ArticleCancer research2018
AMPK-Akt Double-Negative Feedback Loop in Breast Cancer Cells Regulates Their Adaptation to Matrix Deprivation.
Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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.
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Who cites it
36 citing papers in PubMed, 68 citations in OpenAlex.
- Programmed cell death and metastatic evolution in breast cancer: the role of anoikis, necroptosis, and ferroptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Glucose metabolic reprogramming: a novel strategy to enhance radiotherapy response to triple-negative breast cancer.Frontiers in public health · 2026Review
- Dual Inhibition of PARP and Akt Induces Metabolic Collapse and Apoptosis in Breast Cancer Cells.Cancers · 2025Article
- GPD1L as a potential biomarker associated with Treg cell infiltration and lipid metabolism in clear cell renal cell carcinoma.Journal of translational medicine · 2025Article
- Rethinking AMPK: A Reversible Switch Fortifying Cancer Cell Stress-Resilience.The Yale journal of biology and medicine · 2025Review
- Experimentally-driven mathematical model to understand the effects of matrix deprivation in breast cancer metastasis.NPJ systems biology and applications · 2024Article
- miR-4448/Girdin/Akt/AMPK axis inhibits EZH2-mediated EMT and tumorigenesis in small-cell lung cancer.Cancer medicine · 2024Article
- CD24 negativity reprograms mitochondrial metabolism to PPARα and NF-κB-driven fatty acid β-oxidation in triple-negative breast cancer.Cancer letters · 2024Article
- Extracellular matrix detached cancer cells resist oxidative stress by increasing histone demethylase KDM6 activity.Saudi journal of biological sciences · 2024Article
- Anoikis resistance--protagonists of breast cancer cells survive and metastasize after ECM detachment.Cell communication and signaling : CCS · 2023Review
- Extracellular matrix remodeling in tumor progression and immune escape: from mechanisms to treatments.Molecular cancer · 2023Review
- AMPK is required for recovery from metabolic stress induced by ultrasound microbubble treatment.iScience · 2023Article
- Novel Anti-Cancer Products Targeting AMPK: Natural Herbal Medicine against Breast Cancer.Molecules (Basel, Switzerland) · 2023Review
- Inhibition of protein translation under matrix-deprivation stress in breast cancer cells.Frontiers in medicine · 2023Article
- AMP-activated protein kinase promotes breast cancer stemness and drug resistance.Disease models & mechanisms · 2022Article
- Mechanisms during Osteogenic Differentiation in Human Dental Follicle Cells.International journal of molecular sciences · 2022Review
- AMPKα loss promotes KRAS-mediated lung tumorigenesis.Cell death and differentiation · 2021Article
- Combined intermittent fasting and ERK inhibition enhance the anti-tumor effects of chemotherapy via the GSK3β-SIRT7 axis.Nature communications · 2021Article
- Role of AMPK and Akt in triple negative breast cancer lung colonization.Neoplasia (New York, N.Y.) · 2021Article
- Molecular profiling of epigenetic landscape of cancer cells during extracellular matrix detachment.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Cell detachment from the extracellular matrix triggers anoikis. Disseminated tumor cells must adapt to survive matrix deprivation, while still retaining the ability to attach at secondary sites and reinitiate cell division. In this study, we elucidate mechanisms that enable reversible matrix attachment by breast cancer cells. Matrix deprival triggered AMPK activity and concomitantly inhibited AKT activity by upregulating the Akt phosphatase PHLPP2. The resultant pAMPK
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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.