Evidence map›Paper›PMID 25003983›Full record

ArticleOncotarget2014

The tumor suppressive role of CAMK2N1 in castration-resistant prostate cancer.

Tao Wang, Zhuo Liu, Shuiming Guo, Licheng Wu, Mingchao Li, Jun Yang, Ruibao Chen, Hua Xu, Shaoxin Cai, Hui Chen and 11 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 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.5field-weighted citation impact, top 10% 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, 44 citations in OpenAlex.

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  12. Elucidation of the Molecular Mechanism UnderlyingInternational journal of molecular sciences · 2019
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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

21 authors at 6 institutions in 2 countries.

Tao WangDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei, China; Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei, China.
Zhuo Liu
Shuiming Guo
Licheng Wu
Mingchao Li
Jun Yang
Ruibao Chen
Hua Xu
Shaoxin Cai
Hui Chen
Weiyong Li
Liang Wang
Zhiquan Hu
Qianyuan Zhuang
Shaohua Xu
Liping Wang
Jihong Liu
Zhangqun Ye
Jun-Yuan Ji
Chenguang Wang
Ke ChenDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei, China; Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Hubei, China.
Tongji Hospital · CNHuazhong University of Science and Technology · CNThomas Jefferson University · USUnion Hospital · CNSidney Kimmel Cancer Center · USTexas A&M University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer at advanced stages including metastatic and castration-resistant cancer remains incurable due to the lack of effective therapies. The CAMK2N1 gene, cloned and characterized as an inhibitor of CaMKII (calcium/calmodulin-dependent protein kinase II), has been shown to affect tumorigenesis and tumor growth. However, it is still unknown whether CAMK2N1 plays a role in prostate cancer development. We first examined the protein and mRNA levels of CAMK2N1 and observed a significant decrease in human prostate cancers comparing to normal prostate tissues. Re-expression of CAMK2N1 in prostate cancer cells reduced cellular proliferation, arrested cells in G0/G1 phases, and induced apoptotic cell death accompanied by down-regulation of IGF-1, ErbB2, and VEGF downstream kinases PI3K/AKT, as well as the MEK/ERK-mediated signaling pathways. Conversely, knockdown of CAMK2N1 had a significant opposite effects on these phenotypes. Our analyses suggest that CAMK2N1 plays a tumor suppressive role in prostate cancer cells. Reduced CAMK2N1 expression correlates to human prostate cancer progression and predicts poor clinical outcome, indicating that CAMK2N1 may serve as a biomarker. The inhibition of tumor growth by expressing CAMK2N1 established a role of CAMK2N1 as a therapeutic target.

Indexed as

AnimalsApoptosisCell ProliferationDisease ProgressionGenes, Tumor SuppressorHeterograftsHumansMaleMice, NudeProstatic Neoplasms, Castration-ResistantProteinsRNA, MessengerSignal TransductionCAMK2N1 protein, humanProteinsRNA, Messenger

Identifiers

PMID25003983
PMCPMC4116507
OpenAlexW1541668489

What OpenQuestion holds

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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.