Evidence map›Paper›PMID 32867831›Full record

ArticleBMC pharmacology & toxicology2020

Boswellic acid sensitizes gastric cancer cells to Cisplatin-induced apoptosis via p53-mediated pathway.

Shadia Al-Bahlani, Ikram A Burney, Buthaina Al-Dhahli, Safiya Al-Kharusi, Fakhra Al-Kharousi, Amani Al-Kalbani, Ikhlas Ahmed

Open access · goldAbstract read
In one paragraph

Article in BMC pharmacology & toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  8. 3-O-Acetyl-11-Keto-Oncology research · 2025
    Article
  9. Review
  10. Review
  11. Cellular and Molecular Mechanisms of Chemoresistance for Gastric Cancer.International journal of general medicine · 2024
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
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 1 institution in 1 country.

Shadia Al-BahlaniDepartment of Allied Health Sciences, College of Medicine and Health Sciences, Sultan Qaboos University, P. O. Box 35, PC 123 AlKhoud, Muscat, Oman. bahlani@squ.edu.om.
Ikram A BurneyDepartment of Medicine, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Oman.
Buthaina Al-DhahliDepartment of Allied Health Sciences, College of Medicine and Health Sciences, Sultan Qaboos University, P. O. Box 35, PC 123 AlKhoud, Muscat, Oman.
Safiya Al-KharusiDepartment of Allied Health Sciences, College of Medicine and Health Sciences, Sultan Qaboos University, P. O. Box 35, PC 123 AlKhoud, Muscat, Oman.
Fakhra Al-KharousiDepartment of Allied Health Sciences, College of Medicine and Health Sciences, Sultan Qaboos University, P. O. Box 35, PC 123 AlKhoud, Muscat, Oman.
Amani Al-KalbaniDepartment of Allied Health Sciences, College of Medicine and Health Sciences, Sultan Qaboos University, P. O. Box 35, PC 123 AlKhoud, Muscat, Oman.
Ikhlas AhmedDepartment of Pharmacology and Clinical Pharmacy, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Oman.
Sultan Qaboos University · OM

Funding

Sultan Qaboos University (OM) Grant No. IG/MED/ALIE/16/01
6 · The paper itself

Abstract

backgroundCisplatin (CDDP) is an effective anticancer drug for Gastric cancer (GC) that induces apoptosis by altering pro- (p53) and anti-apoptotic (Akt and NFkB) proteins; however, chemoresistance remains a big challenge. Additional compounds with promising anticancer effects such as AKBA (Acetyl-keto-beta boswellic acid) may overcome the resistance. However, its role in CDDP-induced apoptosis in GC has not been studied. This study aimed to examine the effectiveness of AKBA on p53-mediated, CDDP-induced apoptosis in GC cells. AGS and NCI-N87 cells were treated with different concentrations (0, 25, 50, 100 μM) of CDDP and/or AKBA.

methodsP53, Akt and NFkB proteins and apoptosis were assessed by Western blot and flow cytometry. The role of p53 was determined by inhibiting its function via the siRNA approach.

resultsThe results revealed that CDDP and AKBA significantly increased p53 content in both cells, while Akt and NFkB were significantly decreased. Both compounds significantly induced apoptosis in a dose-dependent manner. AKBA sensitized GC cells to CDDP-induced apoptosis by altering the protein expression. P53 downregulation affected Akt and NFkB proteins with a slight increase in apoptosis induction in the combination treated groups.

conclusionsAltogether, our findings suggest that AKBA enhances GC cell sensitivity to CDDP-induced apoptosis via the p53 pathway.

Indexed as

Adjuvants, PharmaceuticAntineoplastic AgentsApoptosisCell Line, TumorCisplatinHumansNF-kappa BProto-Oncogene Proteins c-aktSignal TransductionStomach NeoplasmsTriterpenesTumor Suppressor Protein p53Adjuvants, PharmaceuticAntineoplastic Agentsboswellic acidCisplatinNF-kappa BProto-Oncogene Proteins c-aktTriterpenesTumor Suppressor Protein p53AKBAApoptosis and gastric cancerCDDPP53

Identifiers

PMID32867831
PMCPMC7460741
OpenAlexW3082308923

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.