ArticleOncogene2019
TGFβ promotes breast cancer stem cell self-renewal through an ILEI/LIFR signaling axis.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Role of STAT3 signaling pathway in breast cancer.Cell communication and signaling : CCS · 2020Pooled it
- Fam3C alters Golgi apparatus morphology and function in triple negative breast cancer.Journal of molecular cell biology · 2026Article
- Breast cancer stem cells and circulating tumor cells: Dual drivers of progression and relapse.World journal of stem cells · 2025Review
- Stromal transcriptomics uncover LIF as a key effector in high tumor budding triple-negative breast cancer.Scientific reports · 2025Article
- Cellular and molecular characterisation of the peripheral immune environment in migraine.Pain reports · 2025Article
- Breast neoplasm epithelial-mesenchymal transition and cytokines: a systematic review.Cancer cell international · 2025Review
- In Vitro Effects ofAntioxidants (Basel, Switzerland) · 2025Article
- An update on cancer stem cell survival pathways involved in chemoresistance in triple-negative breast cancer.Future oncology (London, England) · 2025Review
- Comprehensive single-cell aging atlas of healthy mammary tissues reveals shared epigenomic and transcriptomic signatures of aging and cancer.Nature aging · 2025Article
- FAM3C Regulates Glioma Cell Proliferation, Invasion, Apoptosis, and Epithelial Mesenchymal Transition via the Notch Pathway.Cancer medicine · 2024Article
- TGFβ family signaling in human stem cell self-renewal and differentiation.Cell regeneration (London, England) · 2024Review
- NSDHL contributes to breast cancer stem-like cell maintenance and tumor-initiating capacity through TGF-β/Smad signaling pathway in MCF-7 tumor spheroid.BMC cancer · 2024Article
- PCBP1 regulates LIFR through FAM3C to maintain breast cancer stem cell self-renewal and invasiveness.Cancer biology & therapy · 2023Article
- Comprehensive single cell aging atlas of mammary tissues reveals shared epigenomic and transcriptomic signatures of aging and cancer.bioRxiv : the preprint server for biology · 2023Article
- FAM3 family genes are associated with prognostic value of human cancer: a pan-cancer analysis.Scientific reports · 2023Article
- FAM3C/ILEI protein is elevated in psoriatic lesions and triggers psoriasiform hyperproliferation in mice.EMBO molecular medicine · 2023Article
- Review
- Targeting Cancer Stem Cells as the Key Driver of Carcinogenesis and Therapeutic Resistance.International journal of molecular sciences · 2023Review
- FAM3C in circulating tumor-derived extracellular vesicles promotes non-small cell lung cancer growth in secondary sites.Theranostics · 2023Article
- Neutrophils promote tumor invasionInternational journal of biological sciences · 2023Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
FAM3C/Interleukin-like EMT Inducer (ILEI) is an oncogenic member of the FAM3 cytokine family and serves essential roles in both epithelial-mesenchymal transition (EMT) and breast cancer metastasis. ILEI expression levels are regulated through a non-canonical TGFβ signaling pathway by 3'-UTR-mediated translational silencing at the mRNA level by hnRNP E1. TGFβ stimulation or silencing of hnRNP E1 increases ILEI translation and induces an EMT program that correlates with enhanced invasion and migration. Recently, EMT has been linked to the formation of breast cancer stem cells (BCSCs) that confer both tumor cell heterogeneity as well as chemoresistant properties. Herein, we demonstrate that hnRNP E1 knockdown significantly shifts normal mammary epithelial cells to mesenchymal BCSCs in vitro and in vivo. We further validate that modulating ILEI protein levels results in the abrogation of these phenotypes, promoting further investigation into the unknown mechanism of ILEI signaling that drives tumor progression. We identify LIFR as the receptor for ILEI, which mediates signaling through STAT3 to drive both EMT and BCSC formation. Reduction of either ILEI or LIFR protein levels results in reduced tumor growth, fewer tumor initiating cells and reduced metastasis within the hnRNP E1 knock-down cell populations in vivo. These results reveal a novel ligand-receptor complex that drives the formation of BCSCs and represents a unique target for the development of metastatic breast cancer therapies.
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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.