The molecular landscape of colorectal cancer cell lines unveils clinically actionable kinase targets
Open accessAbstract
The development of molecularly targeted anticancer agents relies on large panels of tumour-specific preclinical models closely recapitulating the molecular heterogeneity observed in patients. Here we describe the mutational and gene expression analyses of 151 colorectal cancer (CRC) cell lines. We find that the whole spectrum of CRC molecular and transcriptional subtypes, previously defined in patients, is represented in this cell line compendium. Transcriptional outlier analysis identifies RAS/BRAF wild-type cells, resistant to EGFR blockade, functionally and pharmacologically addicted to kinase genes including ALK, FGFR2, NTRK1/2 and RET. The same genes are present as expression outliers in CRC patient samples. Genomic rearrangements (translocations) involving the ALK and NTRK1 genes are associated with the overexpression of the corresponding proteins in CRC specimens. The approach described here can be used to pinpoint CRCs with exquisite dependencies to individual kinases for which clinically approved drugs are already available. Precision oncology relies on model systems that reflect the genomic heterogeneity of human cancers. Here the authors characterize a panel of 151 colorectal cancer cell lines with respect to genetic mutations, expression profiles and drug sensitivity to identify new therapeutic targets.
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In Medico CRC cell lines (n = 154), a gene expression signature correlation analysis shows a strong correlation of MEKi-resistance with EMT, SRC activation and dasatinib sensitivity.
“In agreeing with this, a gene expression signature correlation analysis in Medico CRC cell lines (n = 154) shows a strong correlation of MEKi-resistance with EMT, SRC activation and dasatinib sensitivity (see Fig S10a).”
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 [24]
The Genetic and transcriptional profiling section describes Medico et al.'s gene-expression profiling of CRC cell lines, so the source supports identifying the cell-line dataset. But the paper reports 151 lines after excluding one non-CRC line, not 154; the passages found do not report a correlation between MEK-inhibitor resistance, EMT, SRC activation, and dasatinib sensitivity. The citing sentence points to its own Fig. S10a for that analysis. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAmong Medico 113 CMS1-4 CRC cell lines, HCT116 (CMS4, KRAS G13D) and LIM2405 (CMS1, BRAF V600E) were shown to be sensitive to MEKi + SRCi in vitro.
“Notably, the finding is also supported by the analysis of Medico 113 CMS1-4 CRC cell lines (Fig. 8e) among which HCT116 (CMS4, KRAS G13D) and LIM2405 (CMS1, BRAF (V600E) (both within Fig. 8e RUQs) were shown to be sensitive to MEKi + SRCi in vitro (Additional File 3_Fig S10 and S11).”
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 [24]
The Genetic and transcriptional profiling section includes HCT116 and LIM2405 in Medico et al.’s CRC cell-line collection, supporting the identification of the lines. Our copy describes 151 lines and tests cetuximab and other targeted drugs, but does not report a 113-line CMS1–4 analysis or show that these two lines were sensitive to combined MEK and SRC inhibition. The citing sentence points to its own supplementary figures for that treatment result. (LLM, conf=0.87)
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- Authors
- Medico, E., Russo, M., Picco, G., Cancelliere, C., Valtorta, E., Corti, G., Buscarino, M., Isella, C., Lamba, S., Martinoglio, B., Veronese, S., Siena, S., Sartore-Bianchi, A., Beccuti, M., Mottolese, M., Linnebacher, M., Cordero, F., Di Nicolantonio, F., & Bardelli, A.
- Affiliations
- IFOM (IT)
- Candiolo Cancer Institute (IT)
- Azienda Socio Sanitaria Territoriale Grande Ospedale Metropolitano Niguarda (IT)
- University of Turin (IT)
- Instituto Nazionale Tumori Regina Elena (IT)
- University of Rostock (DE)
- Corresponding author
- Bardelli, Alberto
- ORCID
- Venue
- Nature Communications
- Published
- 2015-04-30
- Volume
- 6
- Issue
- 1
- Pages
- 7002-7002
- ISSN
- 2041-1723 (ISSN-L)
- OpenAlex
- W2066560754
- Cited by
- 302
- References
- 47
- Citations by year
- 2026: 10 · 2025: 14 · 2024: 31 · 2023: 25 · 2022: 26 · 2021: 41 · 2020: 28 · 2019: 29 · 2018: 31 · 2017: 36 · 2016: 21 · 2015: 10
- FWCI
- 14.27
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion, other-oa)
- RePEc: Research Papers in Economics (submittedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Funders
- European Commission (602901)
- Ministero della Salute
- Ministero dell’Istruzione, dell’Università e della Ricerca
- Associazione Italiana per la Ricerca sul Cancro (12812, 12944)
- Topics
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- colorectal cancer, cancer cell lines, RAS/BRAF wild-type, anaplastic lymphoma kinase, FGFR2, NTRK1, NTRK2, RET, genome rearrangement, translocation, precision oncology, molecular subtypes, drug sensitivity, therapeutic target
- MeSH terms
- Cetuximab, Anaplastic Lymphoma Kinase, Humans, Colorectal Neoplasms, Genetic Heterogeneity, Genes, erbB-1, Receptor Protein-Tyrosine Kinases, Cell Line, Tumor, Proto-Oncogene Proteins c-ret, Receptor, Fibroblast Growth Factor, Type 2, Molecular Targeted Therapy, ErbB Receptors
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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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