Evidence map›Paper›PMID 25797267›Full record

ArticleOncotarget2015

Ku80 cooperates with CBP to promote COX-2 expression and tumor growth.

Yao Xiao, Jingshu Wang, Yu Qin, Yang Xuan, Yunlu Jia, Wenxian Hu, Wendan Yu, Meng Dai, Zhenglin Li, Canhui Yi and 14 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
7.6field-weighted citation impact, top 3% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. COX-2 in lung cancer: Mechanisms, development, and targeted therapies.Chronic diseases and translational medicine · 2024
    Review
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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

24 authors at 5 institutions in 1 country.

Yao XiaoInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Jingshu WangSun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Yu QinInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Yang XuanInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Yunlu JiaDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, China.
Wenxian HuDepartment of Surgical Oncology, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, China.
Wendan YuInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Meng DaiInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Zhenglin LiInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Canhui YiInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Shilei ZhaoInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Mei LiInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Sha DuInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Wei ChengInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Xiangsheng XiaoSun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Yiming ChenInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Taihua WuInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Songshu MengInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Yuhui YuanInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Quentin LiuInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Wenlin HuangSun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Wei GuoInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Shusen WangSun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Wuguo DengInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
First Affiliated Hospital of Dalian Medical University · CNDalian Medical University · CNSun Yat-sen University Cancer Center · CNZhejiang University · CNState Key Laboratory of Oncology in South China

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclooxygenase-2 (COX-2) plays an important role in lung cancer development and progression. Using streptavidin-agarose pulldown and proteomics assay, we identified and validated Ku80, a dimer of Ku participating in the repair of broken DNA double strands, as a new binding protein of the COX-2 gene promoter. Overexpression of Ku80 up-regulated COX-2 promoter activation and COX-2 expression in lung cancer cells. Silencing of Ku80 by siRNA down-regulated COX-2 expression and inhibited tumor cell growth in vitro and in a xenograft mouse model. Ku80 knockdown suppressed phosphorylation of ERK, resulting in an inactivation of the MAPK pathway. Moreover, CBP, a transcription co-activator, interacted with and acetylated Ku80 to co-regulate the activation of COX-2 promoter. Overexpression of CBP increased Ku80 acetylation, thereby promoting COX-2 expression and cell growth. Suppression of CBP by a CBP-specific inhibitor or siRNA inhibited COX-2 expression as well as tumor cell growth. Tissue microarray immunohistochemical analysis of lung adenocarcinomas revealed a strong positive correlation between levels of Ku80 and COX-2 and clinicopathologic variables. Overexpression of Ku80 was associated with poor prognosis in patients with lung cancers. We conclude that Ku80 promotes COX-2 expression and tumor growth and is a potential therapeutic target in lung cancer.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAnimalsAntigens, NuclearCell Line, TumorCell MovementCell ProliferationCyclooxygenase 2Disease ProgressionDNA-Binding ProteinsHeterograftsHumansKu AutoantigenLung NeoplasmsMicePromoter Regions, GeneticAntigens, NuclearCyclooxygenase 2DNA-Binding ProteinsKu AutoantigenPTGS2 protein, humanRNA, Small InterferingXrcc6 protein, humanXrcc6 protein, mouseCBPCOX-2Ku80lung cancer

Identifiers

PMID25797267
PMCPMC4480734
OpenAlexW1501165518

What OpenQuestion holds

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LicenceCC BY
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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.