Evidence map›Paper›PMID 21385902›Full record

ArticleCancer research2011

PrLZ protects prostate cancer cells from apoptosis induced by androgen deprivation via the activation of Stat3/Bcl-2 pathway.

Dong Zhang, Dalin He, Yan Xue, Ruoxiang Wang, Kaijie Wu, Hongjun Xie, Jin Zeng, Xinyang Wang, Haiyen E Zhau, Leland W K Chung and 2 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
  2. Article
  3. Molecular insights for the tumor suppressor role of SPOP in prostate cancer.Biochimica et biophysica acta. Reviews on cancer · 2026
    Review
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  7. The Tumor Suppressor TPD52-Governed Endoplasmic Reticulum Stress is Modulated by APCAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
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  10. Article
  11. Article
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  20. Isoform 1 of TPD52 (PC-1) promotes neuroendocrine transdifferentiation in prostate cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Dong ZhangDepartment of Urology, The First Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, Shaanxi, PR China.
Dalin He
Yan Xue
Ruoxiang Wang
Kaijie Wu
Hongjun Xie
Jin Zeng
Xinyang Wang
Haiyen E Zhau
Leland W K Chung
Luke S Chang
Lei Li
Cedars-Sinai Medical Center · USFirst Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

Prostate Cancer Bone Metastasis: Biology and TargetingP01CA098912 · NCI · EMORY UNIVERSITY · PI TIGHIOUART, MOURAD · 2003 to 2019
$24.0M
Beta 2-Microglobulin signaling and targeting in bone metastasisR01CA122602 · NCI · CEDARS-SINAI MEDICAL CENTER · PI CHUNG, LELAND W.K. · 2009 to 2013
$1.5M
NCI NIH HHS P01 CA098912NCI NIH HHS R01 CA122602
6 · The paper itself

Abstract

PrLZ/PC-1 is a newly identified, prostate-specific and androgen-inducible gene. Our previous study showed that PrLZ can enhance the proliferation and invasive capability of LNCaP cells, contributing to the development of prostate cancer. However, its potential role in androgen-independent processes remains elusive. In this study, we showed that PrLZ enhanced in vitro growth and colony formation of prostate cancer cells on androgen deprivation as well as tumorigenicity in castrated nude mice. In addition, PrLZ stabilized mitochondrial transmembrane potential, prevented release of cytochrome c from mitochondria to cytoplasm, and inhibited intrinsic apoptosis induced by androgen depletion. Mechanistically, PrLZ elevated the phosphorylation of Akt and Stat3 and upregulated Bcl-2 expression. Our data indicate that PrLZ protects prostate cancer cells from apoptosis and promotes tumor progression following androgen deprivation. In summary, we propose that PrLZ is a novel antiapoptotic gene that is specifically activated in prostate cancer cells escaping androgen deprivation may offer an appealing therapeutic target to prevent or treat advanced prostate malignancy.

Indexed as

ApoptosisAndrogensAnimalsBlotting, WesternCell Line, TumorCharcoalChromonesDextransEnzyme InhibitorsHumansMaleMembrane Potential, MitochondrialMiceMice, Inbred BALB CMice, NudeMorpholines2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneAndrogensCharcoalChromonesDextransEnzyme InhibitorsMorpholinesNeoplasm ProteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2STAT3 protein, humanSTAT3 Transcription FactorTPD52 protein, human

Identifiers

PMID21385902
PMCPMC3680512
OpenAlexW1999821224

What OpenQuestion holds

Textmetadata
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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.