ArticleOncotarget2017
The WAVE3-YB1 interaction regulates cancer stem cells activity in breast cancer.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 36 citations in OpenAlex.
- Review
- The subcellular distribution of phosphorylated Y-box-binding protein-1 at S102 in colorectal cancer patients, stratified by KRAS mutational status and clinicopathological features.Molecular oncology · 2025Article
- Role of WAVE3 as an actin binding protein in the pathology of triple negative breast cancer.Cytoskeleton (Hoboken, N.J.) · 2025Review
- Kindlin-2 regulates the oncogenic activities of integrins and TGF-β in triple-negative breast cancer progression and metastasis.Oncogene · 2024Article
- WAVE3 Facilitates the Tumorigenesis and Metastasis of Tongue Squamous Cell Carcinoma via EMT.Applied biochemistry and biotechnology · 2024Article
- YB-1 regulates mesothelioma cell migration via snail but not EGFR, MMP1, EPHA5 or PARK2.Molecular oncology · 2024Article
- Y-Box Binding Protein 1: Unraveling the Multifaceted Role in Cancer Development and Therapeutic Potential.International journal of molecular sciences · 2024Review
- The WAVE3/β-catenin oncogenic signaling regulates chemoresistance in triple negative breast cancer.Breast cancer research : BCR · 2023Article
- YB-1 as an Oncoprotein: Functions, Regulation, Post-Translational Modifications, and Targeted Therapy.Cells · 2022Review
- Article
- A comprehensive review of the functions of YB-1 in cancer stemness, metastasis and drug resistance.Cellular signalling · 2021Review
- Phosphorylation of the proline-rich domain of WAVE3 drives its oncogenic activity in breast cancer.Scientific reports · 2021Article
- Targeting WASF3 Signaling in Metastatic Cancer.International journal of molecular sciences · 2021Review
- WAVE3 phosphorylation regulates the interplay between PI3K, TGF-β, and EGF signaling pathways in breast cancer.Oncogenesis · 2020Article
- PTEN suppresses epithelial-mesenchymal transition and cancer stem cell activity by downregulating Abi1.Scientific reports · 2020Article
- Perspectives on molecular signaling in cancer and update on therapeutic options for the treatment of metastatic cancer.Annals of translational medicine · 2020Article
- Elucidating the molecular signaling pathways of WAVE3.Annals of translational medicine · 2020Review
- MicroRNA-93 targets WASF3 and functions as a metastasis suppressor in breast cancer.Cancer science · 2020Article
- CRISPR/Cas9 for overcoming drug resistance in solid tumors.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2020Review
- Inhibition of breast cancer growth via miR-7 suppressing ALDH1A3 activity concomitant with decreasing breast cancer stem cell subpopulation.Journal of cellular physiology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Resistance to therapy is the main cause of tumor recurrence and metastasis and cancer stem cells (CSCs) play a crucial role in this process, especially in triple-negative breast cancers (TNBCs). Unfortunately, no FDA-approved treatment is currently available for this subtype of BC, which explains the high rate of mortality in patients with TNBC tumors. WAVE3, a member of the WASP/WAVE actin-cytoskeleton remodeling family of protein, has been established as a major driver of tumor progression and metastasis of several solid tumors, including those originating in the breast. Our recently published studies found WAVE3 to mediate the process of chemoresistance in TNBCs. The molecular mechanisms whereby WAVE3 regulates chemoresistance in TNBC tumors remains largely unknown, as does the role of WAVE3 in CSC maintenance. Here we show that WAVE3 promotes CSC self-renewal and regulates transcription of CSC-specific genes, which, in part, provides a mechanistic explanation for the function of WAVE3 in chemoresistance in TNBCs. Our data show that WAVE3 is enriched in the CSC-subpopulation of TNBC cell lines. Knockout of WAVE3 via CRISPR/Cas9 significantly attenuates the CSC-subpopulation and inhibits transcription of CSC transcription factors. Mechanistically, we established a link between WAVE3 and the Y-box-binding protein-1 (YB1), a transcription factor and CSC-maintenance gene. Indeed, the interaction of WAVE3 with YB1 is required for YB1 translocation to the nucleus of cancer cells, and activation of transcription of CSC-specific genes. Our findings identify a new WAVE3/YB1 signaling axis that regulates the CSC-mediated resistance to therapy and opens a new therapeutic window for TNBCs treatment.
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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.