Evidence map›Paper›PMID 42088408›Full record

ArticleFrontiers in toxicology2026

Acute anti-proliferative and anti-migratory effects of cannabidiol on C6 rat glioma, SH-SY5Y human neuroblastoma, and HT22 mouse hippocampal neuronal cell cultures.

Kittikun Viwatpinyo, Sujira Mukda, Aktsar Roskiana Ahmad, Sakan Warinhomhoun

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Article in Frontiers in toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Kittikun ViwatpinyoSchool of Medicine, Walailak University, Nakorn Si Thammarat, Thailand.
Sujira MukdaResearch Center for Neuroscience, Institute of Molecular Biosciences, Mahidol University, Nakorn Pathom, Thailand.
Aktsar Roskiana AhmadDepartment of Pharmacognosy and Phytochemistry, Faculty of Pharmacy, Universitas of Muslim Indonesia, Makassar, South Sulawesi, Indonesia.
Sakan WarinhomhounCollege of Oriental Medicine, Rangsit University, Pathum Thani, Thailand.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The treatment of central nervous system tumors remains challenging owing to their highly proliferative nature, aggressiveness, and poor prognosis. Additionally, existing treatment methods have several problems, including high risk of complications, systemic side effects, and impact on patients' quality of life. Recently, cannabidiol (CBD), a non-psychoactive cannabinoid found in Methods: We evaluated the cell viability, clonogenicity, migration, apoptotic nuclear morphology, and cell cycle phases of C6 rat glioma, SH-SY5Y human neuroblastoma, and HT22 immortalized mouse hippocampus neuronal cultures treated with CBD ranged between 0 and 10 μg/mL. Results: CBD concentrations exceeding 5 μg/mL induced significant reductions in cell viability in C6 glioma and SH-SY5Y neuroblastoma cultures, accompanied by decreased clonogenicity in both cultures at 10 μg/mL. A scratch assay for cell migration revealed that 5 μg/mL CBD suppressed C6 glioma cell migration. Additionally, late apoptotic nuclear morphology was observed in C6 glioma cultures treated with 10 μg/mL cannabidiol. Similarly, HT22 hippocampal neuronal cultures exhibited decreased cell viability and clonogenicity, with apparent nuclear signs of apoptosis at CBD concentrations over 5 μg/mL. Notably, CBD disrupted HT22 cell migration at concentrations of 2.5 and 5 μg/mL. Proteomic profiling of C6 glioma revealed upregulation of ribosomal proteins, molecular chaperones, and modulators of cytoskeletal dynamics upon treatment with 1 μg/mL CBD. In comparison, treatment with 2.5 μg/mL CBD led to marked downregulation of endoplasmic reticulum chaperones, mitochondrial ATP synthase, and cytoskeletal regulators. Conclusion: Our findings confirm the sensitivity of glioma, neuroblastoma, and hippocampal neuronal cultures to CBD, providing valuable insights for further research into its therapeutic potential against glioma, neuroblastoma, and neuronal disorders.

Indexed as

apoptosiscannabidiolcytotoxicitygliomahippocampal neuronneuroblastoma

Identifiers

PMID42088408
PMCPMC13138797

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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 Socratic graph.