ArticleCell death & disease2019
The paracrine induction of prostate cancer progression by caveolin-1.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Endocrine and paracrine characteristics of neuroendocrine prostate cancer.Frontiers in endocrinology · 2022Pooled it
- Trial
- Elevated Expression of Caveolin-1 Reflects a Poor Prognosis in Patients With Primary Central Nervous System Lymphomas.Neuropathology : official journal of the Japanese Society of Neuropathology · 2026Article
- Caveolae in cancer: mechanochemical signaling in tumor progression, immunity, and therapy.Cell communication and signaling : CCS · 2026Review
- LRRC8D Suppresses Prostate Cancer Growth and Enhances Platinum Sensitivity via Modulation of CAV-1/STAT3 Signaling.Membranes · 2026Article
- Targeting caveolin-1: dual challenges in tumor immunity and drug therapy strategies.Cancer cell international · 2026Review
- The dual roles of exosomes in prostate cancer: mechanisms in tumorigenesis and avenues for clinical translation.Frontiers in immunology · 2026Review
- Extracellular vesicles as mediators of prostatic diseases: connecting function to diagnostic and therapeutic applications.Extracellular vesicles and circulating nucleic acids · 2026Review
- Orchestrating movement: the role of Caveolin-1 in migration and metastasis.Molecular cancer · 2025Review
- Caveolin-1: an ambiguous entity in breast cancer.Molecular cancer · 2025Review
- Small extracellular vesicles: crucial mediators for prostate cancer.Journal of nanobiotechnology · 2025Review
- Role of exosomes in castration-resistant prostate cancer.Frontiers in oncology · 2025Review
- Extracellular vesicles in anti-tumor drug resistance: Mechanisms and therapeutic prospects.Journal of pharmaceutical analysis · 2024Review
- CAV1 Protein Encapsulated in Mouse BMSC-Derived Extracellular Vesicles Alleviates Myocardial Fibrosis Following Myocardial Infarction by Blocking the TGF-β1/SMAD2/c-JUN Axis.Journal of cardiovascular translational research · 2024Article
- Article
- Decoding the secrets of small extracellular vesicle communications: exploring the inhibition of vesicle-associated pathways and interception strategies for cancer treatment.American journal of cancer research · 2024Review
- Prostate cancer-derived small extracellular vesicle proteins: the hope in diagnosis, prognosis, and therapeutics.Journal of nanobiotechnology · 2023Review
- Estrogen-related genes for thyroid cancer prognosis, immune infiltration, staging, and drug sensitivity.BMC cancer · 2023Article
- Targeting Key Players of Neuroendocrine Differentiation in Prostate Cancer.International journal of molecular sciences · 2023Review
- Tissue-specific cancer stem/progenitor cells: Therapeutic implications.World journal of stem cells · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 6 institutions in 3 countries.
Funding
Abstract
A subpopulation of cancer stem cells (CSCs) plays a critical role of cancer progression, recurrence, and therapeutic resistance. Many studies have indicated that castration-resistant prostate cancer (CRPC) is associated with stem cell phenotypes, which could further promote neuroendocrine transdifferentiation. Although only a small subset of genetically pre-programmed cells in each organ has stem cell capability, CSCs appear to be inducible among a heterogeneous cancer cell population. However, the inductive mechanism(s) leading to the emergence of these CSCs are not fully understood in CRPC. Tumor cells actively produce, release, and utilize exosomes to promote cancer development and metastasis, cancer immune evasion as well as chemotherapeutic resistance; the impact of tumor-derived exosomes (TDE) and its cargo on prostate cancer (PCa) development is still unclear. In this study, we demonstrate that the presence of Cav-1 in TDE acts as a potent driver to induce CSC phenotypes and epithelial-mesenchymal transition in PCa undergoing neuroendocrine differentiation through NFκB signaling pathway. Furthermore, Cav-1 in mCRPC-derived exosomes is capable of inducing radio- and chemo-resistance in recipient cells. Collectively, these data support Cav-1 as a critical driver for mCRPC progression.
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.