancer cell to the chemotherapeutic treatment despite of the critical role in governing DNA damage response and cellular recovery from genotoxic stress.
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