ArticleAmerican journal of cancer research2015
YES oncogenic activity is specified by its SH4 domain and regulates RAS/MAPK signaling in colon carcinoma cells.
Article in American journal of cancer research, 2015. 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.
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.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- Comprehensive analysis of a palmitoylation-related prognostic signature in colorectal cancer: Implications for immune therapy and personalized treatment.Oncology letters · 2025Article
- Palmitoylation in cancer: decoding its roles in signal transduction, tumor immunity, and emerging therapeutic opportunities.Frontiers in immunology · 2025Review
- Exploring the role of YES1 kinase in regulating cisplatin resistance through iTRAQ-based quantitative proteomic analysis in urothelial carcinoma.American journal of cancer research · 2025Article
- Protein lipidation in cancer: mechanisms, dysregulation and emerging drug targets.Nature reviews. Cancer · 2024Review
- A renaissance for YES in cancer.Oncogene · 2023Review
- YES1 Kinase Mediates the Membrane Removal of Rescued F508del-CFTR in Airway Cells by Promoting MAPK Pathway Activation via SHC1.Biomolecules · 2023Article
- Protein palmitoylation in cancer: molecular functions and therapeutic potential.Molecular oncology · 2023Review
- Novel inhibitor of hematopoietic cell kinase as a potential therapeutic agent for acute myeloid leukemia.Cancer immunology, immunotherapy : CII · 2022Article
- The Activity of Novel BCR-ABL Small-Molecule Degraders Containing Pyrimidine Rings and Their Role in Overcoming Drug Resistance.Journal of oncology · 2022Article
- Hematopoietic Cell Kinase (HCK) Is a Player of the Crosstalk Between Hematopoietic Cells and Bone Marrow Niche Through CXCL12/CXCR4 Axis.Frontiers in cell and developmental biology · 2021Article
- Recent Advances of Functional Proteomics in Gastrointestinal Cancers- a Path towards the Identification of Candidate Diagnostic, Prognostic, and Therapeutic Molecular Biomarkers.International journal of molecular sciences · 2020Review
- Src Family Tyrosine Kinases in Intestinal Homeostasis, Regeneration and Tumorigenesis.Cancers · 2020Review
- Nuclear Functions of the Tyrosine Kinase Src.International journal of molecular sciences · 2020Review
- Review
- Role of Membrane Cholesterol Levels in Activation of Lyn upon Cell Detachment.International journal of molecular sciences · 2018Review
- Article
- The Yin and Yang of Tyrosine Kinase Inhibition During Experimental Polymicrobial Sepsis.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the SRC family of tyrosine kinases (SFK) display important functions in human cancer, but their specific role in tumorigenesis remains unclear. We previously demonstrated that YES regulates a unique oncogenic signaling important for colorectal cancer (CRC) progression that is not shared with SRC. Here, we addressed the underlying mechanism involved in this process. We show that YES oncogenic signaling relies on palmitoylation of its SH4 domain that controls YES localization in cholesterol-enriched membrane micro-domains. Specifically, deletion of the palmitoylation site compromised YES transforming activity, while addition of a palmitoylation site in the SH4 domain of SRC was sufficient for SRC to restore the transforming properties of cells in which YES had been silenced. Subsequently, SILAC phosphoproteomic analysis revealed that micro-domain-associated cell adhesive components and receptor tyrosine kinases are major YES substrates. YES also phosphorylates upstream regulators of RAS/MAPK signaling, including EGFR, SHC and SHP2, which were not targeted by SRC due to the absence of palmitoylation. Accordingly, EGFR-induced MAPK activity was attenuated by YES down-regulation, while increased RAS activity significantly restored cell transformation that was lost upon YES silencing. Collectively, these results uncover a critical role for the SH4 domain in the specification of SFK oncogenic activity and a selective role for YES in the induction of RAS/MAPK signaling in CRC cells.
Indexed as
Identifiers
26269757PMC4529617W2402867314What 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.