Evidence map›Paper›PMID 25268751›Full record

ArticlePloS one2014

Fluvastatin mediated breast cancer cell death: a proteomic approach to identify differentially regulated proteins in MDA-MB-231 cells.

Anantha Koteswararao Kanugula, Vishnu M Dhople, Uwe Völker, Ramesh Ummanni, Srigiridhar Kotamraju

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

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  6. From structural resilience to cell specification - Intermediate filaments as regulators of cell fate.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Anantha Koteswararao KanugulaCentre for Chemical Biology, CSIR-Indian Institute of Chemical Technology, Hyderabad, India.
Vishnu M DhopleInterfacultary Institute of Genetics and Functional Genomics, University Medicine Greifswald, Greifswald, Germany.
Uwe VölkerInterfacultary Institute of Genetics and Functional Genomics, University Medicine Greifswald, Greifswald, Germany.
Ramesh UmmanniCentre for Chemical Biology, CSIR-Indian Institute of Chemical Technology, Hyderabad, India.
Srigiridhar KotamrajuCentre for Chemical Biology, CSIR-Indian Institute of Chemical Technology, Hyderabad, India.
Indian Institute of Chemical Technology · INUniversitätsmedizin Greifswald · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Statins are increasingly being recognized as anti-cancer agents against various cancers including breast cancer. To understand the molecular pathways targeted by fluvastatin and its differential sensitivity against metastatic breast cancer cells, we analyzed protein alterations in MDA-MB-231 cells treated with fluvastatin using 2-DE in combination with LC-MS/MS. Results revealed dys-regulation of 39 protein spots corresponding to 35 different proteins. To determine the relevance of altered protein profiles with breast cancer cell death, we mapped these proteins to major pathways involved in the regulation of cell-to-cell signaling and interaction, cell cycle, Rho GDI and proteasomal pathways using IPA analysis. Highly interconnected sub networks showed that vimentin and ERK1/2 proteins play a central role in controlling the expression of altered proteins. Fluvastatin treatment caused proteolysis of vimentin, a marker of epithelial to mesenchymal transition. This effect of fluvastatin was reversed in the presence of mevalonate, a downstream product of HMG-CoA and caspase-3 inhibitor. Interestingly, fluvastatin neither caused an appreciable cell death nor did modulate vimentin expression in normal mammary epithelial cells. In conclusion, fluvastatin alters levels of cytoskeletal proteins, primarily targeting vimentin through increased caspase-3- mediated proteolysis, thereby suggesting a role for vimentin in statin-induced breast cancer cell death.

Indexed as

Electrophoresis, Gel, Two-DimensionalAcyl Coenzyme AAnticholesteremic AgentsApoptosisBreast NeoplasmsCaspase 3Cell Line, TumorChromatography, High Pressure LiquidEpithelial-Mesenchymal TransitionFatty Acids, MonounsaturatedFemaleFluvastatinHumansIndolesMetabolic Networks and PathwaysMevalonic Acid3-hydroxy-3-methylglutaryl-coenzyme AAcyl Coenzyme AAnticholesteremic AgentsCaspase 3Fatty Acids, MonounsaturatedFluvastatinIndolesMevalonic AcidMitogen-Activated Protein Kinase 1ProteomeVimentin

Identifiers

PMID25268751
PMCPMC4182601
OpenAlexW2004422184

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.