Dual Src and MEK Inhibition Decreases Ovarian Cancer Growth and Targets Tumor Initiating Stem-Like Cells
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Abstract
Purpose: Rational targeted therapies are needed for treatment of ovarian cancers. Signaling kinases Src and MAPK are activated in high-grade serous ovarian cancer (HGSOC). Here, we tested the frequency of activation of both kinases in HGSOC and the therapeutic potential of dual kinase inhibition. Experimental Design: MEK and Src activation was assayed in primary HGSOC from The Cancer Genome Atlas (TGGA). Effects of dual kinase inhibition were assayed on cell-cycle, apoptosis, gene, and proteomic analysis; cancer stem cells; and xenografts. Results: Both Src and MAPK are coactivated in 31% of HGSOC, and this associates with worse overall survival on multivariate analysis. Frequent dual kinase activation in HGSOC led us to assay the efficacy of combined Src and MEK inhibition. Treatment of established lines and primary ovarian cancer cultures with Src and MEK inhibitors saracatinib and selumetinib, respectively, showed target kinase inhibition and synergistic induction of apoptosis and cell-cycle arrest in vitro, and tumor inhibition in xenografts. Gene expression and proteomic analysis confirmed cell-cycle inhibition and autophagy. Dual therapy also potently inhibited tumor-initiating cells. Src and MAPK were both activated in tumor-initiating populations. Combination treatment followed by drug washout decreased sphere formation and ALDH1+ cells. In vivo, tumors dissociated after dual therapy showed a marked decrease in ALDH1 staining, sphere formation, and loss of tumor-initiating cells upon serial xenografting. Conclusions: Selumetinib added to saracatinib overcomes EGFR/HER2/ERBB2–mediated bypass activation of MEK/MAPK observed with saracatinib alone and targets tumor-initiating ovarian cancer populations, supporting further evaluation of combined Src–MEK inhibition in clinical trials. Clin Cancer Res; 24(19); 4874–86. ©2018 AACR.
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Preclinical studies suggest that inhibition of SRC may revert resistance to cytotoxic drugs.
“preclinical studies suggest that inhibition of SRC may revert this resistance.”
From Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer (2025) · cites this paper as [30]
The Results and Discussion report that combined Src and MEK inhibition overcame resistance to either inhibitor in preclinical ovarian cancer models. The resistance studied was to those targeted inhibitors, not to cytotoxic drugs, and Src inhibition alone did not reverse it. The Discussion also notes no added clinical benefit when a Src inhibitor was combined with chemotherapy for platinum-resistant ovarian cancer. (LLM, conf=0.85)
Experimental — accuracy not yet measuredActivation of SRC contributes to resistance to cytotoxic drugs such as platinum agents in several malignancies.
“activation of SRC contributes to resistance to different cytotoxic drugs (i.e. platinum agents) in several malignancies [29–31]”
From Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer (2025) · cites this paper as [30]
The Discussion says platinum chemotherapy selects for ovarian stem-like cells, and the Results report elevated activated Src in an ovarian ALDH1+ stem-like population. These passages connect Src activity with cells implicated in platinum resistance, but do not establish that Src activation causes resistance to cytotoxic drugs or show this across several malignancies. Page numbers are unavailable in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredDrug combinations of MEK and SRC inhibitors have been carried out in vitro using various types of cancer cell lines and to a less degree in vivo using mouse models, where enhanced anti-cancer effects have been reported.
“Notably, exploration of drug combinations of MEK and SRC inhibitors have been carried out in vitro using various types of cancer cell lines and to a less degree in vivo using mouse models, where enhanced anti-cancer effects have been reported [53–57].”
From An integrative gene expression signature analysis identifies CMS4 KRAS-mutated colorectal cancers sensitive to combined MEK and SRC targeted therapy (2022) · cites this paper as [57]
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Small molecule inhibitors targeting the cancers
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Synergistic Anti-Tumor Activity by Targeting Multiple Signaling Pathways in Ovarian Cancer
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BCL2L11 Induction Mediates Sensitivity to Src and MEK1/2 Inhibition in Thyroid Cancer
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Network controllability solutions for computational drug repurposing using genetic algorithms
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PTPRS drives adaptive resistance to MEK/ERK inhibitors through SRC
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Gut–Vaginal Microbiome Crosstalk in Ovarian Cancer: Implications for Early Diagnosis
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Strategic Combination Therapies for Ovarian Cancer
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Combinatorial Strategies to Target Molecular and Signaling Pathways to Disarm Cancer Stem Cells
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Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer
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Pathway profiling of a novel SRC inhibitor, AZD0424, in combination with MEK inhibitorsPreprint
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- Authors
- Simpkins, F., Jang, K., Yoon, H., Hew, K. E., Kim, M., Azzam, D. J., Sun, J., Zhao, D., Ince, T. A., Liu, W., Guo, W., Wei, Z., Zhang, G., Mills, G. B., & Slingerland, J. M.
- Affiliations
- University of Miami (US)
- The University of Texas MD Anderson Cancer Center (US)
- New Jersey Institute of Technology (US)
- The Wistar Institute (US)
- Corresponding author
- Simpkins, Fiona
- Slingerland, Joyce M.
- ORCID
- Venue
- Clinical Cancer Research
- Published
- 2018-10-01
- Volume
- 24
- Issue
- 19
- Pages
- 4874-4886
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- PMC
- PMC6557165
- OpenAlex
- W2811339164
- Cited by
- 67
- References
- 115
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 5 · 2023: 12 · 2022: 13 · 2021: 10 · 2020: 7 · 2019: 13
- FWCI
- 8.04
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NCI (K08 CA151892-01)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Ovarian cancer diagnosis and treatment
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cancer Mechanisms and Therapy
- Keywords
- high-grade serous ovarian cancer, Src kinase, MEK inhibition, MAPK signaling, dual kinase inhibition, saracatinib, selumetinib, cancer stem cells, ALDH1, apoptosis, cell cycle arrest, autophagy, combination therapy
- MeSH terms
- Animals, Antineoplastic Combined Chemotherapy Protocols, Benzimidazoles, Female, Humans, Middle Aged, Ovarian Neoplasms, Quinazolines, Neoplastic Stem Cells, Apoptosis, Disease-Free Survival, Drug Resistance, Neoplasm, src-Family Kinases, Xenograft Model Antitumor Assays, Proteomics, Cell Line, Tumor, Protein Kinase Inhibitors, Estrogen Receptor alpha, MAP Kinase Kinase 1, Cell Proliferation, Mice, Benzodioxoles
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