Evidence map›Paper›PMID 34360785›Full record

ArticleInternational journal of molecular sciences2021

Rapamycin Plus Doxycycline Combination Affects Growth Arrest and Selective Autophagy-Dependent Cell Death in Breast Cancer Cells.

Titanilla Dankó, Gábor Petővári, Dániel Sztankovics, Dorottya Moldvai, Regina Raffay, Péter Lőrincz, Tamás Visnovitz, Viktória Zsiros, Gábor Barna, Ágnes Márk and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 26 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

12 authors at 2 institutions in 1 country.

Titanilla Dankó1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, H-1085 Budapest, Hungary.
Gábor Petővári1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, H-1085 Budapest, Hungary.ORCID 0000-0002-1957-2864
Dániel Sztankovics1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, H-1085 Budapest, Hungary.
Dorottya Moldvai1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, H-1085 Budapest, Hungary.
Regina Raffay1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, H-1085 Budapest, Hungary.
Péter LőrinczDepartment of Anatomy, Cell and Developmental Biology, Eotvos Lorand University, Pázmány Péter sétány 1/c, H-1117 Budapest, Hungary.ORCID 0000-0001-7374-667X
Tamás VisnovitzDepartment of Genetics, Cell- and Immunobiology, Semmelweis University, Nagyvárad tér 4, H-1089 Budapest, Hungary.ORCID 0000-0002-7962-5083
Viktória ZsirosDepartment of Anatomy, Histology and Embryology, Semmelweis University, Tűzoltó utca 58, H-1094 Budapest, Hungary.
Gábor Barna1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, H-1085 Budapest, Hungary.
Ágnes Márk1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, H-1085 Budapest, Hungary.
Ildikó Krencz1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, H-1085 Budapest, Hungary.ORCID 0000-0003-3601-8723
Anna Sebestyén1st Department of Pathology and Experimental Cancer Research, Semmelweis University, Üllői út 26, H-1085 Budapest, Hungary.ORCID 0000-0001-8814-4794
Semmelweis University · HUEötvös Loránd University · HU

Funding

Higher Education Excellence Program at Semmelweis University FKIPHungarian Scientific Research Fund Higher Education Institutional Excellence Program - Therapeutic development OTKA120237Magyar Tudományos Akadémia PPD-222/2018National Research, Development and Innovation Office NKFI-FK-128404National Research, Development and Innovation Office VEKOP-2.3.2-16-2016-00002Nemzeti Kutatási Fejlesztési és Innovációs Hivatal National Bionics Program (Project no. ED_17-1-2017-0009)Semmelweis University Scientific and Innovation Funds STIA-KFI-2020
6 · The paper itself

Abstract

Metabolic alteration is characteristic during tumour growth and therapy; however, targeting metabolic rewiring could overcome therapy resistance. mTOR hyperactivity, autophagy and other metabolic processes, including mitochondrial functions, could be targeted in breast cancer progression. We investigated the growth inhibitory mechanism of rapamycin + doxycycline treatment in human breast cancer model systems. Cell cycle and cell viability, including apoptotic and necrotic cell death, were analysed using flow cytometry, caspase activity measurements and caspase-3 immunostainings. mTOR-, autophagy-, necroptosis-related proteins and treatment-induced morphological alterations were analysed by Wes

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsAutophagyBreast NeoplasmsCell ProliferationDoxycyclineFemaleHT29 CellsHumansMCF-7 CellsMitochondriaNeoplasm ProteinsSirolimusDoxycyclineNeoplasm ProteinsSirolimusautophagycell deathdoxycyclinemitophagyrapamycintumour growth

Identifiers

PMID34360785
PMCPMC8347279
OpenAlexW3185852598

What Socratic 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 Socratic graph.