AKT3 expression in mesenchymal colorectal cancer cells drives growth and is associated with epithelial-mesenchymal transition
Open accessAbstract
Colorectal cancer (CRC) is a heterogeneous disease that can currently be subdivided into four distinct consensus molecular subtypes (CMS) based on gene expression profiling. The CMS4 subtype is marked by high expression of mesenchymal genes and is associated with a worse overall prognosis compared to other CMSs. Importantly, this subtype responds poorly to the standard therapies currently used to treat CRC. We set out to explore what regulatory signalling networks underlie the CMS4 phenotype of cancer cells, specifically, by analysing which kinases were more highly expressed in this subtype compared to others. We found AKT3 to be expressed in the cancer cell epithelium of CRC specimens, patient derived xenograft (PDX) models and in (primary) cell cultures representing CMS4. Importantly, chemical inhibition or knockout of this gene hampers outgrowth of this subtype, as AKT3 controls expression of the cell cycle regulator p27KIP1. Furthermore, high AKT3 expression was associated with high expression of epithelial-mesenchymal transition (EMT) genes, and this observation could be expanded to cell lines representing other carcinoma types. More importantly, this association allowed for the identification of CRC patients with a high propensity to metastasise and an associated poor prognosis. High AKT3 expression in the tumour epithelial compartment may thus be used as a surrogate marker for EMT and may allow for a selection of CRC patients that could benefit from AKT3-targeted therapy.
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Elevated AKT3 and KIT, reduced mitochondrial respiratory complex I activity, and modified alternative splicing landscape are biological hallmarks of CMS4.
“Among other biological hallmarks of this subtype shown to contribute to CMS4 traits feature elevated AKT3 (42) and KIT (43), reduced mitochondrial respiratory complex I activity (44)—possibly resulting from KIT overexpression (43)—or modified alternative splicing landscape (45).”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [42]
MK2206 reduced cell growth in preclinical models of CMS4 colorectal cancer (AKT3 target).
“| AKT3 | MK2206 | Reduced cell growth | (42) |”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [42]
HSP90, PAK2, and AKT3 have emerged as candidate targets from preclinical studies of CMS4 colorectal cancer.
“Other candidate targets have emerged from preclinical studies, including HSP90, combined with 5-FU (7), PAK2 (67) or AKT3 (42)”
From Clinical Challenges of Consensus Molecular Subtype CMS4 Colon Cancer in the Era of Precision Medicine (2024) · cites this paper as [42]
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Mouillet-Richard, S., Cazelles, A., Sroussi, M., Gallois, C., Taieb, J., & Laurent-Puig, P. (2024) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-23-3964 · Cited by 43 · see citing works
- Authors
- Buikhuisen, J. Y., Gomez Barila, P. M., Torang, A., Dekker, D., de Jong, J. H., Cameron, K., Vitale, S., Stassi, G., van Hooff, S. R., Castro, M. A. A., Vermeulen, L., & Medema, J. P.
- Affiliations
- Oncode Institute (NL)
- Laboratory for Experimental Oncology and Radiobiology, Center for Experimental Molecular Medicine, Cancer Center Amsterdam, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands
- Università Cattolica del Sacro Cuore (IT)
- University of Palermo (IT)
- Universidade Federal do Paraná (BR)
- Corresponding author
- Medema, Jan Paul
- ORCID
- Venue
- Cancers
- Publisher
- MDPI AG
- Published
- 2021-02-14
- Volume
- 13
- Issue
- 4
- Pages
- 801
- ISSN
- 2072-6694 (ISSN-L)
- PMC
- PMC7918753
- OpenAlex
- W3130651220
- Cited by
- 33
- References
- 69
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 6 · 2023: 9 · 2022: 5 · 2021: 5
- FWCI
- 2.28
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cancers (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (acceptedVersion, cc-by)
- IRIS UniPA (University of Palermo) (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- KWF Kankerbestrijding (UVA2014-7245, 10150)
- Oncode Institute (n/a)
- AMC Graduate School (PhD Scholarship)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- AKT3, colorectal cancer, epithelial-mesenchymal transition, p27, tumor growth, metastasis, prognosis, patient-derived xenografts
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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