ArticleFrontiers in cell and developmental biology2018
Microenvironment-Induced Non-sporadic Expression of the AXL and cKIT Receptors Are Related to Epithelial Plasticity and Drug Resistance.
Article in Frontiers in cell and developmental biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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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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.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Navigating TAM receptor dynamics in tumour immunotherapy.Cancer immunology, immunotherapy : CII · 2025Review
- Functional delineation of the luminal epithelial microenvironment in breast using cell-based screening in combinatorial microenvironments.Cellular signalling · 2024Article
- Extracellular matrix-derived mechanical force governs breast cancer cell stemness and quiescence transition through integrin-DDR signaling.Signal transduction and targeted therapy · 2023Article
- Characteristics and molecular mechanism of drug-tolerant cells in cancer: a review.Frontiers in oncology · 2023Review
- Dissecting the Role of AXL in Cancer Immune Escape and Resistance to Immune Checkpoint Inhibition.Frontiers in immunology · 2022Review
- High-Throughput Microenvironment Microarray (MEMA) High-Resolution Imaging.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Intrinsic Differences in Spatiotemporal Organization and Stromal Cell Interactions Between Isogenic Lung Cancer Cells of Epithelial and Mesenchymal Phenotypes Revealed by High-Dimensional Single-Cell Analysis of Heterotypic 3D Spheroid Models.Frontiers in oncology · 2022Article
- Aged Breast Extracellular Matrix Drives Mammary Epithelial Cells to an Invasive and Cancer-Like Phenotype.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Integration of mechanical and ECM microenvironment signals in the determination of cancer stem cell states.Current stem cell reports · 2021Article
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- The actin modulator hMENA regulates GAS6-AXL axis and pro-tumor cancer/stromal cell cooperation.EMBO reports · 2020Article
- Article
- Decoding cancer's camouflage: epithelial-mesenchymal plasticity in resistance to immune checkpoint blockade.Cancer drug resistance (Alhambra, Calif.) · 2020Review
- AXL as a Target in Breast Cancer Therapy.Journal of oncology · 2020Review
- Breast Tissue Biology Expands the Possibilities for Prevention of Age-Related Breast Cancers.Frontiers in cell and developmental biology · 2019Review
- Does Axl have potential as a therapeutic target in pancreatic cancer?Expert opinion on therapeutic targets · 2018Review
- Gas6 is dispensable for pubertal mammary gland development.PloS one · 2018Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
Abstract
The existence of rare cancer cells that sporadically acquire drug-tolerance through epigenetic mechanisms is proposed as one mechanism that drives cancer therapy failure. Here we provide evidence that specific microenvironments impose non-sporadic expression of proteins related to epithelial plasticity and drug resistance. Microarrays of robotically printed combinatorial microenvironments of known composition were used to make cell-based functional associations between microenvironments, which were design-inspired by normal and tumor-burdened breast tissues, and cell phenotypes. We hypothesized that specific combinations of microenvironment constituents non-sporadically impose the induction of the AXL and cKIT receptor tyrosine kinase proteins, which are known to be involved in epithelial plasticity and drug-tolerance, in an isogenic human mammary epithelial cell (HMEC) malignant progression series. Dimension reduction analysis reveals type I collagen as a dominant feature, inducing expression of both markers in pre-stasis finite lifespan HMECs, and transformed non-malignant and malignant immortal cell lines. Basement membrane-associated matrix proteins, laminin-111 and type IV collagen, suppress AXL and cKIT expression in pre-stasis and non-malignant cells. However, AXL and cKIT are not suppressed by laminin-111 in malignant cells. General linear models identified key factors, osteopontin, IL-8, and type VIα3 collagen, which significantly upregulated AXL and cKIT, as well as a plasticity-related gene expression program that is often observed in stem cells and in epithelial-to-mesenchymal-transition. These factors are co-located with AXL-expressing cells
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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 Socratic graph.