ArticleHeliyon2024
Asperuloside regulates the proliferation, apoptosis, and differentiation of chronic myeloid leukemia cell line K562 through the RAS/MEK/ERK pathway.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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
4 citing papers in PubMed, 4 citations in OpenAlex.
- Epigenetic Reactivation of <italic>SOCS-3</italic> and Inhibition of ERK1/2 Underlie Thymoquinone-Induced Apoptosis in a Chronic Myeloid Leukemia Xenograft Model.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2026Article
- Integrating Nature Into Oncology: Enhancing Hematological Malignancies Therapies With Natural Medicine.Cancer medicine · 2025Review
- Asperuloside as a promising multi-target agent for Alzheimer's disease: molecular mechanisms and therapeutic perspectives.Inflammopharmacology · 2025Review
- Synergistic effects of 6-shogaol and hyperthermia on ACHN renal cancer cells: modulation of ROS and heat shock pro-teins in cancer therapy.Frontiers in pharmacology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Context: Chronic myeloid leukemia (CML) is a malignant hematopoietic stem cell disease caused by excessive proliferation and abnormal differentiation of hematopoietic stem cells. Objective: This study aimed to explore the effects and possible mechanisms of ASP on the biological behavior of K562 cells based on RNA-seq. Materials and methods: The IC Results: ASP significantly inhibited the proliferation, and promoted apoptosis and differentiation of K562 cells. A total of 117 differentially expressed genes were screened by RNA-seq, mainly involved in the RAS/MEK/ERK pathway. PD98059 was used to inhibit the RAS/MEK/ERK pathway in K562 cells, and results confirmed that PD98059 could not only inhibit the RAS/MEK/ERK pathway, but also inhibit the regulation of ASP on the proliferation and differentiation of K562 cells. Conclusion: ASP inhibited the proliferation, promoted apoptosis and differentiation of K562 cells by regulating the RAS/MEK/ERK pathway, and played a good anti-CML role.
Indexed as
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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.