Evidence map›Paper›PMID 26755645›Full record

ArticleOncotarget2016

STAT3-survivin signaling mediates a poor response to radiotherapy in HER2-positive breast cancers.

Jae-Sung Kim, Hyun-Ah Kim, Min-Ki Seong, Hyesil Seol, Jeong Su Oh, Eun-Kyu Kim, Jong Wook Chang, Sang-Gu Hwang, Woo Chul Noh

Open access · diamondAbstract readComparative Study
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 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
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  5. Overexpression ofEuropean journal of breast health · 2024
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  20. Radiation with STAT3 Blockade Triggers Dendritic Cell-T cell Interactions in the Glioma Microenvironment and Therapeutic Efficacy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020
    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

9 authors at 4 institutions in 1 country.

Jae-Sung KimDivision of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Hyun-Ah KimDepartment of Surgery, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Min-Ki SeongDepartment of Surgery, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Hyesil SeolDepartment of Pathology, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Jeong Su OhDepartment of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
Eun-Kyu KimDepartment of Surgery, Breast Cancer Center, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Gyeonggi-do, Korea.
Jong Wook ChangStem Cell Regenerative Medicine Center, Research Institute for Future Medicine, Samsung Medical Center, Seoul, Korea.
Sang-Gu HwangDivision of Radiation Cancer Research, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Woo Chul NohDepartment of Surgery, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Korea Institute of Radiological and Medical Sciences · KRSamsung Medical Center · KRSeoul National University Bundang Hospital · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although radiotherapy resistance is associated with locoregional recurrence and distant metastasis in breast cancers, clinically relevant molecular markers and critical signaling pathways of radioresistant breast cancer are yet to be defined. Herein, we show that HER2-STAT3-survivin regulation is associated with radiotherapy resistance in HER2-positive breast cancers. Depletion of HER2 by siRNA sensitized HER2-positive breast cancer cells to irradiation by decreasing STAT3 activity and survivin, a STAT3 target gene, expression in HER2-positive breast cancer cells. Furthermore, inhibition of STAT3 activation or depletion of survivin also sensitized HER2-positive breast cancer cells to irradiation, suggesting that the HER2-STAT3-survivin axis is a key pathway in radiotherapy resistance of HER2-positive breast cancer cells. In addition, our clinical analysis demonstrated the association between HER2-positive breast cancers and radiotherapy resistance. Notably, we found that increased expression of phosphorylated STAT3, STAT3, and survivin correlated with a poor response to radiotherapy in HER2-positive breast cancer tissues. These findings suggest that the HER2-STAT3-survivin axis might serve as a predictive marker and therapeutic target to overcome radiotherapy resistance in HER2-positive breast cancers.

Indexed as

Radiation ToleranceApoptosisBlotting, WesternBreast NeoplasmsCase-Control StudiesCell ProliferationErb-b2 Receptor Tyrosine KinasesFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansImmunoenzyme TechniquesInhibitor of Apoptosis ProteinsMiddle AgedNeoplasm Recurrence, LocalNeoplasm StagingBIRC5 protein, humanErb-b2 Receptor Tyrosine KinasesInhibitor of Apoptosis ProteinsReceptors, EstrogenReceptors, ProgesteroneRNA, Small InterferingSTAT3 Transcription FactorSurvivinbreast cancerHER2radioresistanceSTAT3survivin

Identifiers

PMID26755645
PMCPMC4872768
OpenAlexW2285791739

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.