Evidence map›Paper›PMID 27462784›Full record

ArticleOncotarget2016

Ligand activated progesterone receptor B drives autophagy-senescence transition through a Beclin-1/Bcl-2 dependent mechanism in human breast cancer cells.

Francesca De Amicis, Carmela Guido, Marta Santoro, Francesca Giordano, Ada Donà, Pietro Rizza, Michele Pellegrino, Ida Perrotta, Daniela Bonofiglio, Diego Sisci and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. 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
2.4field-weighted citation impact, top 11% 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, 21 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

14 authors at 2 institutions in 1 country.

Francesca De AmicisCentro Sanitario, University of Calabria, Rende, Italy.
Carmela GuidoCentro Sanitario, University of Calabria, Rende, Italy.
Marta SantoroCentro Sanitario, University of Calabria, Rende, Italy.
Francesca GiordanoDepartment of Pharmacy, Health Science and Nutrition, University of Calabria, Rende, Italy.
Ada DonàCentro Sanitario, University of Calabria, Rende, Italy.
Pietro RizzaDepartment of Pharmacy, Health Science and Nutrition, University of Calabria, Rende, Italy.
Michele PellegrinoDepartment of Pharmacy, Health Science and Nutrition, University of Calabria, Rende, Italy.
Ida PerrottaDiBEST University of Calabria, Rende, Italy.
Daniela BonofiglioCentro Sanitario, University of Calabria, Rende, Italy.
Diego SisciCentro Sanitario, University of Calabria, Rende, Italy.
Maria Luisa PannoDepartment of Pharmacy, Health Science and Nutrition, University of Calabria, Rende, Italy.
Donatella TramontanoDepartment of Molecular Medicine and Medical Biotechnologies, University of Naples "Federico II", Naples, Italy.
Saveria AquilaCentro Sanitario, University of Calabria, Rende, Italy.
Sebastiano AndòCentro Sanitario, University of Calabria, Rende, Italy.
University of Calabria · ITUniversity of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of progesterone-receptors (PR) expression is associated with breast cancer progression. Herein we provide evidence that OHPg/PR-B through Beclin-1 evoke autophagy-senescence transition, in breast cancer cells. Specifically, OHPg increases Beclin-1 expression through a transcriptional mechanism due to the occupancy of Beclin-1 promoter by PR-B, together with the transcriptional coactivator SRC-2. This complex binds at a canonical half progesterone responsive element, which is fundamental for OHPg effects, as shown by site-directed mutagenesis. Beside, OHPg via non-genomic action rapidly activates JNK, which phosphorylates Bcl-2, producing the functional release from Beclin-1 interaction. This is not linked to an efficient autophagic flux, since p62 levels, marker of degradation via lysosomes, were not reduced after sustained OHPg stimulus. Instead, the cell cycle inhibitor p27 was induced, together with an irreversible G1 arrest, hallmark of cellular senescence. Specifically the increase of senescence-associated β-galactosidase activity was blocked by Bcl-2 siRNA but also by Beclin-1 siRNA. Collectively these findings support the importance of PR-B expression in breast cancer cells, thus targeting PR-B may be a useful strategy to provide additional approaches to existing therapies for breast cancer patients.

Indexed as

AutophagyCellular SenescenceBeclin-1beta-GalactosidaseBreast NeoplasmsCell CycleCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p16Gene Expression Regulation, NeoplasticGenomicsHumansLigandsMCF-7 CellsMutagenesis, Site-DirectedPlasmidsBCL2 protein, humanBeclin-1BECN1 protein, humanbeta-GalactosidaseCDKN2A protein, humanCyclin-Dependent Kinase Inhibitor p16LigandsProgesteroneprogesterone receptor BProto-Oncogene Proteins c-bcl-2Receptors, ProgesteroneRNA, Small InterferingTranscription FactorsBcl-2cell cycle arrestp16pRbprogesterone

Identifiers

PMID27462784
PMCPMC5295403
OpenAlexW2506811219

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.