Evidence map›Paper›PMID 26694491›Full record

ArticleDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences2015

Cardanol isolated from Thai Apis mellifera propolis induces cell cycle arrest and apoptosis of BT-474 breast cancer cells via p21 upregulation.

Sureerat Buahorm, Songchan Puthong, Tanapat Palaga, Kriengsak Lirdprapamongkol, Preecha Phuwapraisirisan, Jisnuson Svasti, Chanpen Chanchao

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

9 citing papers in PubMed, 25 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.

Sureerat BuahormProgram in Biotechnology, Faculty of Science, Chulalongkorn University, 254 Phayathai Road, Bangkok, 10330, Thailand.
Songchan PuthongInstitute of Biotechnology and Genetic Engineering, Chulalongkorn University, 254 Phayathai Road, Bangkok, 10330, Thailand.
Tanapat PalagaDepartment of Microbiology, Faculty of Science, Chulalongkorn University, 254 Phayathai Road, Bangkok, 10330, Thailand.
Kriengsak LirdprapamongkolLaboratory of Biochemistry, Chulabhorn Research Institute, Vipawadee Rangsit Highway, Bangkok, 10210, Thailand.
Preecha PhuwapraisirisanDepartment of Chemistry, Faculty of Science, Chulalongkorn University, 254 Phayathai Road, Bangkok, 10330, Thailand.
Jisnuson SvastiLaboratory of Biochemistry, Chulabhorn Research Institute, Vipawadee Rangsit Highway, Bangkok, 10210, Thailand.
Chanpen ChanchaoDepartment of Biology, Faculty of Science, Chulalongkorn University, 254 Phayathai Road, Bangkok, 10330, Thailand. chanpen@sc.chula.ac.th.
Chulalongkorn University · THChulabhorn Research Institute · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardanol was previously reported to be an antiproliferative compound purified from Thai Apis mellifera propolis. By morphology, it could induce the cell death to many cancer cell lines but not the control (non-transformed human foreskin fibroblast cell line, Hs27). Here, it was aimed to evaluate the molecular effects of cardanol on breast cancer derived cell line (BT-474).

methodsMorphological changes in BT-474 cells induced by cardanol compared to doxorubicin were evaluated by light microscopy, cytotoxicity by using the 3- (4, 5-dimethyl-thiazol-2-yl) 2, 5-diphenyl-tetrazolium bromide (MTT) assay, induction of cell cycle arrest and cell death by flow cytometric analysis of propidium iodide and annexin-V stained cells, and changes in the expression level of genes involved in the control of apoptosis and the cell cycle by quantitative reverse transcriptase-PCR (qRT-PCR) and western blot analyses.

resultsIt revealed that cardanol induced a time- and dose-dependent cytotoxicity along with cell shrinkage and detachment from substratum. Cardanol caused cell cycle arrest at the G1 subphase (as opposed to at the G2/M subphase seen with doxorubicin) and cell death by late apoptosis, with both late apoptosis (27.2 ± 1.1 %) and necrosis (25.4 ± 1.4 %) being found in cardanol treated cells after 72 h, compared to a lower proportion of apoptosis (4.3 ± 0.4 %) and higher proportion of necrosis (35.8 ± 13.0 %) induced by doxorubicin. Moreover, cardanol changed the transcript expression levels of genes involved in the control of apoptosis (increased DR5 and Bcl-2 expression and decreased Mcl-1, MADD and c-FLIPP) and cell division (increased p21 and E2FI and decreased cyclin D1, cyclin E, CDK4 and CDK2 expression), as well as increasing the level of p21 p-ERK, p-JNK and p-p38 and decreasing cyclin D. This accounts for the failure to progress from the G1 to the S subphase.

conclusionCardanol is a potential chemotherapeutic agent for breast cancer.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBeesBreast NeoplasmsCell CycleCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21DoxorubicinFemaleGene Expression Regulation, NeoplasticHumansPhenolsAntineoplastic AgentscardanolCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DoxorubicinPhenols

Identifiers

PMID26694491
PMCPMC4687141
OpenAlexW2202348479

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.