ArticleMolecular and cellular biology2005
DNA topoisomerase I is a cofactor for c-Jun in the regulation of epidermal growth factor receptor expression and cancer cell proliferation.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 53 citations in OpenAlex.
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- E6-mediated activation of JNK drives EGFR signalling to promote proliferation and viral oncoprotein expression in cervical cancer.Cell death and differentiation · 2021Article
- Two-pore channels affect EGF receptor signaling by receptor trafficking and expression.iScience · 2021Article
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- Inhibition of prostate cancer cell line (PC-3) by anhydrodihydroartemisinin (ADHA) through caspase-dependent pathway.EXCLI journal · 2020Article
- Chemotherapeutic Drugs Inhibiting Topoisomerase 1 Activity Impede Cytokine-Induced and NF-κB p65-Regulated Gene Expression.Cancers · 2019Article
- MAP3K1 and MAP2K4 mutations are associated with sensitivity to MEK inhibitors in multiple cancer models.Cell research · 2018Article
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- Natural Compounds as Anticancer Agents Targeting DNA Topoisomerases.Current genomics · 2017Review
- Relevance Rank Platform (RRP) for Functional Filtering of High Content Protein-Protein Interaction Data.Molecular & cellular proteomics : MCP · 2015Article
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- Human cancer cell line microRNAs associated with in vitro sensitivity to paclitaxel.Oncology reports · 2014Article
- Identification of protein interactions involved in cellular signaling.Molecular & cellular proteomics : MCP · 2013Review
- Nucleolar AATF regulates c-Jun-mediated apoptosis.Molecular biology of the cell · 2012Article
- c-Fos overexpression increases the proliferation of human hepatocytes by stabilizing nuclear Cyclin D1.World journal of gastroenterology · 2008Article
- The role of topoisomerases and RNA transcription in the action of the antitumour benzonaphthyridine derivative SN 28049.Cancer chemotherapy and pharmacology · 2008Article
- Involvement of Hif-1 in desferrioxamine-induced invasion of glioblastoma cells.Clinical & experimental metastasis · 2007Article
- Topoisomerase I inhibitors: camptothecins and beyond.Nature reviews. Cancer · 2006Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA topoisomerase I (Topo I) is a molecular target for the anticancer agent topotecan in the treatment of small cell lung cancer and ovarian carcinomas. However, the molecular mechanisms by which topotecan treatment inhibits cancer cell proliferation are unclear. We describe here the identification of Topo I as a novel endogenous interaction partner for transcription factor c-Jun. Reciprocal coimmunoprecipitation analysis showed that Topo I and c-Jun interact in transformed human cells in a manner that is dependent on JNK activity. c-Jun target gene epidermal growth factor receptor (EGFR) was identified as a novel gene whose expression was specifically inhibited by topotecan. Moreover, Topo I overexpression supported c-Jun-mediated reporter gene activation and both genetic and chemical inhibition of c-Jun converted cells resistant to topotecan-elicited EGFR downregulation. Topotecan-elicited suppression of proliferation was rescued by exogenously expressed EGFR. Furthermore, we demonstrate the cooperation of the JNK-c-Jun pathway, Topo I, and EGFR in the positive regulation of HT-1080 cell proliferation. Together, these results have identified transcriptional coactivator Topo I as a first endogenous cofactor for c-Jun in the regulation of cell proliferation. In addition, the results of the present study strongly suggest that inhibition of EGFR expression is a novel mechanism by which topotecan inhibits cell proliferation in cancer therapy.
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