ArticleCell reports2015
Wild-Type N-Ras, Overexpressed in Basal-like Breast Cancer, Promotes Tumor Formation by Inducing IL-8 Secretion via JAK2 Activation.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Relationship of possible biomarkers with malignancy of thymic tumors: a meta-analysis.BMC cancer · 2020Pooled it
- Elevated FBXL6 activates both wild-type KRAS and mutant KRASMilitary Medical Research · 2023Trial
- NF1 loss in estrogen receptor-positive breast cancer induces osteoclast formation and immunosuppression to promote bone metastasis.Cancer letters · 2026Article
- Secretory carrier membrane protein 3 modulates nuclear ERK1/2 signaling and drug response in triple-negative breast cancer.Frontiers in oncology · 2026Article
- Decoding BRCA1 promoter hypermethylation: a new frontier in understanding sporadic breast cancer.Cancer gene therapy · 2025Article
- The Hippo-YAP signaling pathway promotes hepatocellular carcinoma progression by inducing FHL3 expression.Cell death & disease · 2025Article
- Review
- Regulation of nucleotide excision repair by wild-type HRAS signaling in head and neck cancer.Cancer gene therapy · 2025Article
- The RAL Small G Proteins Are Clinically Relevant Targets in Triple Negative Breast Cancer.Cancers · 2024Article
- Influenza A virus infection activates STAT3 to enhance SREBP2 expression, cholesterol biosynthesis, and virus replication.iScience · 2024Article
- Unmutated RRAS2 emerges as a key oncogene in post-partum-associated triple negative breast cancer.Molecular cancer · 2024Article
- Role of EGFR and FASN in breast cancer progression.Journal of cell communication and signaling · 2023Review
- RAS‑stimulated release of exosomalInternational journal of molecular medicine · 2023Article
- Proteogenomic Approaches for the Identification of NF1/Neurofibromin-depleted Estrogen Receptor-positive Breast Cancers for Targeted Treatment.Cancer research communications · 2023Article
- Efficient cancer modeling through CRISPR-Cas9/HDR-based somatic precision gene editing in mice.Science advances · 2023Article
- Epitranscriptic regulation ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Elevated NRAS expression during DCIS is a potential driver for progression to basal-like properties and local invasiveness.Breast cancer research : BCR · 2022Article
- Polyphenol-Enriched Blueberry Preparation Controls Breast Cancer Stem Cells by Targeting FOXO1 and miR-145.Molecules (Basel, Switzerland) · 2021Article
- CircPVT1 attenuates negative regulation of NRAS by let-7 and drives cancer cells towards oncogenicity.Scientific reports · 2021Article
- Triple Negative Breast Cancer: A Review of Present and Future Diagnostic Modalities.Medicina (Kaunas, Lithuania) · 2021Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Basal-like breast cancers (BLBCs) are aggressive, and their drivers are unclear. We have found that wild-type N-RAS is overexpressed in BLBCs but not in other breast cancer subtypes. Repressing N-RAS inhibits transformation and tumor growth, whereas overexpression enhances these processes even in preinvasive BLBC cells. We identified N-Ras-responsive genes, most of which encode chemokines; e.g., IL8. Expression levels of these chemokines and N-RAS in tumors correlate with outcome. N-Ras, but not K-Ras, induces IL-8 by binding and activating the cytoplasmic pool of JAK2; IL-8 then acts on both the cancer cells and stromal fibroblasts. Thus, BLBC progression is promoted by increasing activities of wild-type N-Ras, which mediates autocrine/paracrine signaling that can influence both cancer and stroma 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 OpenQuestion graph.