ArticleOncotarget2014
FOXF1 mediates mesenchymal stem cell fusion-induced reprogramming of lung cancer cells.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 94 citations in OpenAlex.
- How Do Cancer Cells Fuse and Why?Advances in experimental medicine and biology · 2026Review
- Mitochondrion-targeted therapies for diabetic wound healing: from mechanism to therapeutic opportunity.Burns & trauma · 2026Review
- Genomic Reshuffling After Cell Fusion: Catalyst for Cancer Evolution and Progression.Advances in experimental medicine and biology · 2026Review
- Changes in epistatic green-beard alleles induce domain shift in hypostatic rock-paper-scissors-like green-beard competition.NPJ systems biology and applications · 2025Article
- Fusion of tumor cells and mesenchymal stem/stroma cells: a source of tumor heterogeneity, evolution and recurrence.Medical oncology (Northwood, London, England) · 2025Review
- The molecular features of lung cancer stem cells in dedifferentiation process-driven epigenetic alterations.The Journal of biological chemistry · 2024Review
- FOXF1 inhibits invasion and metastasis of lung adenocarcinoma cells and enhances anti-tumor immunity via MFAP4/FAK signal axis.Scientific reports · 2024Article
- Gastric cancer and mesenchymal stem cell-derived exosomes: from pro-tumorigenic effects to anti-cancer vehicles.Archives of pharmacal research · 2024Review
- Cell Fusion and Syncytia Formation in Cancer.Results and problems in cell differentiation · 2024Review
- Unraveling the Molecular Puzzle: Exploring Gene Networks across Diverse EMT Status of Cell Lines.International journal of molecular sciences · 2023Review
- Role of Fork-Head Box Genes in Breast Cancer: From Drug Resistance to Therapeutic Targets.Biomedicines · 2023Review
- The impact and outcomes of cancer-macrophage fusion.BMC cancer · 2023Article
- Fibroblasts as Turned Agents in Cancer Progression.Cancers · 2023Review
- Lung Cancer Gene Regulatory Network of Transcription Factors Related to the Hallmarks of Cancer.Current issues in molecular biology · 2023Article
- Extracellular Events Involved in Cancer Cell-Cell Fusion.International journal of molecular sciences · 2022Review
- Identifying General Tumor and Specific Lung Cancer Biomarkers by Transcriptomic Analysis.Biology · 2022Article
- An integrated analysis of the competing endogenous RNA network associated of prognosis of stage I lung adenocarcinoma.BMC cancer · 2022Article
- Tumor Hybrid Cells: Nature and Biological Significance.Frontiers in cell and developmental biology · 2022Review
- Cell fusion in cancer hallmarks: Current research status and future indications.Oncology letters · 2021Review
- Spontaneous Fusion of MSC with Breast Cancer Cells Can Generate Tumor Dormancy.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
11 authors at 7 institutions in 2 countries.
Funding
Abstract
Several reports suggest that malignant cells generate phenotypic diversity through fusion with various types of stromal cells within the tumor microenvironment. Mesenchymal stem cell (MSC) is one of the critical components in the tumor microenvironment and a promising fusogenic candidate, but the underlying functions of MSC fusion with malignant cell have not been fully examined. Here, we demonstrate that MSCs fuse spontaneously with lung cancer cells, and the latter is reprogrammed to slow growth and stem-like state. Transcriptome profiles reveal that lung cancer cells are reprogrammed to a more benign state upon MSC fusion. We further identified FOXF1 as a reprogramming mediator that contributes not only to the reprogramming toward stemness but also to the p21-regulated growth suppression in fusion progeny. Collectively, MSC fusion does not enhance the intrinsic malignancy of lung cancer cells. The anti-malignant effects of MSC fusion-induced reprogramming on lung cancer cells were accomplished by complementation of tumorigenic defects, including restoration of p21 function and normal terminal differentiation pathways as well as up-regulation of FOXF1, a putative tumor suppressor. Such fusion process raises the therapeutic potential that MSC fusion can be utilized to reverse cellular phenotypes in cancer.
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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.