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Targeting the PI 3K signaling pathway in KRAS mutant colon cancer
Open accessAbstract
Metastatic colorectal cancer (CRC) patients with v‐Ki‐ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations are resistant to monoclonal antibody that targets the epidermal growth factor receptor such as cetuximab. BKM 120 targets phosphatidylinositide‐3‐kinase (PIK 3 CA), but it is unknown whether BKM 120 can reverse cetuximab resistance in KRAS mutant CRC. Human CRC cell lines with KRAS mutations (DLD‐1, HCT 116, and LoVo) were used to test the effect of cetuximab, BKM 120, and cetuximab plus BKM 120 on cell proliferation in vitro and in vivo. BKM 120 reduced cell proliferation in a concentration‐dependent manner in the LoVo (PI 3 KCA wild type) as well as the HCT 116 and DLD 1 cells (that carry a PI 3 KCA mutation). BKM 120 only inhibited ERK phosphorylation in LoVo cells (PIK 3 CA wild type), but not in DLD 1 or HCT 116 cells at a concentration of 1 μ mol/L. Treatment with cetuximab and BKM 120 significantly reduced the growth of xenograft tumors originating from KRAS mutant cells compared with cetuximab alone (P = 0.034). BKM 120 may overcome cetuximab resistance in colon cancer cells with KRAS mutation.
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“Another PI3K inhibitor, BKM120, was found to impede KRAS mutation-induced colorectal cancer growth both in vitro and in vivo, regardless of PI3K genotype [45].”
From Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies (2021) · cites this paper as [45]
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Zhou, J., Ji, Q., & Li, Q. (2021) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-021-02130-2 · Cited by 246
Metadata
- Authors
- Hong, S., Kim, S., Kim, H. Y., Kang, M., Jang, H. H., & Lee, W.
- Affiliations
- Gachon University (KR)
- Department of Surgery Gil Medical Center Gachon University Incheon Korea
- Corresponding author
- Lee, Won‐Suk
- Venue
- Cancer Medicine
- Publisher
- Wiley
- Published
- 2015-12-29
- Volume
- 5
- Issue
- 2
- Pages
- 248-255
- ISSN
- 2045-7634 (ISSN-L)
- PMC
- PMC4735771
- OpenAlex
- W2199689631
- Cited by
- 37
- References
- 20
- Citations by year
- 2026: 1 · 2024: 4 · 2023: 4 · 2022: 2 · 2021: 5 · 2020: 1 · 2019: 3 · 2018: 6 · 2017: 9 · 2016: 2
- FWCI
- 2.47
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cancer Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Gachon University (FRD2014‐9, FRD2014‐28)
- Topics
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- KRAS mutation, colorectal cancer, PI3K signaling, BKM120, PIK3CA, cetuximab resistance, anti-EGFR therapy, combination therapy, ERK1/2 phosphorylation, xenograft tumor growth, cell proliferation
- MeSH terms
- Cetuximab, Phosphoinositide-3 Kinase Inhibitors, Aminopyridines, Animals, Antineoplastic Agents, Cell Survival, Colonic Neoplasms, Disease Models, Animal, Drug Synergism, Humans, Male, Morpholines, Mutation, Signal Transduction, Apoptosis, ras Proteins, Phosphatidylinositol 3-Kinases, MAP Kinase Signaling System, Xenograft Model Antitumor Assays, Cell Line, Tumor, Tumor Burden, Cell Proliferation, Proto-Oncogene Proteins c-akt, Caspase 3, Molecular Targeted Therapy
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