ArticleNature communications2016
RAS signalling through PI3-Kinase controls cell migration via modulation of Reelin expression.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Applicability of Plant Extracts in Preclinical Studies of Melanoma: A Systematic Review.Mediators of inflammation · 2018Pooled it
- A renaissance in targeting the PI3K/AKT/mTOR pathway.Nature reviews. Drug discovery · 2026Review
- Polarized SOS activity orchestrates FGF-directed cell migration in vivo.Current biology : CB · 2026Article
- Advanced dual primary male breast cancer and lung cancer: A case report and literature review.Oncology letters · 2026Article
- Review
- Forcing the code: tension modulates signaling to drive morphogenesis and malignancy.Genes & development · 2025Review
- RET Inhibitor SPP86 Triggers Apoptosis and Activates the DNA Damage Response Through the Suppression of Autophagy and the PI3K/AKT Signaling Pathway in Melanoma Cells.Drug design, development and therapy · 2025Article
- Regulatory mechanism of Reelin activity: a platform for exploiting Reelin as a therapeutic agent.Frontiers in molecular neuroscience · 2025Review
- The Potential Role of the Extracellular Matrix Glycoprotein Reelin in Glioblastoma Biology.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Molecular Mechanisms of Reelin in the Enteric Nervous System and the Microbiota-Gut-Brain Axis: Implications for Depression and Antidepressant Therapy.International journal of molecular sciences · 2024Review
- Developments in Genetics: Better Management of Ovarian Cancer Patients.International journal of molecular sciences · 2023Review
- Analysis of genomic and immune intratumor heterogeneity in linitis plastica via multiregional exome and T-cell receptor sequencing.Molecular oncology · 2023Article
- Reelin through the years: From brain development to inflammation.Cell reports · 2023Review
- Reelin and APP Cooperatively Modulate Dendritic Spine FormationExperimental neurobiology · 2023Article
- CD34Frontiers in cell and developmental biology · 2023Article
- Predictive miRNAs Patterns in Blood of Breast Cancer Patients Demonstrating Resistance Towards Neoadjuvant Chemotherapy.Breast cancer (Dove Medical Press) · 2023Article
- Neurotransmitter signaling: a new frontier in colorectal cancer biology and treatment.Oncogene · 2022Review
- Reelin Protects against Colon Pathology via p53 and May Be a Biomarker for Colon Cancer Progression.Biology · 2022Article
- Review
- Engineered variants of the Ras effector protein RASSF5 (NORE1A) promote anticancer activities in lung adenocarcinoma.The Journal of biological chemistry · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
RAS signalling through phosphoinositide 3-kinase (PI3-Kinase) has been shown to have an essential role in tumour initiation and maintenance. RAS also regulates cell motility and tumour invasiveness, but the role of direct RAS binding to PI3-Kinase in this remains uncertain. Here, we provide evidence that disruption of RAS interaction with PI3-Kinase p110α decreases cell motility and prevents activation of Rac GTPase. Analysis of gene expression in cells lacking RAS interaction with p110α reveals increased levels of the extracellular matrix glycoprotein Reelin and activation of its downstream pathway resulting in upregulation of E-cadherin expression. Induction of the Reelin/E-cadherin axis is also observed in Kras mutant lung tumours that are regressing due to blockade of RAS interaction with PI3-Kinase. Furthermore, loss of Reelin correlates with decreased survival of lung and breast cancer patients. Reelin thus plays a role in restraining RAS and PI3-kinase promotion of cell motility and potentially tumour metastasis.
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What OpenQuestion holds
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.