Evidence map›Paper›PMID 41307591›Full record

ArticleDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences2025

Synergistic effects of Calebin A and docetaxel on apoptosis and migration in prostate cancer cells.

MohammadMostafa Askarnia Faal, Tandiseh Tasbandi, Mahdieh Aliyari, Maryam Shojaei, Moeen Eskandari, Amirhossein Sahebkar, Hossein Hosseini, Mohammad Jalili-Nik

Abstract read
In one paragraph

Article in Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

MohammadMostafa Askarnia Faal *Department of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Tandiseh Tasbandi *Department of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Mahdieh AliyariDepartment of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Maryam ShojaeiDepartment of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Moeen EskandariDepartment of Clinical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Amirhossein SahebkarBiotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
Hossein HosseiniSyndrome Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. HoseiniHS@mums.ac.ir.
Mohammad Jalili-NikPharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran. Mohammad.Jalilinik@gmail.com.

Funding

Mashhad University of Medical Sciences 4031830
6 · The paper itself

Abstract

backgroundResistance to docetaxel (DTX), a frontline chemotherapeutic agent for prostate cancer (PC), remains a major therapeutic challenge, often driven by impaired apoptosis and enhanced metastatic potential. Calebin A (CA), a natural polyphenol derived from turmeric, has demonstrated anticancer properties in various malignancies. This study investigated the individual and combined effects of CA and DTX on proliferation, apoptosis, cell cycle progression, migration, and gene expression in human PC3 prostate cancer cells.

methodsPC3 cells were treated with varying concentrations of CA and DTX, alone or in combination. Cell viability was assessed using the MTT assay, and drug interactions were evaluated using the combination index (CI) analysis. Flow cytometry was employed to analyze apoptosis and cell cycle distribution. Gene expression of Bax, Bcl-2, MMP-2, and MMP-9 was quantified using qRT-PCR, while gelatin zymography and wound healing assays evaluated protease activity and migratory behavior, respectively.

resultsBoth CA and DTX exhibited time- and dose-dependent cytotoxicity, with combination treatment producing synergistic effects (CI < 1). Co-treatment significantly increased apoptotic cell populations and induced marked sub-G1 and G2/M cell cycle arrest. The combination therapy upregulated the pro-apoptotic Bax/Bcl-2 ratio and downregulated MMP-2 expression, with modest reductions in MMP-2 and MMP-9 enzymatic activities. Furthermore, migratory capacity was significantly diminished under combinatorial treatment compared to monotherapies.

conclusionCA enhances the antitumor efficacy of DTX by potentiating apoptosis, inhibiting migration, and modulating gene expression associated with metastasis and survival. These findings suggest CA as a promising adjuvant to overcome chemoresistance and improve therapeutic outcomes in prostate cancer.

Indexed as

Antineoplastic AgentsApoptosisDocetaxelProstatic NeoplasmsCell CycleCell Line, TumorCell MovementCell ProliferationCell SurvivalDrug SynergismGene Expression Regulation, NeoplasticHumansMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9PC-3 CellsAntineoplastic AgentsDocetaxelMatrix Metalloproteinase 2Matrix Metalloproteinase 9Proto-Oncogene Proteins c-bcl-2

Identifiers

PMID41307591
PMCPMC12660546

What Socratic holds

Textmetadata
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.