Evidence map›Paper›PMID 30781465›Full record

ReviewInternational journal of molecular sciences2019

Endoplasmic Reticulum Stress and Unfolded Protein Response in Breast Cancer: The Balance between Apoptosis and Autophagy and Its Role in Drug Resistance.

Lorenza Sisinni, Michele Pietrafesa, Silvia Lepore, Francesca Maddalena, Valentina Condelli, Franca Esposito, Matteo Landriscina

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

104 citing papers in PubMed, 182 citations in OpenAlex.

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44 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 1 country.

Lorenza SisinniLaboratory of Pre-Clinical and Translational Research, IRCCS, Referral Cancer Center of Basilicata, 85028 Rionero in Vulture, Italy. lorisi@hotmail.com.
Michele PietrafesaLaboratory of Pre-Clinical and Translational Research, IRCCS, Referral Cancer Center of Basilicata, 85028 Rionero in Vulture, Italy. michele.pietrafesa@crob.it.
Silvia LeporeLaboratory of Pre-Clinical and Translational Research, IRCCS, Referral Cancer Center of Basilicata, 85028 Rionero in Vulture, Italy. silvia.lepore@crob.it.
Francesca MaddalenaLaboratory of Pre-Clinical and Translational Research, IRCCS, Referral Cancer Center of Basilicata, 85028 Rionero in Vulture, Italy. francesca.maddalena@crob.it.
Valentina CondelliLaboratory of Pre-Clinical and Translational Research, IRCCS, Referral Cancer Center of Basilicata, 85028 Rionero in Vulture, Italy. valentina.condelli@crob.it.
Franca EspositoDepartment of Molecular Medicine and Medical Biotechnology, University of Napoli Federico II, 80131 Naples, Italy. franca.esposito@unina.it.ORCID 0000-0001-9340-6875
Matteo LandriscinaLaboratory of Pre-Clinical and Translational Research, IRCCS, Referral Cancer Center of Basilicata, 85028 Rionero in Vulture, Italy. matteo.landriscina@unifg.it.ORCID 0000-0003-0591-9799
Centro di Riferimento Oncologico della Basilicata · ITUniversity of Foggia · ITUniversity of Naples Federico II · IT

Funding

Associazione Italiana per la Ricerca sul Cancro IG2015 Id.16738
6 · The paper itself

Abstract

The unfolded protein response (UPR) is a stress response activated by the accumulation of unfolded or misfolded proteins in the lumen of the endoplasmic reticulum (ER) and its uncontrolled activation is mechanistically responsible for several human pathologies, including metabolic, neurodegenerative, and inflammatory diseases, and cancer. Indeed, ER stress and the downstream UPR activation lead to changes in the levels and activities of key regulators of cell survival and autophagy and this is physiologically finalized to restore metabolic homeostasis with the integration of pro-death or/and pro-survival signals. By contrast, the chronic activation of UPR in cancer cells is widely considered a mechanism of tumor progression. In this review, we focus on the relationship between ER stress, apoptosis, and autophagy in human breast cancer and the interplay between the activation of UPR and resistance to anticancer therapies with the aim to disclose novel therapeutic scenarios. The hypothesis that autophagy and UPR may provide novel molecular targets in human malignancies is discussed.

Indexed as

ApoptosisAutophagyBreast NeoplasmsDrug Resistance, NeoplasmEndoplasmic ReticulumEndoplasmic Reticulum StressFemaleHumansSignal TransductionUnfolded Protein Responseapoptosisautophagybreast cancerdrug resistanceendoplasmic reticulum stresshormone therapyunfolded protein response

Identifiers

PMID30781465
PMCPMC6412864
OpenAlexW2914672066

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.