ArticleeLife2021
KSR1- and ERK-dependent translational regulation of the epithelial-to-mesenchymal transition.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 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
13 citing papers in PubMed, 22 citations in OpenAlex.
- Epithelial interferon-stimulated gene programs modulate chemotherapy sensitivity in colorectal cancer via EPSTI1.Oncogene · 2026Article
- DUSP family phosphatases in cell signaling, inflammation, and chronic diseases.Journal of biomedical science · 2026Review
- KSR1 is a scaffold for the Hippo signaling pathway.Communications biology · 2025Article
- Diagnostic and prognostic biomarkers associated with histotype in advanced epithelial ovarian cancer.Scientific reports · 2025Article
- Integrated In Silico and Experimental Validation of Antrocin as a Plant-Derived Multi-Target Therapeutic for BRAF/MEK/PI3K-Driven Colorectal Cancer.International journal of molecular sciences · 2025Article
- KSR1 Mediates Small Cell Lung Carcinoma Tumor Initiation and Cisplatin Resistance.Molecular cancer research : MCR · 2025Article
- The feasible role of soluble E‑cadherin in spheroidogenesis of HCT116 colorectal cancer cells, a candidate biomarker for liquid biopsy.Oncology letters · 2025Article
- ERK1/2 mitogen-activated protein kinase dimerization is essential for the regulation of cell motility.Molecular oncology · 2025Article
- Exosomal circ-0100519 promotes breast cancer progression via inducing M2 macrophage polarisation by USP7/NRF2 axis.Clinical and translational medicine · 2024Article
- SOS1 and KSR1 modulate MEK inhibitor responsiveness to target resistant cell populations based on PI3K and KRAS mutation status.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Kinase Suppressor of RAS 1 (KSR1) Maintains the Transformed Phenotype of BRAFV600E Mutant Human Melanoma Cells.International journal of molecular sciences · 2023Article
- Review
- PPA1 Promotes Breast Cancer Proliferation and Metastasis Through PI3K/AKT/GSK3β Signaling Pathway.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
The epithelial-to-mesenchymal transition (EMT) is considered a transcriptional process that induces a switch in cells from a polarized state to a migratory phenotype. Here, we show that KSR1 and ERK promote EMT-like phenotype through the preferential translation of Epithelial-Stromal Interaction 1 (EPSTI1), which is required to induce the switch from E- to N-cadherin and coordinate migratory and invasive behavior. EPSTI1 is overexpressed in human colorectal cancer (CRC) cells. Disruption of KSR1 or EPSTI1 significantly impairs cell migration and invasion in vitro, and reverses EMT-like phenotype, in part, by decreasing the expression of N-cadherin and the transcriptional repressors of E-cadherin expression, ZEB1 and Slug. In CRC cells lacking KSR1, ectopic EPSTI1 expression restored the E- to N-cadherin switch, migration, invasion, and anchorage-independent growth. KSR1-dependent induction of EMT-like phenotype via selective translation of mRNAs reveals its underappreciated role in remodeling the translational landscape of CRC cells to promote their migratory and invasive behavior.
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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.