Evidence map›Paper›PMID 35356807›Full record

ArticleNeuro-oncology advances

Cannabidiol inhibits RAD51 and sensitizes glioblastoma to temozolomide in multiple orthotopic tumor models.

Liliana Soroceanu, Eric Singer, Pratiksha Dighe, Max Sidorov, Chandani Limbad, Aida Rodriquez-Brotons, Peter Rix, Rinette W L Woo, Lawrence Dickinson, Pierre-Yves Desprez and 1 more

Open access · goldAbstract read
In one paragraph

Article in Neuro-oncology advances. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Liliana SoroceanuCalifornia Pacific Medical Center Research Institute, San Francisco, CA 94107, USA.
Eric SingerCalifornia Pacific Medical Center Research Institute, San Francisco, CA 94107, USA.
Pratiksha DigheCalifornia Pacific Medical Center Research Institute, San Francisco, CA 94107, USA.
Max SidorovCalifornia Pacific Medical Center Research Institute, San Francisco, CA 94107, USA.
Chandani LimbadCalifornia Pacific Medical Center Research Institute, San Francisco, CA 94107, USA.
Aida Rodriquez-BrotonsCalifornia Pacific Medical Center Research Institute, San Francisco, CA 94107, USA.
Peter RixLaunch Bioscience, San Diego, CA 92130, USA.
Rinette W L WooCalifornia Pacific Medical Center Research Institute, San Francisco, CA 94107, USA.
Lawrence DickinsonEden Medical Center Sutter Research, Castro Valley, CA 94546, USA.
Pierre-Yves DesprezCalifornia Pacific Medical Center Research Institute, San Francisco, CA 94107, USA.
Sean D McAllisterCalifornia Pacific Medical Center Research Institute, San Francisco, CA 94107, USA.ORCID https://orcid.org/0000-0002-1749-1251
California Pacific Medical Center · USEden Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Cannabidiol (CBD), a nonpsychoactive cannabinoid with a low toxicity profile, has been shown to produce antitumor activity across cancers in part through selective production of reactive oxygen species (ROS) in tumor cells. The alkylating agent, temozolomide (TMZ), is standard of care for treatment of glioblastoma (GBM). It can trigger increased ROS to induce DNA damage. It has also been reported that downregulating the expression of RAD51, an important DNA damage repair protein, leads to sensitization of GBM to TMZ. Methods: We determined the extent to which CBD enhanced the antitumor activity of TMZ in multiple orthotopic models of GBM. In addition, we investigated the potential for CBD to enhance the antitumor activity of TMZ through production of ROS and modulation of DNA repair pathways. Results: CBD enhanced the activity of TMZ in U87 MG and U251 GBM cell lines and in patient-derived primary GBM163 cells leading to stimulation of ROS, activation of the ROS sensor AMP-activated protein kinase (AMPK), and upregulation of the autophagy marker LC3A. CBD produced a sensitization of U87 and GBM163-derived intracranial (i.c.) tumors to TMZ and significantly increased survival of tumor-bearing mice. However, these effects were not observed in orthotopic models derived from GBM with intact methylguanine methyltransferase (MGMT) expression. We further demonstrate that CBD inhibited RAD51 expression in MGMT-methylated models of GBM, providing a potential mechanism for tumor sensitization to TMZ by CBD. Conclusion: These data support the potential therapeutic benefits of using CBD to enhance the antitumor activity of TMZ in GBM patients.

Indexed as

cannabidiolglioblastomapatient-derived-xenograftsensitization to temozolomide

Identifiers

PMID35356807
PMCPMC8962752
OpenAlexW4212961825

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.