Evidence map›Paper›PMID 26893781›Full record

ArticleOncology letters2016

Overexpression of ErbB2 renders breast cancer cells susceptible to 3-BrPA through the increased dissociation of hexokinase II from mitochondrial outer membrane.

Sujie Gao, Xuebo Chen, Hongyong Jin, Shengnan Ren, Zhuo Liu, Xuedong Fang, Guizhen Zhang

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.2field-weighted citation impact, top 41% 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

7 citing papers in PubMed, 16 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

7 authors at 3 institutions in 1 country.

Sujie GaoDepartment of Anesthesiology, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China; Central Research Laboratory, The Second Hospital, Jilin University, Changchun, Jilin 130041, P.R. China.
Xuebo ChenDepartment of General Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.
Hongyong JinDepartment of General Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.
Shengnan RenDepartment of General Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.
Zhuo LiuDepartment of General Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.
Xuedong FangDepartment of General Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.
Guizhen ZhangCentral Research Laboratory, The Second Hospital, Jilin University, Changchun, Jilin 130041, P.R. China.
Jilin University · CNUnion Hospital · CNSecond Affiliated Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ErbB2 is known to upregulate glycolysis in breast cancer, however, the precise mechanisms remain unclear. In the present study, ErbB2 upregulated Hexokinase II (HK II) activity by increasing the binding of HK II to the mitochondrial outer membrane. Dysregulated glucose metabolism in high ErbB2-expressing breast cancer cells induces susceptibility to glucose starvation and glycolysis inhibition. Additionally, HK II has a tendency to dissociate from the mitochondria outer membrane in ErbB2-overexpressing cells following treatment with the HK II inhibitor, 3-BrPA. Furthermore, 3-BrPA treatment results in decreased mitochondria membrane potential and release of cytochrome

Indexed as

3-BrPAErbB2hexokinase II

Identifiers

PMID26893781
PMCPMC4734279
OpenAlexW2204180886

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.