ArticleNPJ precision oncology2021
PARP inhibitors promote stromal fibroblast activation by enhancing CCL5 autocrine signaling in ovarian cancer.
Article in NPJ precision oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Overlapping gene dependencies for PARP inhibitors and carboplatin response identified by functional CRISPR-Cas9 screening in ovarian cancer.Cell death & disease · 2022Pooled it
- The dual immune landscape of homologous recombination-deficient tumors: mechanisms and therapeutic implications.Cancer metastasis reviews · 2026Review
- Selected Chemokines as Prognostic Biomarkers and Therapeutic Targets in Ovarian Cancer.Current issues in molecular biology · 2026Review
- Mitochondrial superoxide sustains a senescence-like phenotype in PARP- inhibited ovarian cancer cells by stabilizing HIF1α.Redox biology · 2026Article
- Tumor cell-derived IFN spatially reprograms osteopontin-enriched macrophage niches to promote PARP inhibitor resistance.The Journal of clinical investigation · 2026Article
- Immune-Centered Cross-Talk Between Cancer Cells and the Tumor Microenvironment-Implications for Therapy.Cancers · 2026Review
- FGF7-FGFR2 Signaling Enhances Contractile Activation of CAFs in Ovarian Cancer: Integrative Single-Cell and Spatial Transcriptomics.Journal of inflammation research · 2026Article
- PARP inhibitors accumulate B7-H3 on fibroblasts via blocking autophagic flux to potentiate immune evasion in ovarian cancer.Oncoimmunology · 2025Article
- Systematic profiling of cancer-fibroblast interactions reveals drug combinations in ovarian cancer.Molecular oncology · 2025Article
- The distinct landscape of tumor immune microenvironment in homologous recombination deficient cancers.Biomarker research · 2025Review
- The immunological landscape and silico analysis of key paraptosis regulator LPAR1 in gastric cancer patients.Translational oncology · 2024Article
- Leveraging PARP-1/2 to Target Distant Metastasis.International journal of molecular sciences · 2024Review
- High expression of SLC7A1 in high-grade serous ovarian cancer promotes tumor progression and is involved in MAPK/ERK pathway and EMT.Cancer medicine · 2024Article
- Article
- Prognostic risk factors of serous ovarian carcinoma based on mesenchymal stem cell phenotype and guidance for therapeutic efficacy.Journal of translational medicine · 2023Article
- Roles of the PARP Inhibitor inCancers · 2023Review
- Review
- Review
- Deciphering the immune landscape dominated by cancer-associated fibroblasts to investigate their potential in indicating prognosis and guiding therapeutic regimens in high grade serous ovarian carcinoma.Frontiers in immunology · 2022Article
- Secretome Analysis of Rabbit and Human Mesenchymal Stem and Endothelial Progenitor Cells: A Comparative Study.International journal of molecular sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer-associated fibroblasts (CAFs) play significant roles in drug resistance through different ways. Antitumor therapies, including molecular targeted interventions, not only effect tumor cells but also modulate the phenotype and characteristics of CAFs, which can in turn blunt the therapeutic response. Little is known about how stromal fibroblasts respond to poly (ADP-ribose) polymerase inhibitors (PARPis) in ovarian cancer (OC) and subsequent effects on tumor cells. This is a study to evaluate how CAFs react to PARPis and their potential influence on PARPi resistance in OC. We discovered that OC stromal fibroblasts exhibited intrinsic resistance to PARPis and were further activated after the administration of PARPis. PARPi-challenged fibroblasts displayed a specific secretory profile characterized by increased secretion of CCL5, MIP-3α, MCP3, CCL11, and ENA-78. Mechanistically, increased secretion of CCL5 through activation of the NF-κB signaling pathway was required for PARPi-induced stromal fibroblast activation in an autocrine manner. Moreover, neutralizing CCL5 partly reversed PARPi-induced fibroblast activation and boosted the tumor inhibitory effect of PARPis in both BRCA1/2-mutant and BRCA1/2-wild type xenograft models. Our study revealed that PARPis could maintain and improve stromal fibroblast activation involving CCL5 autocrine upregulation. Targeting CCL5 might offer a new treatment modality in overcoming the reality of PARPi resistance in OC.
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.