Evidence map›Paper›PMID 28728544›Full record

ArticleBMC cell biology2017

Cladosporol A triggers apoptosis sensitivity by ROS-mediated autophagic flux in human breast cancer cells.

Mytre Koul, Ashok Kumar, Ramesh Deshidi, Vishal Sharma, Rachna D Singh, Jasvinder Singh, Parduman Raj Sharma, Bhahwal Ali Shah, Sundeep Jaglan, Shashank Singh

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in BMC cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

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  12. Vanadocene dichloride induces apoptosis in HeLa cells through depolymerization of microtubules and inhibition of Eg5.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Mytre KoulCancer Pharmacology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, India.
Ashok KumarCancer Pharmacology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, India.
Ramesh DeshidiNatural Product Chemistry, CSIR-Indian Institute of Integrative Medicine, Jammu, India.
Vishal SharmaMicrobial Biotechnology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, India.
Rachna D SinghDepartment of Conservative Dentistry & Endodontics, Indira Gandhi Govt. Dental College and Hospital, Jammu, India.
Jasvinder SinghCancer Pharmacology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, India.
Parduman Raj SharmaCancer Pharmacology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, India.
Bhahwal Ali ShahNatural Product Chemistry, CSIR-Indian Institute of Integrative Medicine, Jammu, India. bashah@iiim.ac.in.
Sundeep JaglanMicrobial Biotechnology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, India.
Shashank SinghCancer Pharmacology Division, CSIR-Indian Institute of Integrative Medicine, Jammu, India. sksingh@iiim.ac.in.
Academy of Scientific and Innovative Research · INIndian Institute of Integrative Medicine · INGovt. Dental College & Hospital · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndophytes have proven to be an invaluable resource of chemically diverse secondary metabolites that act as excellent lead compounds for anticancer drug discovery. Here we report the promising cytotoxic effects of Cladosporol A (HPLC purified >98%) isolated from endophytic fungus Cladosporium cladosporioides collected from Datura innoxia. Cladosporol A was subjected to in vitro cytotoxicity assay against NCI60 panel of human cancer cells using MTT assay. We further investigated the molecular mechanism(s) of Cladosporol A induced cell death in human breast (MCF-7) cancer cells. Mechanistically early events of cell death were studied using DAPI, Annexin V-FITC staining assay. Furthermore, immunofluorescence studies were carried to see the involvement of intrinsic pathway leading to mitochondrial dysfunction, cytochrome c release, Bax/Bcl-2 regulation and flowcytometrically measured membrane potential loss of mitochondria in human breast (MCF-7) cancer cells after Cladosporol A treatment. The interplay between apoptosis and autophagy was studied by microtubule dynamics, expression of pro-apoptotic protein p21 and autophagic markers monodansylcadaverine staining and LC3b expression.

resultsAmong NCI60 human cancer cell line panel Cladosporol A showed least IC

conclusionOur experimental data suggests that Cladosporol A depolymerize microtubules, sensitize programmed cell death via ROS mediated autophagic flux leading to mitophagic cell death. The proposed mechanism of Cladosporol A -triggered apoptotic as well as autophagic death of human breast cancer (MCF-7) cells. The figure shows that Cladosporol A induced apoptosis through ROS mediated mitochondrial pathway and increased p21 protein expression in MCF-7 cells in vitro.

Indexed as

AcetylcysteineApoptosisAutophagyBreast NeoplasmsCell CycleCell Line, TumorCell ProliferationChromosomesCladosporiumCyclin-Dependent Kinase Inhibitor p21Cytochromes cDrug Screening Assays, AntitumorFemaleHumansMCF-7 CellsMembrane Potential, MitochondrialAcetylcysteineCDKN1A protein, humancladosporol ACyclin-Dependent Kinase Inhibitor p21Cytochromes cNaphtholsReactive Oxygen SpeciesApoptosisBreast cancerCladosporium cladosporioidesCladosporol aEndophytesReactive oxygen species

Identifiers

PMID28728544
PMCPMC5520384
OpenAlexW2738380285

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.