ArticleCell death discovery2021
ETV4 promotes breast cancer cell stemness by activating glycolysis and CXCR4-mediated sonic Hedgehog signaling.
Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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
45 citing papers in PubMed, 64 citations in OpenAlex.
- IGF2BP3 promotes gastric cancer progression by inhibiting ferroptosis through ETV4-mediated regulation of GCH1.Cancer biology & therapy · 2026Article
- Cancer stem cell plasticity: mechanisms, immune microenvironment crosstalk, and therapeutic implications.Journal of hematology & oncology · 2026Review
- Review
- ETV4 as a potential target gene for alleviating proliferation metastasis of HCC.BMC gastroenterology · 2026Article
- ETV4 promotes colorectal cancer progression through SLC7A11-mediated ferroptosis inhibition.Biology direct · 2026Article
- Aumolertinib combined with targetingJournal of thoracic disease · 2026Article
- Gene regulatory network transitions reveal the central transcription factors in lung adenocarcinoma progression.NPJ systems biology and applications · 2026Article
- Emerging role of ETV4 in colorectal cancer: from molecular mechanisms to clinical implications.Frontiers in oncology · 2026Review
- Deubiquitination of ETV4 by USP7 Promotes NSCLC Tumorigenesis via MAPK7 Activation.Human mutation · 2026Article
- PRAS40 promotes colorectal cancer stemness by enhancing glycolysis through triggering PGK1 acetylation.Oncogenesis · 2025Article
- Single-cell RNA sequencing identifies ZBP1-dependent mechanisms in OSCC progression.Cell death & disease · 2025Article
- Review
- E2F7 transcriptionally upregulates SPC24 to mediate aerobic Glycolysis and facilitate stemness of breast cancer.Journal of bioenergetics and biomembranes · 2025Article
- E2F2/MUC1 Enhances Cell Stemness of Hepatocellular Carcinoma by Regulating the Notch Signaling Pathway.Digestive diseases and sciences · 2025Article
- ETV4/ALYREF-mediated glycolytic metabolism through PKM2 enhances resistance to ferroptosis and promotes the development of intrahepatic cholangiocarcinoma.Cancer & metabolism · 2025Article
- Cancer metastasis: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2025Review
- PEA3 Transcription Factors, Role in Invasion, Proliferation and Radioresistance of Glioblastoma Stem Cells.Journal of cellular and molecular medicine · 2025Article
- Oxidative Stress and Redox Imbalance: Common Mechanisms in Cancer Stem Cells and Neurodegenerative Diseases.Cells · 2025Review
- Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025Review
- FOSL1 transcriptionally dictates the Warburg effect and enhances chemoresistance in triple-negative breast cancer.Journal of translational medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem cells (CSCs) are a major cause of tumor treatment resistance, relapse and metastasis. Cancer cells exhibit reprogrammed metabolism characterized by aerobic glycolysis, which is also critical for sustaining cancer stemness. However, regulation of cancer cell metabolism rewiring and stemness is not completely understood. Here, we report that ETV4 is a key transcription factor in regulating glycolytic gene expression. ETV4 loss significantly inhibits the expression of HK2, LDHA as well as other glycolytic enzymes, reduces glucose uptake and lactate release in breast cancer cells. In human breast cancer and hepatocellular carcinoma tissues, ETV4 expression is positively correlated with glycolytic signaling. Moreover, we confirm that breast CSCs (BCSCs) are glycolysis-dependent and show that ETV4 is required for BCSC maintenance. ETV4 is enriched in BCSCs, its knockdown and overexpression suppresses and promotes breast cancer cell stem-like traits, respectively. Mechanistically, on the one hand, we find that ETV4 may enhance glycolysis activity to facilitate breast cancer stemness; on the other, ETV4 activates Sonic Hedgehog signaling by transcriptionally promoting CXCR4 expression. A xenograft assay validates the tumor growth-impeding effect and inhibition of CXCR4/SHH/GLI1 signaling cascade after ETV4 depletion. Together, our study highlights the potential roles of ETV4 in promoting cancer cell glycolytic shift and BCSC maintenance and reveals the molecular basis.
Identifiers
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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.