ArticleInternational journal of clinical and experimental pathology2017
Hyperoside inhibited the migration and invasion of lung cancer cells through the upregulation of PI3K/AKT and p38 MAPK pathways.
Article in International journal of clinical and experimental pathology, 2017. 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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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- The multiple biological activities of hyperoside: from molecular mechanisms to therapeutic perspectives in neoplastic and non-neoplastic diseases.Frontiers in pharmacology · 2025Review
- Quercetin Derivatives as Potential Therapeutic Agents: An Updated Perspective on the Treatment of Nicotine-Induced Non-Small Cell Lung Cancer.International journal of molecular sciences · 2023Review
- Role of Plant-Derived Compounds in the Molecular Pathways Related to Inflammation.International journal of molecular sciences · 2023Review
- Potential Implications of Hyperoside on Oxidative Stress-Induced Human Diseases: A Comprehensive Review.Journal of inflammation research · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) is one of the most common human malignancies. Malignant tumor is characterized by the Invasion and metastasis of tumor. Based on previous research, human A549 cells could be induced to apoptosis by Hyperoside (Hyp). The aim of the present study was to investigate whether low concentrations of Hyp (1-10 μM) could inhibit the invasion and migration of lung cancer cells through regulation of phosphoinositide-3-kinase/serine threonine kinase (PI3K/AKT) and p38 mitogen-activated protein kinase (p38 MAPK) pathways.CCK8 assay was performed to identify the cell viability after human A549 cells treated with Hyp (1, 2 and 5 μM) 12, 24 and 48 h. Hyp (1, 2 and 5 μM) significantly suppressed the invasion and migration of A549 cells in a dose-dependant manner. Phosphorylation of AKT and P38 protein level were measured by western blot. By RT-PCR and western blot analysis, non-metastatic gene23-H1 (nm23-H1), metastasis-associated gene 1 (MTA1), tissue inhibitor of metalloproteinase-1 (TIMP-2) and matrix metalloproteinases-2/9 (MMP-2/9) expression was estimated. The results showed that the level of nm23-H1, MTA1, TIMP-2 and MMP-2/9 expression were all regulated dramatically in Hyp groups compared with the control group. The p-ATK and p-P38 were descended notably. These results suggested that Hyp significantly suppressed the invasion and migration of A549 cells by mediating the AKT/PI3K and p38 MAPK pathways and regulated the expressions of invasion and migration related genes.
Indexed as
Identifiers
31966810PMC6965916W3010558197What 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.