Evidence map›Paper›PMID 24742333›Full record

ArticleMolecular cancer2014

E2F1 renders prostate cancer cell resistant to ICAM-1 mediated antitumor immunity by NF-κB modulation.

Zijia Ren, Wenyao Kang, Lihua Wang, Baoliang Sun, Jiajia Ma, Chaogu Zheng, Jie Sun, Zhigang Tian, Xiaoyi Yang, Weihua Xiao

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

24 citing papers in PubMed, 44 citations in OpenAlex.

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  20. Checkpoint Kinase 1 Inhibition Enhances Cisplatin Cytotoxicity and Overcomes Cisplatin Resistance in SCLC by Promoting Mitotic Cell Death.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2019
    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

10 authors at 4 institutions in 1 country.

Zijia Ren
Wenyao Kang
Lihua Wang
Baoliang Sun
Jiajia Ma
Chaogu Zheng
Jie Sun
Zhigang Tian
Xiaoyi YangCAS Key Laboratory of Innate Immunity and Chronic Disease, Innovation Center for Cell Biology, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, Anhui 230027, China. xyyang@tsmc.edu.cn.
Weihua Xiao
Hefei National Center for Physical Sciences at Nanoscale · CNUniversity of Science and Technology of China · CNTaishan Medical University · CNWeifang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundE2F1 is the gatekeeper of the cell cycle controlling an analogous balance between proliferation and cell death. E2F1 expression is elevated in advanced prostate cancer. However, it is still unclear that the roles and mechanisms of E2F1 on prostate cancers.

methodsTargeted knockdown by interferon RNA was applied on two prostate cancer and Hela cell lines to examine the inverse correlation expression of E2F1 and ICAM-1. ICAM-1 promoter reporter and ChIP assays were used for analysis of the molecular basis of transcriptional regulation of E2F1 on ICAM-1. Co-IP assays were employed for testing the protein interaction between E2F1 and NF-κB. Tumor xenograft mice model with E2F1 and ICAM-1-knockdown prostate cancer cells were used to investigate the effects of E2F1 and ICAM-1 on antitumor immunity.

resultsE2F1 knockdown by a specific short hairpin RNA increased gene transcription and protein expression of ICAM-1. By using wild type and a series of mutant ICAM-1 promoter luciferase constructs, the NF-κB binding sites were found to be important for E2F1 regulation of ICAM-1 promoter. Targeted knockdown of E2F1 did not affect expression and phosphorylation of NF-κB and IκBα, but facilitated NF-κB binding to the ICAM-1 promoter, subsequently induced ICAM-1 transcription and production in prostate carcinoma cells. Furthermore, knockdown of E2F1 inhibited tumor growth of prostate cancer in vivo through increasing the susceptibility of tumor cells to ICAM-1-mediated anti-tumor immunity including enhancement of monocyte adhesion, leucocytes infiltration, as well as cytotoxicity against tumor cells.

conclusionsE2F1 knockdown inhibited prostate tumor growth in vitro and in vivo through sensitizing tumor cells to ICAM-1 mediated anti-immunity by NF-κB modulation, highlighting the potential of E2F1 as a therapeutic target.

Indexed as

AnimalsApoptosisE2F1 Transcription FactorGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeLa CellsHumansI-kappa B ProteinsImmunity, InnateIntercellular Adhesion Molecule-1MaleMiceNF-kappa BNF-KappaB Inhibitor alphaPromoter Regions, GeneticProstatic NeoplasmsE2F1 protein, humanE2F1 Transcription FactorI-kappa B ProteinsIntercellular Adhesion Molecule-1NF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanNfkbia protein, mouse

Identifiers

PMID24742333
PMCPMC4004456
OpenAlexW2115290743

What OpenQuestion holds

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LicenceCC BY
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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.