Evidence map›Paper›PMID 36307019›Full record

ArticleJournal of advanced research2023

Crosstalk between aryl hydrocarbon receptor (AhR) and BCL-2 pathways suggests the use of AhR antagonist to maintain normal differentiation state of mammary epithelial cells during BCL-2 inhibition therapy.

Abdullah Al-Dhfyan, Ayodele Alaiya, Falah Al-Mohanna, Mohamed W Attwa, Abdullah F AlAsmari, Saleh A Bakheet, Hesham M Korashy

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. 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

7 authors at 3 institutions in 2 countries.

Abdullah Al-DhfyanDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia; Stem Cell & Tissue Re-Engineering Program, King Faisal Specialist Hospital and Research Center, Riyadh 11211, Saudi Arabia.
Ayodele AlaiyaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Falah Al-MohannaDepartment of Comparative Medicine, King Faisal Specialist Hospital and Research Center, Riyadh 11211, Saudi Arabia.
Mohamed W AttwaDepartment of Pharmaceutical Chemistry, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Abdullah F AlAsmariDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Saleh A BakheetDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia.
Hesham M KorashyDepartment of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, Doha 2713, Qatar. Electronic address: hkorashy@qu.edu.qa.
King Saud University · SAKing Faisal Specialist Hospital & Research Centre · SAQatar University · QA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionActivating the aryl hydrocarbon receptor upon exposure to environmental pollutants promotes development of breast cancer stem cell (CSCs). BCL-2 family proteins protect cancer cells from the apoptotic effects of chemotherapeutic drugs. However, the crosstalk between AhR and the BCL-2 family in CSC development remains uninvestigated.

objectivesThis study explored the interaction mechanisms between AhR and BCL-2 in CSC development and chemoresistance.

methodsA quantitative proteomic analysis study was performed as a tool for comparative expression analysis of breast cancer cells treated by AhR agonist. The basal and inducible levels of BCL-2, AhR, and CYP1A1 in vitro breast cancer and epithelial cell lines and in vivo mice animal models were determined by RT-PCR, Western blot analysis, immunofluorescence, flow cytometry, silencing of the target, and immunohistochemistry. In addition, an in silico toxicity study was conducted using DEREK software.

resultsActivation of the AhR/CYP1A1 pathway in mice increased EpCAM

conclusionsThis is the first study to report crosstalk between AhR and BCL-2 in breast CSCs and provides the rationale for using a combined treatment of BCL-2 inhibitor and AhR antagonist for more effective cancer prevention and treatment.

Indexed as

Cytochrome P-450 CYP1A1Receptors, Aryl HydrocarbonAnimalsCell DifferentiationCell Line, TumorEpithelial Cell Adhesion MoleculeEpithelial CellsIntegrin alpha6MiceProteomicsCytochrome P-450 CYP1A1Epithelial Cell Adhesion MoleculeIntegrin alpha6Receptors, Aryl HydrocarbonAhR/CYP1A1BCL-2Breast cancer stem cellsIn vivo miceProteomicsVenetoclax

Identifiers

PMID36307019
PMCPMC10403657
OpenAlexW4307397053

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.