ArticleJournal of extracellular vesicles2014
Anti-proliferative and anti-tumour effects of lymphocyte-derived microparticles are neither species- nor tumour-type specific.
Article in Journal of extracellular vesicles, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Nanomaterials in Targeting Cancer Cells with Nanotherapeutics: Transitioning Towards Responsive Systems.Current pharmaceutical design · 2024Review
- MiR-181a-5p inhibits uveal melanoma development by targeting GNAQ and AKT3.American journal of cancer research · 2023Article
- MicroRNA-181a suppresses norethisterone-promoted tumorigenesis of breast epithelial MCF10A cells through the PGRMC1/EGFR-PI3K/Akt/mTOR signaling pathway.Translational oncology · 2021Article
- Immunoregulatory Roles of Extracellular Vesicles and Associated Therapeutic Applications in Lung Cancer.Frontiers in immunology · 2020Review
- Generation of lymphocytic microparticles and detection of their proapoptotic effect on airway epithelial cells.Journal of visualized experiments : JoVE · 2015Article
- Prediction of the Therapeutic Effects of Pembrolizumab and Nivolumab in Advanced Non-Small Cell Lung Cancer by Platelet-Derived Microparticles in Circulating Blood.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUnregulated cell proliferation or growth is a prominent characteristic of cancer. We have previously demonstrated that LMPs (cell membrane microparticles derived from apoptotic human CEM T lymphoma cells stimulated with actinomycin D) strongly suppress the proliferation of not only human endothelial cells but also mouse Lewis lung carcinoma cells.
methodsLMPs were generated either from CEM T cells using different stimuli or from 3 different types of lymphocytes. The effects of LMPs on cancer cell proliferation were examined using cell lines from different species and tissues. The cell cycle kinetics was evaluated by FACS and the expression of cell cycle-related genes was determined using quantitative RT-PCR. The in vivo anti-tumor effect of LMPs was investigated using xenografts and allografts.
resultsLMPs at doses far above physiological levels dramatically suppressed the proliferation of cancer cells in a non species-specific manner. LMPs selectively target high proliferating cells and their anti-proliferative effect is not dependent on parental cell origin or stimuli. The anti-proliferative effect of LMPs was due to induction of cell-cycle arrest in G0/G1, with associated increases in expression of the cyclin-dependent kinase inhibitors p15(INK4b), p16(INK4a), and p21(Cip1). In vivo, LMPs significantly suppressed tumor growth in animal tumor models.
conclusionThese results highlight the potential role of LMPs in modulating the growth of high proliferating cells. Given that cell-based therapies are considered less toxic than pharmacologic approaches and have the potential to target multiple pathways in a synergistic manner, LMPs may serve as a veritable option for cancer treatment.
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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.