Evidence map›Paper›PMID 32572774›Full record

ArticleChinese journal of integrative medicine2021

Carvacrol Promotes Cell Cycle Arrest and Apoptosis through PI3K/AKT Signaling Pathway in MCF-7 Breast Cancer Cells.

Ashok Mari, Gopikrishnan Mani, Sirpu Natesh Nagabhishek, Gopalakrishnan Balaraman, Nirmala Subramanian, Fathima Bushra Mirza, Jagan Sundaram, Devaki Thiruvengadam

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In one paragraph

Article in Chinese journal of integrative medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Hyperprogressive disease in carcinoma induced by immune checkpoint inhibitor therapy: a systematic review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Pooled it
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  8. Exploring the Therapeutic Potential ofAnti-cancer agents in medicinal chemistry · 2026
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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

8 authors at 2 institutions in 1 country.

Ashok MariDepartment of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India.
Gopikrishnan ManiDepartment of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India.
Sirpu Natesh NagabhishekCancer Biology Lab, Department of Nanoscience and Nanotechnology, Sathyabama Institute of Science and Technology, Chennai, 600119, India.
Gopalakrishnan BalaramanDepartment of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India.
Nirmala SubramanianDepartment of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India.
Fathima Bushra MirzaVRR Institute of Biomedical Science, Kattupakkam, Chennai, 600056, India.
Jagan SundaramDepartment of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India.
Devaki ThiruvengadamDepartment of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India. devakit@yahoo.co.uk.
University of Madras · INSathyabama Institute of Science and Technology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo examine the role of carvacrol in modulating PI3K/AKT signaling involved in human breast cancer pathogenesis using in vitro experimental model MCF-7 cells.

methodsMTT and lactate dehydrogenase assays were performed with cells treated with different doses of carvacrol (0-250 p mol/L) at different time points (24 and 48 h). The nuclear morphology was assessed in MCF-7 cells with propidium iodide (PI) and acridine orange/ethidium bromide (AO/EB) staining and analyzed by fluorescence microscopy. Events like cell cycle arrest, apoptosis was observed by flow cytometric analysis and expressions of p-Rb, cyclin D1, cyclin-dependent kinase 4 (CDK4), CDK6, Bax, Bcl-2, PI3K/p-AKT was analyzed by immunoblot.

resultsCarvacrol significantly reduced cell viability with the half maximal inhibitory concentration value of 200 µmol/L at 24 and 48 h (P<0.05). importantly, there was a significant increase in the accumulation of the G

conclusionCarvacrol significantly inhibited the breast cancer MCF-7 cell proliferation and induced apoptosis via suppressing PI3/AKT signaling pathway.

Indexed as

Breast NeoplasmsPhosphatidylinositol 3-KinasesApoptosisCell Cycle CheckpointsCell Line, TumorCell ProliferationCymenesFemaleHumansMCF-7 CellsProto-Oncogene Proteins c-aktSignal TransductioncarvacrolCymenesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktapoptosisbreast cancercarvacrolPI3K/AKT signaling pathwayproliferation

Identifiers

PMID32572774
OpenAlexW3036316395

What OpenQuestion 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 OpenQuestion graph.