Trial reportCancer communications (London, England)2023
μ-opioid receptor agonist facilitates circulating tumor cell formation in bladder cancer via the MOR/AKT/Slug pathway: a comprehensive study including randomized controlled trial.
Trial report in Cancer communications (London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 25 citations in OpenAlex.
- μ-opioid receptor agonist facilitates circulating tumor cell formation in bladder cancer via the MOR/AKT/Slug pathway: a comprehensive study including randomized controlled trial.Cancer communications (London, England) · 2023Trial
- Cancer-related pain: A bidirectional modulator of cancer progression.Clinical and translational medicine · 2026Review
- Opioid signaling-related genes and their prognostic role in hepatocellular carcinoma: insights from bioinformatics and functional studies.Discover oncology · 2026Article
- EIF4A3/circPTGR1/miR-4725-5p positive- feedback loop promotes colorectal cancer progression via FAK/AKT signaling pathway.Molecular cancer · 2026Article
- Astrocytes and Microglia Regulate Opioid Receptor-Driven Cancer Brain Metastasis and Neural Injury: Remodeling the Brain Microenvironment.Journal of inflammation research · 2026Article
- Liquid biopsy in genitourinary cancers: Diagnostic and prognostic implications.World journal of clinical oncology · 2025Review
- Cancer and neurotransmitter receptors.Chinese medical journal · 2025Review
- Review
- Opioid System and Epithelial-Mesenchymal Transition.Pharmaceuticals (Basel, Switzerland) · 2025Review
- A revolutionary era in advancing precision immuno-oncology; role of circulating tumor cells.The journal of liquid biopsy · 2024Review
- Bio-energy-powered microfluidic devices.Biomicrofluidics · 2024Article
- Nucleus-targeted Silencer nanoplatform regulating ZEB1-AS1 in head and neck squamous cell carcinoma therapy.Discover nano · 2024Article
- Phenotypic Transitions the Processes Involved in Regulation of Growth and Proangiogenic Properties of Stem Cells, Cancer Stem Cells and Circulating Tumor Cells.Stem cell reviews and reports · 2024Review
- Review
- Impact of opioids and mu-opioid receptors on oncologic metastasis.American journal of cancer research · 2024Review
- The Bladder Tumor Microenvironment Components That Modulate the Tumor and Impact Therapy.International journal of molecular sciences · 2023Review
- Pan-Cancer Analysis and Validation of Opioid-Related Receptors Reveals the Immunotherapeutic Value of Toll-Like Receptor 4.International journal of general medicine · 2023Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundμ-opioid receptor agonists (MORAs) are indispensable for analgesia in bladder cancer (BC) patients, both during surgery and for chronic pain treatment. Whether MORAs affect BC progression and metastasis remains largely unknown. This study focused on the effects of MORAs on the formation of circulating tumor cells (CTCs) in BC and aimed to provide potential therapeutic targets, which would retain the pain-relieving effects of MORAs in BC patients without sacrificing their long-term prognosis.
methodsDifferent preclinical models were used to identify the effects of MORAs on the progression of BC. A novel immunocapture microfluidic chip was utilized to analyze whether MORAs affected the number of CTCs in mouse models and clinical BC patients. Bioinformatic analyses, total transcriptome sequencing, and molecular biology methods were then used to investigate the underlying mechanisms in these models and in BC cell lines.
resultsMouse models of hematogenous metastasis and in situ BC demonstrated that tumor metastasis was significantly increased after MORA treatment. A significant increase in the number of mesenchymal and/or epithelial CTCs was detected after MORA treatment in both the mouse models and clinical trial patients. Mechanistically, MORAs facilitated the formation of CTCs by activating the MOR/PI3K/AKT/Slug signaling pathway, hereby promoting the epithelial-mesenchymal transition (EMT) of BC cells, as knockdown of MOR, Slug or blockade of PI3K inhibited the EMT process and CTC formation.
conclusionMORAs promoted BC metastasis by facilitating CTC formation. The EMT-CTC axis could be targeted for preventive measures during MORA treatment to inhibit the associated tumor metastasis or recurrence in BC patients.
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.