Evidence map›Paper›PMID 30623450›Full record

ReviewJournal of cellular physiology2019

Mechanisms of apoptosis modulation by curcumin: Implications for cancer therapy.

Keywan Mortezaee, Ensieh Salehi, Hanifeh Mirtavoos-Mahyari, Elahe Motevaseli, Masoud Najafi, Bagher Farhood, Rhonda J Rosengren, Amirhossein Sahebkar

Abstract readReview
In one paragraph

Review in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 4 pooled it
13.4field-weighted citation impact, top 1% 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

161 citing papers in PubMed, 4 syntheses or guidelines pooled it, 335 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Toxicology reports · 2026
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  12. Impact ofBiology · 2026
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101 more citing papers are in PubMed but not listed here.

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 at 6 institutions in 2 countries.

Keywan MortezaeeDepartment of Anatomy, School of Medicine, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Ensieh SalehiDepartment of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Hanifeh Mirtavoos-MahyariDepartment of Medical Genetics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Elahe MotevaseliDepartment of Molecular Medicine, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Masoud NajafiRadiology and Nuclear Medicine Department, School of Paramedical Sciences, Kermanshah University of Medical Science, Kermanshah, Iran.
Bagher FarhoodDepartment of Medical Physics and Radiology, Faculty of Paramedical Sciences, Kashan University of Medical Sciences, Kashan, Iran.
Rhonda J RosengrenDepartment of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand.
Amirhossein SahebkarBiotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.ORCID 0000-0002-8656-1444
Tehran University of Medical Sciences · IRKashan University of Medical Sciences · IRKermanshah University of Medical Sciences · IRKurdistan University of Medical Sciences · IRMashhad University of Medical Sciences · IRUniversity of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer incidences are growing and cause millions of deaths worldwide. Cancer therapy is one of the most important challenges in medicine. Improving therapeutic outcomes from cancer therapy is necessary for increasing patients' survival and quality of life. Adjuvant therapy using various types of antibodies or immunomodulatory agents has suggested modulating tumor response. Resistance to apoptosis is the main reason for radioresistance and chemoresistance of most of the cancers, and also one of the pivotal targets for improving cancer therapy is the modulation of apoptosis signaling pathways. Apoptosis can be induced by intrinsic or extrinsic pathways via stimulation of several targets, such as membrane receptors of tumor necrosis factor-α and transforming growth factor-β, and also mitochondria. Curcumin is a naturally derived agent that induces apoptosis in a variety of different tumor cell lines. Curcumin also activates redox reactions within cells inducing reactive oxygen species (ROS) production that leads to the upregulation of apoptosis receptors on the tumor cell membrane. Curcumin can also upregulate the expression and activity of p53 that inhibits tumor cell proliferation and increases apoptosis. Furthermore, curcumin has a potent inhibitory effect on the activity of NF-κB and COX-2, which are involved in the overexpression of antiapoptosis genes such as Bcl-2. It can also attenuate the regulation of antiapoptosis PI3K signaling and increase the expression of MAPKs to induce endogenous production of ROS. In this paper, we aimed to review the molecular mechanisms of curcumin-induced apoptosis in cancer cells. This action of curcumin could be applicable for use as an adjuvant in combination with other modalities of cancer therapy including radiotherapy and chemotherapy.

Indexed as

AnimalsApoptosisCurcuminGene Expression Regulation, NeoplasticHumansNeoplasmsCurcuminapoptosiscancercurcuminJNKNF-κBp53

Identifiers

PMID30623450
PMCPMC13484200
OpenAlexW2908664203

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.