Network Modeling of MDM2 Inhibitor-Oxaliplatin Combination Reveals Biological Synergy in wt-p53 solid tumors
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Asfar S. Azmi 1 , Sanjeev Banerjee 1 , Shadan Ali 1 , Zhiwei Wang 1 , Bin Bao 1 , Frances W.J. Beck 2 , Main Maitah 2 , Minsig Choi 2 , Tony F. Shields 2 , Philip A. Philip 2 , Fazlul H. Sarkar 1 , Ramzi M. Mohammad 2 1 Department of Pathology, Wayne State University School of Medicine 2 Departments of Oncology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan Keywords: MDM2 and p53, MI-219, oxaliplatin Network Modeling Received: April 28, 2011; Accepted: May 11, 2011; Published: May 16, 2011; Correspondence: Fazlul H Sarkar, e-mail: // Ramzi M. Mohammad, e-mail: // // Abstract Earlier we had shown that the MDM2 inhibitor (MI-219) belonging to the spiro-oxindole family can synergistically enhance the efficacy of platinum chemotherapeutics leading to 50% tumor free survival in a genetically complex pancreatic ductal adenocarcinoma (PDAC) xenograft model. In this report, we have taken a systems and network modeling approach in order to understand central mechanisms behind MI219-oxaliplatin synergy with validation in PDAC, colon and breast cancer cell lines. Microarray profiling of drug treatments (MI-219, oxaliplatin or their combination) in capan-2 cells reveal a similar unique set of gene alterations that is duplicated in other solid tumor cells. As single agent, MI-219 or oxaliplatin induced alterations in 48 and 761 genes respectively. The combination treatment resulted in 767 gene alterations with emergence of 286 synergy unique genes. Ingenuity network modeling of combination and synergy unique genes showed the crucial role of five key local networks CREB, CARF, EGR1, NF-kB and E Cadherin. The network signatures were validated at the protein level in all three cell lines. Individually silencing central nodes in these five hubs resulted in abrogation of MI-219-oxaliplatin activity confirming their critical role in aiding p53 mediated apoptotic response. We anticipate that our MI219-oxaliplatin network blueprints can be clinically translated in the rationale design and application of this unique therapeutic combination in a genetically pre-defined subset of patients.
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RelA promotes apoptosis induced by the Mdm2 inhibitor MI-219 plus oxaliplatin in the human pancreatic ductal adenocarcinoma cell line Capan-2.
“Recently, the NFjB subunit RelA was shown to promote apoptosis induced by a combination of the Mdm2 inhibitor MI-219 and oxaliplatin in the human PDAC cell line Capan-2.25”
From Mdm2 inhibitors synergize with topoisomerase II inhibitors to induce p53-independent pancreatic cancer cell death (2013) · cites this paper as [25]
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Self-citation
- Authors
- Azmi, A. S., Banerjee, S., Ali, S., Wang, Z., Bao, B., Beck, F. W. J., Maitah, M., Choi, M., Shields, T. F., Philip, P. A., Sarkar, F. H., & Mohammad, R. M.
- Affiliations
- Wayne State University (US)
- Departments of Oncology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan
- Venue
- Oncotarget
- Publisher
- Impact Journals, LLC
- Published
- 2011-05-16
- Volume
- 2
- Issue
- 5
- Pages
- 378-392
- ISSN
- 1949-2553 (ISSN-L)
- PMC
- PMC3248191
- OpenAlex
- W1869563671
- Cited by
- 48
- References
- 42
- Citations by year
- 2021: 1 · 2020: 2 · 2019: 4 · 2018: 1 · 2017: 1 · 2015: 3 · 2014: 12 · 2013: 8 · 2012: 14
- FWCI
- 5.67
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Oncotarget (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Wayne State University
- Barbara Ann Karmanos Cancer Institute
- National Institutes of Health
- National Cancer Institute (R01CA109389, R01CA101870)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Physical Sciences › Computer Science › Computational Theory and Mathematics › Computational Drug Discovery Methods
- Keywords
- MDM2 inhibitors, oxaliplatin, combination drug synergy, p53, network modeling, pancreatic ductal adenocarcinoma, CREB, CARF, EGR1, NF-kB, E-cadherin, apoptosis, gene expression profiling, spirooxindoles, colon cancer, breast cancer
- MeSH terms
- Oxaliplatin, Oxindoles, Antineoplastic Agents, Computer Simulation, DNA-Binding Proteins, Drug Synergism, Gene Expression Regulation, Humans, Indoles, Organoplatinum Compounds, Pancreatic Neoplasms, Spiro Compounds, Transcription Factors, Tumor Suppressor Protein p53, Apoptosis, Cyclic AMP Response Element-Binding Protein, Platinum Compounds, Computational Biology, Gene Expression Profiling, RNA, Small Interfering, Carcinoma, Ductal, Cell Line, Tumor, Microarray Analysis, Proto-Oncogene Proteins c-mdm2, Early Growth Response Protein 1, Gene Regulatory Networks, Molecular Targeted Therapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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