Evidence map›Paper›PMID 25294805›Full record

ArticleOncotarget2014

Transcriptional coactivator CBP upregulates hTERT expression and tumor growth and predicts poor prognosis in human lung cancers.

Wei Guo, Jianjun Lu, Meng Dai, Taihua Wu, Zhenlong Yu, Jingshu Wang, Wangbing Chen, Dingbo Shi, Wendan Yu, Yao Xiao and 8 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. 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
1.9field-weighted citation impact, top 14% 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, 25 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

18 authors at 6 institutions in 2 countries.

Wei GuoInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China. These authors contributed equally to this work.
Jianjun LuDepartment of Thoracic Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. These authors contributed equally to this work.
Meng DaiInstitute 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.
Zhenlong YuInstitute 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; Colaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Wangbing ChenSun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China; Colaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Dingbo ShiSun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China; Colaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Wendan YuInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Yao XiaoInstitute 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.
Zhipeng TangInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China.
Tingting XuInstitute 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; Colaborative Innovation Center of Cancer Medicine, Guangzhou, 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. Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China; Colaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Guangwei DuDepartment of Integrative Biology and Pharmacology, The University of Texas Health Science Center, Houston, Texas, USA.
Wuguo DengInstitute of Cancer Stem Cell & First Affiliated Hospital, Dalian Medical University, Dalian, China. Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China; Colaborative Innovation Center of Cancer Medicine, Guangzhou, China.
Dalian Medical University · CNFirst Affiliated Hospital of Dalian Medical University · CNSun Yat-sen University · CNState Key Laboratory of Oncology in South ChinaSun Yat-sen University Cancer Center · CNThe University of Texas Health Science Center at Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Upregulated expression and activation of human telomerase reverse transcriptase (hTERT) is a hallmarker of lung tumorigenesis. However, the mechanism underlying the aberrant hTERT activity in lung cancer cells remains poorly understood. In this study, we found the transcriptional co-activator CBP as a new hTERT promoter-binding protein that regulated hTERT expression and tumor growth in lung adenocarcinoma cells using a biotin-streptavidin-bead pulldown technique. Chromatin immunoprecipitation assay verified the immortalized cell and tumor cell-specific binding of CBP on hTERT promoter. Overexpression of exogenous CBP upregulated the expression of the hTERT promoter-driven luciferase and endogenous hTERT protein in lung cancer cells. Conversely, inhibition of CBP by CBP-specific siRNA or its chemical inhibitor repressed the expression of hTERT promoter-driven luciferase and endogenous hTERT protein as well as telomerase activity. Moreover, inhibition of CBP expression or activity also significantly reduced the proliferation of lung cancer cells in vitro and tumor growth in an xenograft mouse model in vivo. Immunohistochemical analysis of tissue microarrays of lung cancers revealed a positive correlation between CBP and hTERT. Importantly, the patients with high CBP and hTERT expression had a significantly shorter overall survival. Furthermore, CBP was found to interact with and acetylate transactivator Sp1 in lung cancer cells. Inhibition of CBP by CBP-specific siRNA or its chemical inhibitor significantly inhibited Sp1 acetylation and its binding to the hTERT promoter. Collectively, our results indicate that CBP contributes to the upregulation of hTERT expression and tumor growth, and overexpression of CBP predicts poor prognosis in human lung cancers.

Indexed as

AcetylationAdenocarcinomaAdenocarcinoma of LungAnimalsCell Line, TumorCell ProliferationCell SurvivalCREB-Binding ProteinGene Expression Regulation, NeoplasticHumansLung NeoplasmsMiceMice, NudeNeoplasm TransplantationPrognosisPromoter Regions, GeneticCREB-Binding ProteinRNA, Small InterferingSP1 protein, humanSp1 Transcription FactorTelomeraseTERT protein, human

Identifiers

PMID25294805
PMCPMC4253439
OpenAlexW2100774938

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.