Evidence map›Paper›PMID 29391428›Full record

ArticleScientific reports2018

β-Sitosterol targets Trx/Trx1 reductase to induce apoptosis in A549 cells via ROS mediated mitochondrial dysregulation and p53 activation.

Tamilselvam Rajavel, Pandian Packiyaraj, Venkatesan Suryanarayanan, Sanjeev Kumar Singh, Kandasamy Ruckmani, Kasi Pandima Devi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 125 citations in OpenAlex.

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  7. Aspects of β-sitosterol's Pharmacology, Nutrition and Analysis.Current pharmaceutical biotechnology · 2025
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  8. The Phytochemical Profile of the Petroleum Ether Extract ofInternational journal of molecular sciences · 2024
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  10. Pharmaceuticals (Basel, Switzerland) · 2024
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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

6 authors at 2 institutions in 1 country.

Tamilselvam RajavelDepartment of Biotechnology, Science Campus, Alagappa University, Karaikudi-630 003, Tamil Nadu, India.
Pandian PackiyarajDepartment of Biotechnology, Science Campus, Alagappa University, Karaikudi-630 003, Tamil Nadu, India.
Venkatesan SuryanarayananComputer Aided Drug Design and Molecular Modeling Lab, Department of Bioinformatics, Alagappa University, Karaikudi- 630003, Tamil Nadu, India.ORCID http://orcid.org/0000-0002-0412-2369
Sanjeev Kumar SinghComputer Aided Drug Design and Molecular Modeling Lab, Department of Bioinformatics, Alagappa University, Karaikudi- 630003, Tamil Nadu, India.
Kandasamy RuckmaniNational Facility for Drug Development (NFDD) for Academia, Pharmaceutical and Allied Industries, Bharathidasan, Institute of Technology, Anna University, Tiruchirappalli, 620024, Tamil Nadu, India.
Kasi Pandima DeviDepartment of Biotechnology, Science Campus, Alagappa University, Karaikudi-630 003, Tamil Nadu, India. devikasi@yahoo.com.ORCID http://orcid.org/0000-0002-6175-8961
Alagappa University · INAnna University, Chennai · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-Sitosterol (BS), a major bioactive constituent present in plants and vegetables has shown potent anticancer effect against many human cancer cells, but the underlying mechanism remain elusive on NSCLC cancers. We found that BS significantly inhibited the growth of A549 cells without harming normal human lung and PBMC cells. Further, BS treatment triggered apoptosis via ROS mediated mitochondrial dysregulation as evidenced by caspase-3 & 9 activation, Annexin-V/PI positive cells, PARP inactivation, loss of MMP, Bcl-2-Bax ratio alteration and cytochrome c release. Moreover, generation of ROS species and subsequent DNA stand break were found upon BS treatment which was reversed by addition of ROS scavenger (NAC). Indeed BS treatment increased p53 expression and its phosphorylation at Ser15, while silencing the p53 expression by pifithrin-α, BS induced apoptosis was reduced in A549 cells. Furthermore, BS induced apoptosis was also observed in NCI-H460 cells (p53 wild) but not in the NCI-H23 cells (p53 mutant). Down-regulation of Trx/Trx1 reductase contributed to the BS induced ROS accumulation and mitochondrial mediated apoptotic cell death in A549 and NCI-H460 cells. Taken together, our findings provide evidence for the novel anti-cancer mechanism of BS which could be developed as a promising chemotherapeutic drug against NSCLC cancers.

Indexed as

ApoptosisAntineoplastic AgentsCell Line, TumorHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsMitochondriaReactive Oxygen SpeciesSitosterolsTumor Suppressor Protein p53Antineoplastic Agentsgamma-sitosterolIntracellular Signaling Peptides and ProteinsMembrane ProteinsReactive Oxygen SpeciesSitosterolsTP53 protein, humanTumor Suppressor Protein p53VAC14 protein, human

Identifiers

PMID29391428
PMCPMC5794769
OpenAlexW2807143793

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.