Evidence map›Paper›PMID 34364387›Full record

ArticleBMC cancer2021

The combined effect of dichloroacetate and 3-bromopyruvate on glucose metabolism in colorectal cancer cell line, HT-29; the mitochondrial pathway apoptosis.

Hojatolla Nikravesh, Mohammad Javad Khodayar, Babak Behmanesh, Masoud Mahdavinia, Ali Teimoori, Soheila Alboghobeish, Leila Zeidooni

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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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 2 institutions in 1 country.

Hojatolla NikraveshCellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Mohammad Javad KhodayarDepartment of Toxicology, Faculty of Pharmacy, School of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Babak BehmaneshStudent Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Masoud MahdaviniaDepartment of Toxicology, Faculty of Pharmacy, School of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. mahdavinia-m@ajums.ac.ir.
Ali TeimooriDepartment of Virology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
Soheila AlboghobeishDepartment of Pharmacology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Leila ZeidooniDepartment of Toxicology, Faculty of Pharmacy, School of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Ahvaz Jundishapur University of Medical Sciences · IRHamedan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background5-Fluorouracil (5-FU) is regarded as the first line treatment for colorectal cancer; however, its effectiveness is limited by drug resistance. The ultimate goal of cancer therapy is induction of cancer cell death to achieve an effective outcome with minimal side effects. The present work aimed to assess the anti-cancer activities of mitocans which can be considered as an effective anticancer drug due to high specificity in targeting cancer cells.

methodsMTT (3-4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide) assay was performed to determine the effects of our mitocans on cell viability and cell death. Apoptosis and necrosis, caspase 3 activity, mitochondrial membrane potential and ROS production in HT29 cell lines were analyzed by ApopNexin™ FITC/PI Kit, Caspase- 3 Assay Kit, MitoTracker Green and DCFH-DA, respectively. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression level of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) genes in HT29 cell lines.

resultsTreatment with mitocans (3Br-P + DCA) inhibited the growth of HT29. Moreover, 3Br-P + DCA significantly induced apoptosis and necrosis, activation of caspase 3 activity, depolarize the mitochondrial membrane potential, and ROS production. At a molecular level, 3Br-P + DCA treatment remarkably down-regulated the expression of Bcl-2, while up-regulated the expression of Bax.

conclusionMitocans, in particular the combined drug, 3Br-P + DCA, could be regarded and more evaluated as a safe and effective compound for CRC treatment. Targeting hexokinase and pyruvate dehydrogenase kinase enzymes may be an option to overcome 5-FU -mediated chemo-resistant in colorectal cancer.

Indexed as

Antineoplastic AgentsApoptosisCaspase 3Cell Line, TumorCell ProliferationCell SurvivalColorectal NeoplasmsDichloroacetic AcidDrug SynergismFluorouracilGlucoseHT29 CellsHumansMembrane Potential, MitochondrialMetabolic Networks and PathwaysMitochondriaAntineoplastic AgentsbromopyruvateCASP3 protein, humanCaspase 3Dichloroacetic AcidFluorouracilGlucosePyruvates3-Bromopyruvate5-fluorouracilApoptosisColorectal cancer cellsDichloroacetate

Identifiers

PMID34364387
PMCPMC8349486
OpenAlexW3188195129

What OpenQuestion holds

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LicenceCC BY
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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.