ArticleCancer biology & therapy2022
Crosstalk between PI3K/Akt and Wnt/β-catenin pathways promote colorectal cancer progression regardless of mutational status.
Article in Cancer biology & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 71 citations in OpenAlex.
- Pharmacological inhibition of the canonical Wnt/β-catenin signaling pathway sensitizes 5-fluorouracil-resistant colorectal cancer cells.Molecular biology reports · 2026Article
- A novel dihydroisoxazole derivative DHI9 suppresses colorectal cancer cell survival by inducing oxidative stress, DNA damage, and mitochondrial apoptosis while targeting Akt and Wnt/β-catenin signalling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Cancer Stem Cells in Colorectal Cancer: From Molecular Mechanisms to Diagnosis, Prognosis and Therapy Implications.Cancers · 2026Review
- Article
- Evaluation of the Anti-Cancer Effects of KMU-11342 in In Vitro and Ex Vivo Models of Colorectal Cancer.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Molecular mechanisms and multi-organ regulatory roles of anti-Müllerian hormone in female reproduction.Communications biology · 2026Review
- Insulin resistance, inflammation, oxidative stress and dysregulated WNT/β-Catenin signaling in polycystic ovary syndrome: A review.Molecular biology reports · 2026Review
- Cytochrome P450 enzymes as modulators of oncogenic signaling via the Wnt/β-catenin signaling pathway.Archives of toxicology · 2026Review
- Research progress of small molecule protein kinase inhibitors (SMKIs) in the treatment of colorectal cancer: mechanism, application, and future prospects.Frontiers in pharmacology · 2026Review
- Macrophage activation and invasion byJournal of oral microbiology · 2026Article
- Study of ß-catenin signaling pathway modulated by PTHrP in cell and animal colorectal cancer models.Frontiers in oncology · 2026Article
- AI-Guided Discovery of Oncogenic Signaling Crosstalk in Tumor Progression and Drug Resistance.Oncology research · 2026Review
- Targeting mTORC2-dependent AKT/FOXO1/RNF125 signaling exploits a therapeutic vulnerability in c-MET-activated and β-catenin-mutated hepatocellular carcinoma.Hepatology (Baltimore, Md.) · 2025Article
- Roles of Wnt ligands and receptors in oral squamous cell carcinoma.Journal of Zhejiang University. Science. B · 2025Review
- Zinc finger protein 695 facilitates the proliferation of colorectal cancer cells through activation of the NEK2 and PI3K/Akt/mTOR signaling pathways.Oncology reports · 2025Article
- Evolutionary conservation and cancer implications of the WNT signaling pathway.Medical oncology (Northwood, London, England) · 2025Review
- Advances in research on the pathogenesis and signaling pathways associated with postoperative delirium (Review).Molecular medicine reports · 2025Review
- Disruption of the Wnt/β-Catenin and PI3K-AKT-mTOR Crosstalk in Endometrial Stromal Cells: A Case Report of Impaired Decidualization Leading to Recurrent Implantation Failure and Potential Pathway-Specific Therapeutic Interventions.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Warhead-bearing natural compounds for multi-pathway irreversible inhibition to overcome drug resistance in colorectal cancer.Medical oncology (Northwood, London, England) · 2025Article
- Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
The PI3K/Akt and Wnt/β-catenin pathways play an important role in the acquisition of the malignant phenotype in cancer. However, there are few data regarding the role of the interplay between both pathways in colorectal cancer (CRC) progression. The mutational status and the clinicopathological characteristics of PI3K/Akt and Wnt/β-catenin pathways were accessed by bioinformatic analysis whereas that the impact of the interplay between the activity of both pathways to explain tumorigenic potential was performed in vitro using IGF-1 and Wnt3a treatments in CRC cell models. The mutational status of these pathways did not influence the survival of CRC patients, but an association between clinicopathological characteristics in patients with mutations in one, but not in both pathways was observed. A potentiating effect on the activation of both pathways and enhanced cellular migration and proliferation was observed when both pathways were activated simultaneously with IGF-1 and Wnt3a. In addition, these effects were hindered after pretreatment with LY294002, a specific PI3K inhibitor, suggesting some dependence between these two signaling cascades. Our findings show that, regardless of mutational status, there is an interplay between the activity of PI3K/Akt and Wnt/β-catenin pathways that contributes to events related to CRC progression and that the reversal of such events using a PI3K inhibitor highlights the value of targeting these pathways for potential directed therapies in CRC patients.
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