Evidence map›Paper›PMID 24122203›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014

Human kallikrein 2 (KLK2) promotes prostate cancer cell growth via function as a modulator to promote the ARA70-enhanced androgen receptor transactivation.

Zhiqun Shang, Yuanjie Niu, Qiliang Cai, Jing Chen, Jing Tian, Shuyuan Yeh, Kuo-Pao Lai, Chawnshang Chang

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 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
2.0field-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

33 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Human Kallikrein 2: A Novel Lineage-Specific Surface Target in Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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  15. Emerging Immunotherapy Approaches for Treating Prostate Cancer.International journal of molecular sciences · 2023
    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

8 authors at 3 institutions in 2 countries.

Zhiqun Shang
Yuanjie Niu
Qiliang Cai
Jing Chen
Jing Tian
Shuyuan Yeh
Kuo-Pao Lai
Chawnshang Chang
University of Rochester Medical Center · USSecond Hospital of Tianjin Medical University · CNTianjin Medical University · CN

Funding

Non-AR mediated DHT-promoted Bladder Cancer initiation and progressionR01CA155477 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG · 2011 to 2015
$1.6M
Stromal AR Roles in Prostate Hyperplasia and CancerR01CA156700 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2011 to 2015
$1.6M
NCI NIH HHS CA155477NCI NIH HHS CA156700
6 · The paper itself

Abstract

Recent data suggested that tissue human kallikrein 2 (KLK2) might be involved in the carcinogenesis and tumor metastasis of prostate cancer (PCa). However, the detailed pathophysiological roles of KLK2 in PCa remain unclear. We report here that KLK2 may be treated as a potential therapeutic target in castration-resistant PCa (CRPC). Histologic analyses show that the increased KLK2 expression is correlated with higher cell proliferation rate and lower cell apoptosis index in CRPC specimens. Adding functional KLK2 cDNA into high passage LNCaP cells led to increased cell growth, and knockdown of KLK2 expression with KLK2-siRNA in LNCaP cells resulted in increased cell apoptosis with cell growth arrest at the G1 phase. Results from in vitro colony formation assay and in vivo xenografted PCa tissues also demonstrated that targeting KLK2 led to suppressed growth of PCa in the castration-resistant stage. Further mechanism dissection shows that KLK2 may cooperate with the AR coregulator, ARA70, to enhance AR transactivation that may result in alteration of PCa formation. Together, these results suggested KLK2 might become a new therapeutic target to battle the CRPC and KLK2-siRNA may be developed as an alternative approach to suppress PCa growth.

Indexed as

Cell ProliferationAnimalsBlotting, WesternCell Line, TumorFlow CytometryGene Expression Regulation, NeoplasticHeterograftsHumansImmunohistochemistryIn Situ Nick-End LabelingMaleMice, Inbred BALB CNuclear Receptor CoactivatorsProstatic NeoplasmsReal-Time Polymerase Chain ReactionReceptors, AndrogenNCOA4 protein, humanNuclear Receptor CoactivatorsReceptors, AndrogenTissue Kallikreins

Identifiers

PMID24122203
OpenAlexW2021850762

What OpenQuestion holds

Textmetadata
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.