ArticleCancers2021
Exosomal HMGB1 Promoted Cancer Malignancy.
Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 17 citations in OpenAlex.
- Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4/NF-κB/IL-6/STAT3 Signalling Cascade.Journal of cellular and molecular medicine · 2026Article
- The role of platelets in tumor immune evasion and metastasis: mechanisms and therapeutic implications.Cancer cell international · 2025Review
- miRNAs as short non-coding RNAs in regulating doxorubicin resistance.Journal of cell communication and signaling · 2023Review
- Haematopoietic cell-derived exosomes in cancer development and therapeutics: From basic science to clinical practice.Clinical and translational medicine · 2023Review
- The therapeutic potential of exosomes in lung cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- Dialog beyond the Grave: Necrosis in the Tumor Microenvironment and Its Contribution to Tumor Growth.International journal of molecular sciences · 2023Review
- Review
- Effects of the interactions between platelets with other cells in tumor growth and progression.Frontiers in immunology · 2023Review
- Exosome biogenesis: machinery, regulation, and therapeutic implications in cancer.Molecular cancer · 2022Review
- Metformin Mitigated Obesity-Driven Cancer Aggressiveness in Tumor-Bearing Mice.International journal of molecular sciences · 2022Article
- The role of microvesicles as biomarkers in the screening of colorectal neoplasm.Cancer medicine · 2022Article
- Extracellular Vesicles and DAMPs in Cancer: A Mini-Review.Frontiers in immunology · 2021Review
- Bidirectional Interaction Between Cancer Cells and Platelets Provides Potential Strategies for Cancer Therapies.Frontiers in oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 6 institutions in 1 country.
Funding
Abstract
Reciprocal crosstalk between platelets and malignancies underscores the potential of antiplatelet therapy in cancer treatment. In this study, we found that human chronic myeloid leukemia K562 cell-differentiated megakaryocytes and murine platelets produced bioactive substances and these are released into the extracellular space, partly in their exosomal form. High-mobility group box 1 (HMGB1) is a type of exosomal cargo, and the antiplatelet drugs aspirin and dipyridamole interfered with its incorporation into the exosomes. Those released substances and exosomes, along with exogenous HMGB1, promoted cancer cell survival and protected cells from doxorubicin cytotoxicity. In a tumor-bearing model established using murine Lewis lung carcinoma (LLC) cells and C57BL/6 mice, the tumor suppressive effect of dipyridamole correlated well with decreased circulating white blood cells, soluble P-selectin, TGF-β1 (Transforming Growth Factor-β1), exosomes, and exosomal HMGB1, as well as tumor platelet infiltration. Exosome release inhibitor GW4869 exhibited suppressive effects as well. The suppressive effect of dipyridamole on cancer cell survival was paralleled by a reduction of HMGB1/receptor for advanced glycation end-products axis, and proliferation- and migration-related β-catenin, Yes-associated protein 1, Runt-related transcription factor 2, and TGF- β1/Smad signals. Therefore, exosomes and exosomal HMGB1 appear to have roles in platelet-driven cancer malignancy and represent targets of antiplatelet drugs in anticancer treatment.
Indexed as
Identifiers
What Socratic 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 Socratic graph.