ArticleMolecular biology reports2025
Immune modulation by melanoma-derived exosomes: suppression of BALB/c mice splenic cell proliferation, induction of apoptosis, and cell cycle arrest.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMelanoma is an immunogenic malignancy with a high metastatic potential, capable of escaping immune surveillance. Among the mechanisms involved, tumor-derived exosomes have been recognized as potent immune modulators, contributing to immune evasion and tumor progression. In this study, we investigated the effects of exosomes derived from melanoma cells on BALB/c splenocytes, focusing on their impact on cell proliferation, apoptosis, and cell cycle regulation, in light of the pivotal role of splenocytes in immune modulation.
methodsExosomes were isolated from B16-F10 melanoma cell supernatant using ultracentrifugation. Their identity was assessed by scanning electron microscopy (SEM), dynamic light scattering (DLS), and Western blotting for exosomal markers. BALB/c mouse splenocytes were isolated and treated with different concentrations of melanoma-derived exosomes. The optimal exosome concentration was determined based on cell viability assessed by the MTT assay. Then, splenocytes were treated with the selected exosome concentration, and the effects on spleen cells were evaluated by evaluating cell proliferation (MTT assay), apoptosis (Annexin V-FITC/PI staining), and cell cycle phases (DAPI staining) via flow cytometry.
resultsFirstly, the size, morphology, and exosomal markers of the isolated vesicles were assessed, collectively confirming their identity as exosomes. Then, the optimal exosome concentration was found to be 40 µg/mL, and treatment with melanoma-derived exosomes resulted in a dose-dependent inhibition of splenocyte proliferation. Moreover, an arrest in the Sub-G1 cell cycle phase and increased apoptosis rate were also observed in splenocytes exposed to exosomes compared to the control group.
conclusionExosomes derived from B16-F10 melanoma cells were shown to modulate key functional properties of splenocytes. These immunomodulatory effects suggest that melanoma-derived exosomes may contribute to tumor immune evasion by altering the functional dynamics of immune cell populations, highlighting their potential as therapeutic targets in melanoma.
Indexed as
Identifiers
40767919What 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.