Evidence map›Paper›PMID 24268029›Full record

ArticleMolecular cancer2013

PinX1 suppresses bladder urothelial carcinoma cell proliferation via the inhibition of telomerase activity and p16/cyclin D1 pathway.

Jian-Ye Liu, Dong Qian, Li-Ru He, Yong-Hong Li, Yi-Ji Liao, Shi-Juan Mai, Xiao-Peng Tian, Yan-Hui Liu, Jia-Xing Zhang, Hsiang-Fu Kung and 3 more

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Prognostic and Clinicopathological Value ofBioMed research international · 2018
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  19. PinX1 inhibits cell proliferation, migration and invasion in glioma cells.Medical oncology (Northwood, London, England) · 2015
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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

13 authors at 3 institutions in 1 country.

Jian-Ye LiuState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Collaborative Innovation Center for Cancer Medicine, No, 651, Dongfeng Road East, Guangzhou 510060, China. zhoufj@sysucc.org.cn.
Dong Qian
Li-Ru He
Yong-Hong Li
Yi-Ji Liao
Shi-Juan Mai
Xiao-Peng Tian
Yan-Hui Liu
Jia-Xing Zhang
Hsiang-Fu Kung
Yi-Xin Zeng
Fang-Jian Zhou
Dan Xie
Sun Yat-sen University Cancer Center · CNSun Yat-sen University · CNGuangdong Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPIN2/TRF1-interacting telomerase inhibitor1 (PinX1) was recently suggested as a putative tumor suppressor in several types of human cancer, based on its binding to and inhibition of telomerase. Moreover, loss of PinX1 has been detected in many human malignancies. However, the possible involvement of PinX1 and its clinical/prognostic significance in urothelial carcinoma of the bladder (UCB) are unclear.

methodsThe PinX1 expression profile was examined by quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and immunohistochemistry (IHC) in UCB tissues and adjacent normal urothelial bladder epithelial tissues. PinX1 was overexpressed and silenced in UCB cell lines to determine its role in tumorigenesis, development of UCB, and the possible mechanism.

resultsPinX1 expression in UCB was significantly down-regulated at both mRNA and protein level as compared with that in normal urothelial bladder epithelial tissues. PinX1 levels were inversely correlated with tumor multiplicity, advanced N classification, high proliferation index (Ki-67), and poor survival (P < 0.05). Moreover, overexpression of PinX1 in UCB cells significantly inhibited cell proliferation in vitro and in vivo, whereas silencing PinX1 dramatically enhanced cell proliferation. Overexpression of PinX1 resulted in G1/S phase arrest and cell growth/proliferation inhibition, while silencing PinX1 led to acceleration of G1/S transition, and cell growth/proliferation promotion by inhibiting/enhancing telomerase activity and via the p16/cyclin D1 pathway.

conclusionsThese findings suggest that down-regulation of PinX1 play an important role in the tumorigenesis and development of UCB and that the expression of PinX1 as detected by IHC is an independent molecular marker in patients with UCB.

Indexed as

AnimalsCarcinoma, Transitional CellCell Cycle ProteinsCell Line, TumorCell ProliferationCyclin D1Cyclin-Dependent Kinase Inhibitor p16FemaleGene ExpressionGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMaleMiceMice, Inbred BALB CMice, NudeCCND1 protein, humanCell Cycle ProteinsCyclin D1Cyclin-Dependent Kinase Inhibitor p16PINX1 protein, humanTelomeraseTERT protein, humanTumor Suppressor Proteins

Identifiers

PMID24268029
PMCPMC4176126
OpenAlexW2172234106

What OpenQuestion holds

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Registered trials

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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.