Evidence map›Paper›PMID 27588475›Full record

ArticleOncotarget2016

NKAIN2 functions as a novel tumor suppressor in prostate cancer.

Xueying Mao, Fei Luo, Lara K Boyd, Bowei Zhou, Yanling Zhang, Elzbieta Stankiewicz, Jacek Marzec, Natasa Vasiljevic, Yongwei Yu, Ninghan Feng and 8 more

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
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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.

Xueying MaoCentre for Molecular Oncology, Barts Cancer Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Fei LuoDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Lara K BoydCentre for Molecular Oncology, Barts Cancer Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Bowei ZhouDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Yanling ZhangDepartment of Pathology, The First Affiliated Hospital, Zhejiang University Medical College, Hangzhou, 310009, China.
Elzbieta StankiewiczCentre for Molecular Oncology, Barts Cancer Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Jacek MarzecCentre for Molecular Oncology, Barts Cancer Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Natasa VasiljevicCentre for Cancer Prevention, Wolfson Institute of Preventive Medicine, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Yongwei YuDepartment of Pathology, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China.
Ninghan FengDepartment of Urology, Wuxi Second People's Hospital, Nanjing Medical University, Wuxi, 214002, China.
Jia XuKey Laboratory of Proteomics of Guangdong Province and Key Laboratory of Transcriptomics and Proteomics of Human Diseases Supported by The Ministry of Education of China, Southern Medical University, Guangzhou, 510515, China.
Attila LorinczCentre for Cancer Prevention, Wolfson Institute of Preventive Medicine, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Yong JiangKey Laboratory of Proteomics of Guangdong Province and Key Laboratory of Transcriptomics and Proteomics of Human Diseases Supported by The Ministry of Education of China, Southern Medical University, Guangzhou, 510515, China.
Claude ChelalaCentre for Molecular Oncology, Barts Cancer Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Guoping RenDepartment of Pathology, The First Affiliated Hospital, Zhejiang University Medical College, Hangzhou, 310009, China.
Daniel M BerneyCentre for Molecular Oncology, Barts Cancer Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Shan-Chao ZhaoDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Yong-Jie LuCentre for Molecular Oncology, Barts Cancer Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, EC1M 6BQ, UK.
Queen Mary University of London · GBSouthern Medical University · CNFirst Affiliated Hospital Zhejiang University · CNNanfang Hospital · CNSecond Military Medical University · CNWuxi People's Hospital · CN

Funding

Medical Research Council G0701163
6 · The paper itself

Abstract

Recurrent chromosome breakpoints at 6q22.31, leading to truncation and potential loss-of-function of the NKAIN2 gene, in Chinese prostate cancer patients were previously identified. In this study we investigated genomic, methylation and expression changes of NKAIN2 in a large number of prostate cancer samples and determined its functional role in prostate cancer cells. Fluorescence in situ hybridization analysis confirmed that NKAIN2 truncation is specific to Chinese while deletion of the gene is frequent in both Chinese and UK prostate cancers. Significantly reduced expression of NKAIN2 was also detected at both RNA and protein levels. Somatic mutations of NKAIN2 in prostate cancer samples exist but at very low frequency, suggesting that it is a putative tumor suppressor gene (TSG) with haploid insufficiency. Our functional studies showed that overexpression of NKAIN2 in prostate cancer cells inhibits cellular growth by promoting cell apoptosis, and decreasing cell migration and invasion. Conversely, knockdown of NKAIN2 promotes prostate cancer cell growth by inhibiting cell apoptosis, and increasing cell migration and invasion. These data imply that NKAIN2 is a novel TSG whose activity is commonly reduced in prostate cancer. It may restrain the disease development and progression by inducing apoptosis and suppressing cancer cell growth, migration and invasion. This study provides new insights into prostate carcinogenesis and opportunities for development of novel therapies for prostate cancer.

Indexed as

Genes, Tumor SuppressorApoptosisCell Line, TumorCell MovementCell ProliferationDNA MethylationDNA Mutational AnalysisGene DeletionGenomicsHaploidyHigh-Throughput Nucleotide SequencingHumansIn Situ Hybridization, FluorescenceMaleMembrane ProteinsMutationMembrane ProteinsNKAIN2 protein, humanRNA, Small Interferingchromosomal deletion and truncationNKAIN2population differenceprostate cancertumor suppressor

Identifiers

PMID27588475
PMCPMC5325404
OpenAlexW2512353770

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.