ArticleMedical science monitor : international medical journal of experimental and clinical research2019
LaSota Strain Expressing The Rabies Virus Glycoprotein (rL-RVG) Suppresses Gastric Cancer by Inhibiting the Alpha 7 Nicotinic Acetylcholine Receptor (α7 nAChR)/Phosphoinositide 3-Kinase (PI3K)/AKT Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Nicotinic Acetylcholine Receptor Pathways in Cancer: From Psychiatric Clues to Therapeutic Opportunities.Cancer reports (Hoboken, N.J.) · 2025Review
- Cholinergic Mechanisms in Gastrointestinal Neoplasia.International journal of molecular sciences · 2024Review
- Comparative Efficacy of Tumor Microenvironment-responsive Nanotherapeutics Targeting PSD95/Discs-large/ZO-1 Binding Kinase in Different Histological Subgroups of Medulloblastoma.International journal of medical sciences · 2024Article
- Non-conducting functions of ion channels: The case of integrin-ion channel complexes.Channels (Austin, Tex.) · 2022Review
- Review
- Nicotinic receptors modulate antitumor therapy response in triple negative breast cancer cells.World journal of clinical oncology · 2022Article
- Development of Molecular Mechanisms and Their Application on Oncolytic Newcastle Disease Virus in Cancer Therapy.Frontiers in molecular biosciences · 2022Review
- Application progress of RVG peptides to facilitate the delivery of therapeutic agents into the central nervous system.RSC advances · 2021Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The recombinant avirulent Newcastle disease virus (NDV) LaSota strain expressing the rabies virus glycoprotein (rL-RVG) can induce much greater apoptosis than can NDV in gastric carcinoma cells, but the mechanisms involved remains unclear. MATERIAL AND METHODS The 2 gastric carcinoma cell lines were divided into the rL-RVG group, the NDV group, and the PBS group. MTT assay was used to detect and analyze cell viability. siRNA for alpha7-nAChR, alpha7-nAChR antagonist, or alpha7-nAChR agonist, AKT antagonist, and p-AKT agonist were used for pretreatment. The protein expressions of RVG, NDV, alpha7-nAChR, cleaved caspase-3, p-AKT, PI3K, Bcl-2, and Bax proteins were detected by Western blot assay. Immunofluorescence was used to detect expressions of alpha7-nAChR proteins. Light microscopy, flow cytometry, and TUNEL assay were used to assess apoptosis. RESULTS The results showed that 2 virus concentrations over 10³ dilution caused greater cell proliferation inhibition. rL-RVG treatment increased the expression of alpha7-nAChR, cleaved caspase-3, and Bax protein but decreased the expression of p-AKT, PI3K, and Bcl-2 protein. When the groups were pretreated with alpha7-nAChR antagonist, the alpha7-nAChR, cleaved caspase-3, and Bax protein expression increased, but the expression of p-AKT, PI3K, and Bcl-2 protein was clearly decreased. However, the results in the alpha7-nAChR agonist group were the opposite. When treated with the AKT antagonist, the result was the same as in the rL-RVG treatment group. The result in the AKT agonist group was the opposite of that in the AKT antagonist group. Compared with the NDV group, the results of light microscopy, FCM, and TUNEL assay showed that alpha7-nAChR antagonist significantly affected the apoptosis of gastric cancer cells in the rL-RVG group. CONCLUSIONS rL-RVG leads to much greater apoptosis through the alpha7-nAChR/PI3K/AKT pathway.
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