ArticleBiochemical pharmacology2019
Nodal pathway activation due to Akt1 suppression is a molecular switch for prostate cancer cell epithelial-to-mesenchymal transition and metastasis.
Article in Biochemical pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- miR-146b-5p promotes prostate cancer progression by targeting and negatively regulating FOXO3 and its mechanism.World journal of surgical oncology · 2026Article
- Nodal promotes colorectal cancer survival and metastasis through regulating SCD1-mediated ferroptosis resistance.Cell death & disease · 2023Article
- Centipeda minima active components and mechanisms in lung cancer.BMC complementary medicine and therapies · 2023Article
- Discovering Tuberosin and Villosol as Potent and Selective Inhibitors of AKT1 for Therapeutic Targeting of Oral Squamous Cell Carcinoma.Journal of personalized medicine · 2022Article
- Article
- Nodal Enhances Perineural Invasion in Pancreatic Cancer by Promoting Tumor-Nerve Convergence.Journal of healthcare engineering · 2022Article
- Targeting Akt-associated microRNAs for cancer therapeutics.Biochemical pharmacology · 2021Review
- Review
- Bioinformatics Analysis to Screen Key Targets of Curcumin against Colorectal Cancer and the Correlation with Tumor-Infiltrating Immune Cells.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- A Network Pharmacology Approach to Investigate the Anticancer Mechanism and Potential Active Ingredients ofFrontiers in pharmacology · 2020Article
- Distinct functions of AKT isoforms in breast cancer: a comprehensive review.Cell communication and signaling : CCS · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Several studies have unraveled the negative role of Akt1 in advanced cancers, including metastatic prostate cancer (mPCa). Hence, understanding the consequences of targeting Akt1 in the mPCa and identifying its downstream novel targets is essential. We studied how Akt1 deletion in PC3 and DU145 cells activates the Nodal pathway and promotes PCa epithelial-to-mesenchymal transition (EMT) and metastasis. Here we show that Akt1 loss increases Nodal expression in PCa cells accompanied by activation of FoxO1/3a, and EMT markers Snail and N-cadherin as well as loss of epithelial marker E-cadherin. Treatment with FoxO inhibitor AS1842856 abrogated the Nodal expression in Akt1 deleted PCa cells. Akt1 deficient PCa cells exhibited enhanced cell migration and invasion in vitro and lung metastasis in vivo, which were attenuated by treatment with Nodal pathway inhibitor SB505124. Interestingly, Nodal mRNA analysis from two genomic studies in cBioportal showed a positive correlation between Nodal expression and Gleason score indicating the positive role of Nodal in human mPCa. Collectively, our data demonstrate Akt1-FoxO3a-Nodal pathway as an important mediator of PCa metastasis and present Nodal as a potential target to treat mPCa patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.