Evidence map›Paper›PMID 25821797›Full record

ReviewBioMed research international2015

Calcium homeostasis and ER stress in control of autophagy in cancer cells.

Elżbieta Kania, Beata Pająk, Arkadiusz Orzechowski

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed
13.5field-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

122 citing papers in PubMed, 226 citations in OpenAlex.

  1. Review
  2. The influence of exercise duration on inhibiting endoplasmic reticulum stress in ischemic stroke rats.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
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  6. Calcium Signaling Modulator 4-MPTC Reduces Proliferative and Migration Activities of MDA-MB-468 Breast Cancer Cells.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2026
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62 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

3 authors at 2 institutions in 1 country.

Elżbieta KaniaElectron Microscopy Platform, Mossakowski Medical Research Centre, Polish Academy of Sciences, A. Pawińskiego 5 Street, 02-106 Warsaw, Poland.
Beata PająkElectron Microscopy Platform, Mossakowski Medical Research Centre, Polish Academy of Sciences, A. Pawińskiego 5 Street, 02-106 Warsaw, Poland ; Department of Physiological Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences (SGGW), Nowoursynowska 159 Street, 02-776 Warsaw, Poland.
Arkadiusz OrzechowskiElectron Microscopy Platform, Mossakowski Medical Research Centre, Polish Academy of Sciences, A. Pawińskiego 5 Street, 02-106 Warsaw, Poland ; Department of Physiological Sciences, Faculty of Veterinary Medicine, Warsaw University of Life Sciences (SGGW), Nowoursynowska 159 Street, 02-776 Warsaw, Poland.ORCID 0000-0003-1307-2823
Warsaw University of Life Sciences · PLMossakowski Medical Research Institute, Polish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a basic catabolic process, serving as an internal engine during responses to various cellular stresses. As regards cancer, autophagy may play a tumor suppressive role by preserving cellular integrity during tumor development and by possible contribution to cell death. However, autophagy may also exert oncogenic effects by promoting tumor cell survival and preventing cell death, for example, upon anticancer treatment. The major factors influencing autophagy are Ca(2+) homeostasis perturbation and starvation. Several Ca(2+) channels like voltage-gated T- and L-type channels, IP3 receptors, or CRAC are involved in autophagy regulation. Glucose transporters, mainly from GLUT family, which are often upregulated in cancer, are also prominent targets for autophagy induction. Signals from both Ca(2+) perturbations and glucose transport blockage might be integrated at UPR and ER stress activation. Molecular pathways such as IRE 1-JNK-Bcl-2, PERK-eIF2α-ATF4, or ATF6-XBP 1-ATG are related to autophagy induced through ER stress. Moreover ER molecular chaperones such as GRP78/BiP and transcription factors like CHOP participate in regulation of ER stress-mediated autophagy. Autophagy modulation might be promising in anticancer therapies; however, it is a context-dependent matter whether inhibition or activation of autophagy leads to tumor cell death.

Indexed as

Calcium SignalingHomeostasisAnimalsAutophagyCalciumEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPHumansNeoplasmsOxidative StressCalciumEndoplasmic Reticulum Chaperone BiPHSPA5 protein, human

Identifiers

PMID25821797
PMCPMC4363509
OpenAlexW2040767197

What OpenQuestion holds

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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.