Evidence map›Paper›PMID 29288516›Full record

ArticleCancer science2018

Interleukin-6/signal transducer and activator of transcription 3 promotes prostate cancer resistance to androgen deprivation therapy via regulating pituitary tumor transforming gene 1 expression.

Shengquan Huang, Qian Liu, Qianjin Liao, Qingjian Wu, Bishao Sun, Zhenxing Yang, Xiaoyan Hu, Mingjia Tan, Longkun Li

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.7field-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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  8. JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025
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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 3 institutions in 2 countries.

Shengquan HuangDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Qian LiuDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Qianjin LiaoXinqiao Community Health Service Center, Shapingba District, Chongqing, China.
Qingjian WuDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Bishao SunDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Zhenxing YangDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Xiaoyan HuDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Mingjia TanDivision of Radiation and Cancer Biology, Department of Radiation Oncology, University of Michigan, Ann Arbor, MI, USA.
Longkun LiDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.ORCID http://orcid.org/0000-0003-3939-5647
Army Medical University · CNUniversity of Michigan · USXinqiao Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer can progress from androgen dependence to androgen deprivation resistance with some unknown mechanisms. The current study aims to explore the possible role of pituitary tumor transforming gene1 (PTTG1) in castration-resistant prostate cancer (CRPC). Initially, we found that PTTG1 expression was significantly increased in androgen-independent prostate cancer cell lines PC3, DU145 and CRPC specimens compared with that in androgen-dependent prostate cancer cell line LNCaP and initial prostate cancer specimens. PTTG1 overexpression significantly enhanced the cell survival rate, clonality and tumorigenicity in LNCaP cells upon androgen-deprivation therapy (ADT). While knockdown of PTTG1 expression significantly elevated the sensitivity of DU145 cells to ADT. The effects of PTTG1 overexpression on LNCaP cells may be ascribed to the induced EMT and increased CD44

Indexed as

Drug Resistance, Neoplasm3' Untranslated RegionsAndrogen AntagonistsAnimalsCell Line, TumorCell SurvivalEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansInterleukin-6MaleMiceNeoplasm TransplantationProstatic Neoplasms, Castration-ResistantSecurinSTAT3 Transcription Factor3' Untranslated RegionsAndrogen AntagonistsIL6 protein, humanInterleukin-6pituitary tumor-transforming protein 1, humanSecurinSTAT3 protein, humanSTAT3 Transcription Factorcancer stem cellcastration-resistant prostate cancerepithelial-to-mesenchymal transitioninterleukin-6pituitary tumor transforming gene 1

Identifiers

PMID29288516
PMCPMC5834804
OpenAlexW2776681723

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.