Evidence map›Paper›PMID 26876202›Full record

ArticleOncogene2016

Secretory leukocyte protease inhibitor is a survival and proliferation factor for castration-resistant prostate cancer.

D Zheng, B Gui, K P Gray, I Tinay, S Rafiei, Q Huang, C J Sweeney, A S Kibel, L Jia

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 38 citations in OpenAlex.

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  11. Plasma concentrations of secretory leukocyte protease inhibitor (SLPI) differ depending on etiology and severity in community-onset bloodstream infection.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 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

9 authors at 4 institutions in 1 country.

D ZhengCenter for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, MO, USA.
B GuiDivision of Urology, Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
K P GrayDepartment of Biostatistics and Computational Biology, Dana-Farber Cancer Institute and Harvard School of Public Health, Boston, MA, USA.
I TinayDivision of Urology, Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
S RafieiDivision of Urology, Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Q HuangCenter for Pharmacogenomics, Department of Medicine, Washington University School of Medicine, St Louis, MO, USA.
C J SweeneyDepartment of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA, USA.
A S KibelDivision of Urology, Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
L JiaDivision of Urology, Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Brigham and Women's Hospital · USHarvard University · USWashington University in St. Louis · USDana-Farber Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Androgen receptor (AR)-mediated gene expression continues to have a critical role in promoting castration-resistant prostate cancer (CRPC) survival and growth even after androgen deprivation therapy. AR cistrome analyses in CRPC cells have identified a large number of AR target genes involved in proliferative and cell cycle-related functions, and hold promise for development of novel therapeutic approaches for CRPC. However, there is little understanding of how these genes function in vivo and what the clinical implications are. We previously reported that secretory leukocyte peptidase inhibitor (SLPI) is regulated by the AR in a ligand-independent manner in CRPC cells and required for CRPC cell proliferation under androgen-deprived conditions. SLPI is a secreted serine protease inhibitor, which is overexpressed in a number of cancers, including lung, breast and ovarian cancer, and involved in tumor progression. However, the oncogenic potential of SLPI in prostate cancer remains unknown. Here we provide the first evidence that SLPI is upregulated in a subset of CRPC cell lines and CRPC patient tumors. In addition, serum SLPI levels are significantly elevated in metastatic CRPC patients compared with hormone naive patients, raising the possibility that this could serve as a biomarker. We demonstrated that SLPI expression has functional significance, as it promotes CRPC cell survival and growth after androgen withdrawal in vivo and in vitro. Last, we demonstrated that the oncogenic effect of SLPI may be due to protection of growth factor progranulin from enzymatic cleavage or suppression of CRPC cell apoptosis independent of anti-protease activity of SLPI. These findings implicate SLPI as a potential biomarker of resistance to AR inhibition and therapeutic target for CRPC treatment.

Indexed as

AndrogensCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticHumansIntercellular Signaling Peptides and ProteinsMaleProgranulinsProstatic Neoplasms, Castration-ResistantReceptors, AndrogenSecretory Leukocyte Peptidase InhibitorSignal TransductionTranscriptional ActivationAndrogensGRN protein, humanIntercellular Signaling Peptides and ProteinsProgranulinsReceptors, AndrogenSecretory Leukocyte Peptidase InhibitorSLPI protein, human

Identifiers

PMID26876202
OpenAlexW2431032595

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.