ArticleNeoplasia (New York, N.Y.)2011
Identification of H-Ras-specific motif for the activation of invasive signaling program in human breast epithelial cells.
Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 37 citations in OpenAlex.
- CLDN6 inhibits breast cancer growth and metastasis through SREBP1-mediated RAS palmitoylation.Cellular & molecular biology letters · 2024Article
- Xiaozheng pill exerts an anti-mammary hyperplasia effect through Raf/ERK/ELK and HIF-1α/bFGF pathways.Journal of traditional and complementary medicine · 2023Article
- Pathway-Based Personalized Analysis of Pan-Cancer Transcriptomic Data.Biomedicines · 2021Article
- Ras Signaling in Breast Cancer.Advances in experimental medicine and biology · 2021Article
- Interaction between Peptidyl-prolylJournal of cancer prevention · 2020Article
- Individualized genetic network analysis reveals new therapeutic vulnerabilities in 6,700 cancer genomes.PLoS computational biology · 2020Article
- Article
- Cancer gene panel analysis of cultured circulating tumor cells and primary tumor tissue from patients with breast cancer.Oncology letters · 2017Article
- Integrated analysis of differentially expressed genes and pathways in triple‑negative breast cancer.Molecular medicine reports · 2017Article
- IODNE: An integrated optimization method for identifying the deregulated subnetwork for precision medicine in cancer.CPT: pharmacometrics & systems pharmacology · 2017Review
- Effect of low doses of estradiol and tamoxifen on breast cancer cell karyotypes.Endocrine-related cancer · 2016Article
- High-Affinity Interaction of the K-Ras4B Hypervariable Region with the Ras Active Site.Biophysical journal · 2015Article
- Discoidin domain receptor 1 is a novel transcriptional target of ZEB1 in breast epithelial cells undergoing H-Ras-induced epithelial to mesenchymal transition.International journal of cancer · 2015Article
- A novel model to combine clinical and pathway-based transcriptomic information for the prognosis prediction of breast cancer.PLoS computational biology · 2014Article
- Inflammatory lipid sphingosine-1-phosphate upregulates C-reactive protein via C/EBPβ and potentiates breast cancer progression.Oncogene · 2014Article
- Cancer subclonal genetic architecture as a key to personalized medicine.Neoplasia (New York, N.Y.) · 2013Article
- Role of p38 MAP Kinase Signal Transduction in Solid Tumors.Genes & cancer · 2013Review
- Activated Ras as a Therapeutic Target: Constraints on Directly Targeting Ras Isoforms and Wild-Type versus Mutated Proteins.ISRN oncology · 2013Review
- Overcoming intratumor heterogeneity of polygenic cancer drug resistance with improved biomarker integration.Neoplasia (New York, N.Y.) · 2012Article
- The interconnectedness of cancer cell signaling.Neoplasia (New York, N.Y.) · 2011Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased expression and/or activation of H-Ras are often associated with tumor aggressiveness in breast cancer. Previously, we showed that H-Ras, but not N-Ras, induces MCF10A human breast epithelial cell invasion and migration, whereas both H-Ras and N-Ras induce cell proliferation and phenotypic transformation. In an attempt to determine the sequence requirement directing the divergent phenotype induced by H-Ras and N-Ras with a focus on the induction of human breast cell invasion, we investigated the structural and functional relationships between H-Ras and N-Ras using domain-swap and site-directed mutagenesis approaches. Here, we report that the hypervariable region (HVR), consisting of amino acids 166 to 189 in H-Ras, determines the invasive/migratory signaling program as shown by the exchange of invasive phenotype by swapping HVR sequences between H-Ras and N-Ras. We also demonstrate that the H-Ras-specific additional palmitoylation site at Cys184 is not responsible for the signaling events that distinguish between H-Ras and N-Ras. Importantly, this work identifies the C-terminal HVR, especially the flexible linker domain with two consecutive proline residues Pro173 and Pro174, as a critical domain that contributes to activation of H-Ras and its invasive potential in human breast epithelial cells. The present study sheds light on the structural basis for the Ras isoform-specific invasive program of breast epithelial cells, providing information for the development of agents that specifically target invasion-related H-Ras pathways in human cancer.
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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.