ArticleCell death & disease2017
Human cancer-associated fibroblasts enhance glutathione levels and antagonize drug-induced prostate cancer cell death.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
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Who cites it
70 citing papers in PubMed, 111 citations in OpenAlex.
- Physiological Significance and Functions of AA.Reviews of physiology, biochemistry and pharmacology · 2027Review
- Screening anticancer peptides performance in organotypic prostate tumor-stroma 3D models.International journal of cancer · 2026Article
- Dual-action mitochondria-targeted prodrugs that both deplete mitochondrial glutathione and deliver a toxic payload to the matrix.European journal of medicinal chemistry · 2026Article
- Decoding the Integrated Stress Response of Pancreatic Cancer: Identifying a Serine-dependent Tumor Subset Under Metabolic Relationships With CAFs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Modeling CAF-tumor interactions to overcome therapy resistance.Journal of experimental & clinical cancer research : CR · 2026Review
- Cancer-associated fibroblasts: central players in cancer hallmarks and therapeutic resistance.Cell communication and signaling : CCS · 2025Review
- Modelling of immune infiltration in prostate cancer treated with HDR-brachytherapy using Raman spectroscopy and machine learning.Scientific reports · 2025Article
- Cancer‑associated fibroblasts in human malignancies, with a particular emphasis on sarcomas (Review).International journal of oncology · 2025Review
- Advancing prostate cancer research: an exploration of periprostatic adipose stem cells.Journal of translational medicine · 2025Review
- Immune Checkpoint Inhibitor Therapy for Prostate Cancer: Present and Future Prospectives.Biomolecules · 2025Review
- Identification of Cancer Associated Fibroblasts Related Genes Signature to Facilitate Improved Prediction of Prognosis and Responses to Therapy in Patients with Pancreatic Cancer.International journal of molecular sciences · 2025Article
- Article
- Metabolic Atlas of Human Eyelid Infiltrative Basal Cell Carcinoma.Investigative ophthalmology & visual science · 2025Article
- Advances in the study of reversing tumor drug resistance by targeting cancer-associated fibroblasts with nanomaterials.Frontiers in immunology · 2025Review
- Cancer associated fibroblasts in tumors: focusing on solid tumors and hematological malignancies.Frontiers in oncology · 2025Review
- Tumor-stroma type and tumor-stroma ratio predict neoadjuvant chemotherapy response in breast cancer.Revista da Associacao Medica Brasileira (1992) · 2025Article
- Tumor Metabolic Reprogramming and Ferroptosis: The Impact of Glucose, Protein, and Lipid Metabolism.International journal of molecular sciences · 2024Review
- Article
- Glutamine Metabolism and Prostate Cancer.Cancers · 2024Review
- Cancer-associated fibroblasts reprogram cysteine metabolism to increase tumor resistance to ferroptosis in pancreatic cancer.Theranostics · 2024Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance is a major problem in cancer therapy. A growing body of evidence demonstrates that the tumor microenvironment, including cancer-associated fibroblasts (CAFs), can modulate drug sensitivity in tumor cells. We examined the effect of primary human CAFs on p53 induction and cell viability in prostate cancer cells on treatment with chemotherapeutic drugs. Co-culture with prostate CAFs or CAF-conditioned medium attenuated DNA damage and the p53 response to chemotherapeutic drugs and enhanced prostate cancer cell survival. CAF-conditioned medium inhibited the accumulation of doxorubicin, but not taxol, in prostate cancer cells in a manner that was associated with increased cancer cell glutathione levels. A low molecular weight fraction (<3 kDa) of CAF-conditioned medium had the same effect. CAF-conditioned medium also inhibited induction of reactive oxygen species (ROS) in both doxorubicin- and taxol-treated cancer cells. Our findings suggest that CAFs can enhance drug resistance in cancer cells by inhibiting drug accumulation and counteracting drug-induced oxidative stress. This protective mechanism may represent a novel therapeutic target 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.