Evidence map›Paper›PMID 36853473›Full record

ArticleMolecular biology reports2023

Cannabidiol and Cannabis Sativa as a potential treatment in vitro prostate cancer cells silenced with RBBp6 and PC3 xenograft.

Lesetja R Motadi, Zodwa E Jantjies, Boitumelo Moleya

Open access · hybridAbstract read
In one paragraph

Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Cannabidiol Toxicity Driven by Hydroxyquinone Formation.Chemical research in toxicology · 2025
    Article
  7. Article
  8. Current and Potential Use of Biologically Active Compounds Derived fromInternational journal of molecular sciences · 2024
    Review
  9. Article
  10. Review
  11. Article
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

3 authors at 1 institution in 1 country.

Lesetja R MotadiDepartment of Biochemistry, University of Johannesburg, Auckland Park Campus, Johannesburg, South Africa. lmotadi@uj.ac.za.ORCID http://orcid.org/0000-0001-6012-6367
Zodwa E JantjiesDepartment of Biochemistry, University of Johannesburg, Auckland Park Campus, Johannesburg, South Africa.
Boitumelo MoleyaDepartment of Biochemistry, University of Johannesburg, Auckland Park Campus, Johannesburg, South Africa.
University of Johannesburg · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProstate cancer is the second most frequently occurring carcinoma in males worldwide and one of the leading causes of death in men around the world. Recent studies estimate that over 1.4 million males are diagnosed with prostate cancer on an annual basis, with approximately 375,000 succumbing to the disease annually. With current treatments continuing to show severe side effects, there is a need for new treatments. In this study we looked at the effect of cannabis sativa extract, cannabidiol and cisplatin on prostate cancer cells, PC3.

methodsIn addressing the above questions, we employed the MTT assay to measure the antiproliferative effect on PC3 cells following treatment with varying concentrations of Cannabis sativa extract, cisplatin and cannabidiol. xCELLigence was also used to confirm the IC50 activity in which cells were grown in a 16 well plate coated with gold and monitor cell attachment. Caspase 3/7 activity was also measured using 96 well-plate following treatment. Western-blot and qRT-PCR was also used to measure the gene expression of tumour suppressor genes, p53, Bax and Bcl2. Animal studies were employed to measure the growth of PC3-mouse derived cancer to evaluate the effect of compounds in vivo.

resultsFrom the treatment with varying concentrations of Cannabis sativa extract, cannabidiol and cisplatin, we have observed that the three compounds induced antiproliferation of PC3 cancer cell lines through the activation of caspase 3/7 activity. We also observed induction of apoptosis in these cells following silencing of retinoblastoma binding protein 6 (RBBP6), with upregulation of p53 and bax mRNA expression, and a reduction in Bcl2 gene expression. The growth of tumours in the mouse models were reduced following treatment with cisplatin and cannabidiol.

conclusionWe demonstrated that cannabidiol is a viable therapy to treat prostate cancer cells, in combination with silencing of RBBP6. This suggests that cannabidiol rather Cannabis sativa extract may play an important role in reducing cancer progression.

Indexed as

CannabidiolCannabisProstatic NeoplasmsAnimalsApoptosisbcl-2-Associated X ProteinCaspase 3CisplatinDNA-Binding ProteinsHeterograftsHumansMaleMicePC-3 CellsPlant ExtractsProto-Oncogene Proteins c-bcl-2bcl-2-Associated X ProteinCannabidiolCaspase 3CisplatinDNA-Binding ProteinsPlant ExtractsProto-Oncogene Proteins c-bcl-2RBBP6 protein, humanTumor Suppressor Protein p53Ubiquitin-Protein LigasesAnd apoptosisCannabidiolCannabis sativa extractCisplatinsiRBBP6

Identifiers

PMID36853473
PMCPMC10147767
OpenAlexW4322617769

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.