Evidence map›Paper›PMID 27384485›Full record

ArticleOncotarget2016

Inhibition of ERα/ERK/P62 cascades induces "autophagic switch" in the estrogen receptor-positive breast cancer cells exposed to gemcitabine.

Peng Shen, Ming Chen, Mengye He, Luoquan Chen, Yinjing Song, Peng Xiao, Xiaopeng Wan, Feng Dai, Ting Pan, Qingqing Wang

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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 22 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

10 authors at 2 institutions in 1 country.

Peng ShenDepartment of Medical Oncology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, PR China.
Ming ChenDepartment of Medical Oncology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, PR China.
Mengye HeInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, PR China.
Luoquan ChenInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, PR China.
Yinjing SongInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, PR China.
Peng XiaoInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, PR China.
Xiaopeng WanInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, PR China.
Feng DaiInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, PR China.
Ting PanInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, PR China.
Qingqing WangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, PR China.
Zhejiang University · CNFirst Affiliated Hospital Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several clinical trials revealed that estrogen receptor (ER) status had relevance to the response of mammary malignancy to chemotherapy. Autophagy has emerged as an important cellular mechanism of tumor cells in response to anticancer therapy. The aim of this study is to investigate whether gemcitabine induces autophagy, and more importantly, whether such autophagy is functional relevant to the therapeutic effects of gemcitabine in breast cancer cells in relation to the ER status. In our study, autophagy was induced both in ER+ MCF-7 and ER- MDA-MB-231 cells by gemcitabine markedly, while the autophagy plays distinct roles - cytoprotective in ER- MDA-MB-231 and cytotoxic in ER+ MCF-7 cells. Gemcitabine treatment leads to the activation of ERα-ERK-P62 signal pathway in MCF-7 cells which may augment the autophagic degradation, thus results in the excessive activation of autophagy and irreversible autophagic cell death eventually. Inhibition of ERα-ERK-P62 cascades in MCF-7 cells by small interfering RNA or PD98059 impairs the autophagic degradation, and leads to "autophagic switch" - from cytotoxic autophagy to cytoprotection. Moreover, stable overexpression of ERα in the ER- BCap37 breast cancer cell line enhances the gemcitabine-induced autophagy flux and switches the autophagic cytoprotection in ER- BCap37 to cytotoxicity effect in ER+ BCap37 cells. Our study firstly demonstrated that ER status influences gemcitabine efficacy via modulating the autophagy in breast cancer cells.

Indexed as

Antimetabolites, AntineoplasticAutophagyBeclin-1Breast NeoplasmsCytoprotectionDeoxycytidineEstrogen Receptor alphaFemaleFlavonoidsGemcitabineHumansMCF-7 CellsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3ProhibitinsRNA Interference2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneAntimetabolites, AntineoplasticBeclin-1BECN1 protein, humanDeoxycytidineESR1 protein, humanEstrogen Receptor alphaFlavonoidsGemcitabineMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PHB2 protein, humanProhibitinsRNA, Small InterferingSequestosome-1 ProteinSQSTM1 protein, humanautophagybreast cancerestrogen receptorgemcitabineP62

Identifiers

PMID27384485
PMCPMC5217034
OpenAlexW2462025199

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.