Evidence map›Paper›PMID 27560771›Full record

ArticleCancer science2016

Inhibiting autophagy increases epirubicin's cytotoxicity in breast cancer cells.

Wei Guo, Yu Wang, Zhu Wang, Yan-Ping Wang, Hong Zheng

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  14. Autophagy: A Player in response to Oxidative Stress and DNA Damage.Oxidative medicine and cellular longevity · 2019
    Article
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  16. Article
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  18. Article
  19. Autophagy in Cancer Therapy.Frontiers in oncology · 2017
    Review
  20. Article
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

5 authors at 4 institutions in 1 country.

Wei GuoLaboratory of Molecular Diagnosis of Cancer, West China Hospital, West China Medical School, Sichuan University, Chengdu, China.
Yu WangLaboratory of Molecular Diagnosis of Cancer, West China Hospital, West China Medical School, Sichuan University, Chengdu, China.
Zhu WangLaboratory of Molecular Diagnosis of Cancer, West China Hospital, West China Medical School, Sichuan University, Chengdu, China.
Yan-Ping WangLaboratory of Molecular Diagnosis of Cancer, West China Hospital, West China Medical School, Sichuan University, Chengdu, China.
Hong ZhengLaboratory of Molecular Diagnosis of Cancer, West China Hospital, West China Medical School, Sichuan University, Chengdu, China.
Sichuan University · CNState Key Laboratory of BiotherapyWest China Hospital of Sichuan University · CNWest China Medical Center of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy, radiotherapy, and endocrinotherapy are documented to induce autophagy among breast cancer cells, but the role of autophagy in this disease has been attributed as cytoprotective as well as tumor-suppressing. Thus we studied MDA-MB-231 and SK-BR-3 breast cancer cell lines treated with epirubicin (EPI) to assess autophagy and apoptosis. We found out that EPI induced apoptosis and autophagy in both cell lines. The lysosomal inhibitor bafilomycin A1 inhibited cellular autophagy and enhanced EPI-triggered apoptosis, perhaps due to inhibition of autolysosome formation, which then inhibited autophagic effects of engulfing and clearing damaged mitochondria. This inhibition increased mitochondrial cytochrome C release which augmented epirubicin-induced caspase-dependent apoptosis and cytotoxicity. In addition, the lysosomal neutralizing agent ammonia chloride (AC), and Atg7 knockdown by siRNA, could inhibit epirubicin-triggered autophagy, enhance cytotoxicity, and increase caspase-9- and caspase-3-dependent apoptosis. Thus, autophagy plays a prosurvival role in EPI-treated MDA-MB-231 and SK-BR-3 cells, and autophagy inhibition can potentially reverse this effect and increase the cytotoxicity of EPI.

Indexed as

Ammonium ChlorideApoptosisAutophagosomesAutophagyBreast NeoplasmsCaspase 3Caspase 9Cell Line, TumorCytochromes cEpirubicinHumansIn Situ Nick-End LabelingLysosomesMacrolidesMitochondriaNeoplastic Stem CellsAmmonium Chloridebafilomycin A1Caspase 3Caspase 9Cytochromes cEpirubicinMacrolidesAutophagybafilomycin A1breast cancercytotoxicityepirubicin

Identifiers

PMID27560771
PMCPMC5132286
OpenAlexW2514076633

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.