ArticleThe Journal of clinical investigation2018
Proapoptotic PUMA targets stem-like breast cancer cells to suppress metastasis.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 46 citations in OpenAlex.
- Tumor-derived CTHRC1 mediates ITGB3-dependent osteoclast differentiation to promote prostate cancer bone metastasis.Oncogene · 2026Article
- Tumor-derived ITGB3 shapes a primed but functionally constrained NK cell state in breast cancer through HLA-E-NKG2A signaling.Molecular biology reports · 2026Article
- The multifaceted role of PUMA in cell death pathways: its therapeutic potential across cancer types.Cell communication and signaling : CCS · 2025Review
- Biomarkers, isolation methods, and therapeutic implications of breast cancer stem cells.Cancer pathogenesis and therapy · 2025Review
- S100A8/A9 innate immune signaling as a distinct mechanism driving progression of smoking-related breast cancers.Oncogene · 2025Article
- Antitumor Effect of Apcin on Endometrial Carcinoma via p21-Mediated Cell Cycle Arrest and Apoptosis.Current medical science · 2024Article
- STAT3-mediated up-regulation of DAB2 via SRC-YAP1 signaling axis promotes Helicobacter pylori-driven gastric tumorigenesis.Biomarker research · 2024Article
- Upregulation of fibronectin and its integrin receptors - an adaptation to isolation stress that facilitates tumor initiation.Journal of cell science · 2023Article
- Breast cancer stem cells tolerate chromosomal instability during tumor progression via c-Jun/AXL stress signaling.Heliyon · 2023Article
- Pancreatic cancer cells upregulate LPAR4 in response to isolation stress to promote an ECM-enriched niche and support tumour initiation.Nature cell biology · 2023Article
- The role of physics in multiomics and cancer evolution.Frontiers in oncology · 2023Review
- Protein Kinase D1 Signaling in Cancer Stem Cells with Epithelial-Mesenchymal Plasticity.Cells · 2022Article
- Stem-like breast cancer cells in the activated state resist genetic stress via TGFBI-ZEB1.NPJ breast cancer · 2022Article
- TGFBI secreted by tumor-associated macrophages promotes glioblastoma stem cell-driven tumor growth via integrin αvβ5-Src-Stat3 signaling.Theranostics · 2022Article
- The Effect of Educational Intervention on Knowledge, Attitude, and Practice of Women towards Breast Cancer Screening.International journal of breast cancer · 2022Article
- Fas/FasL mediates NF-κBp65/PUMA-modulated hepatocytes apoptosis via autophagy to drive liver fibrosis.Cell death & disease · 2021Article
- The roles of integrins in cancer.Faculty reviews · 2021Review
- A precision approach to breast cancer treatment based on cell lineage-specific vulnerabilities.Oncoscience · 2021Article
- Messing Up the Cancer Stem Cell Chemoresistance Mechanisms Supported by Tumor Microenvironment.Frontiers in oncology · 2021Review
- Combinatorial Strategies to Target Molecular and Signaling Pathways to Disarm Cancer Stem Cells.Frontiers in oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Breast cancer cells with stem cell properties are key contributors to metastatic disease, and there remains a need to better understand and target these cells in human cancers. Here, we identified rare stem-like cells in patients' tumors characterized by low levels of the proapoptotic molecule p53-upregulated modulator of apoptosis (PUMA) and showed that these cells play a critical role in tumor progression that is independent of clinical subtype. A signaling axis consisting of the integrin αvβ3, Src kinase, and the transcription factor Slug suppresses PUMA in these cells, promoting tumor stemness. We showed that genetic or pharmacological disruption of αvβ3/Src signaling drives PUMA expression, specifically depleting these stem-like tumor cells; increases their sensitivity to apoptosis; and reduces pulmonary metastasis, with no effect on primary tumor growth. Taken together, these findings point to PUMA as a key vulnerability of stem-like cells and suggest that pharmacological upregulation of PUMA via Src inhibition may represent a strategy to selectively target these cells in a wide spectrum of aggressive breast cancers.
Indexed as
Identifiers
What OpenQuestion holds
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.