Evidence map›Paper›PMID 22677939›Full record

ArticleCancer gene therapy2012

Overexpression of CIAPIN1 inhibited pancreatic cancer cell proliferation and was associated with good prognosis in pancreatic cancer.

X Chen, X Li, J Chen, P Zheng, S Huang, X Ouyang

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 13 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

X ChenDepartment of Medicine Oncology, Fuzhou General Hospital of Nanjing Military Command, Fujian, China. cxzpc81@gmail.com
X Li
J Chen
P Zheng
S Huang
X Ouyang
Fuzhou General Hospital of Nanjing Military Command · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytokine-induced antiapoptotic molecule (CIAPIN1), a newly identified apoptosis inhibitor, has been found to participate in the process of proliferation and tumorigenicity for several cancers. The aim of this study was to evaluate the prognostic value of CIAPIN1 in pancreatic cancer and to probe its function in pancreatic carcinogenesis. We found that CIAPIN1 protein was absent or reduced in pancreatic cancer cell lines. There was also a loss or decrease in CIAPIN1 expression in 118 cases of pancreatic cancer tissues as compared with that in 82 cases of normal pancreatic tissues. In a Cox proportional hazards model, CIAPIN1 expression independently predicted better survival (P<0.0001). Adenoviral-mediated restoration of CIAPIN1 expression greatly repressed the proliferation of pancreatic cancer cell in vitro and suppressed the tumorigenicity of pancreatic cancer cell in Balb/c nude mice. Our data also revealed that inhibition of pancreatic cancer cells proliferation by enforcing CIAPIN1 expression at least partly through delaying cell cycle progression and inducing cell apoptosis. In summary, our work revealed a novel function of CIAPIN1, which might possibly be used as an independent prognostic factor and a potential therapeutic target for pancreatic cancer.

Indexed as

Gene Expression Regulation, NeoplasticIntracellular Signaling Peptides and ProteinsNeoplasms, ExperimentalPancreatic NeoplasmsAnimalsApoptosisCell Line, TumorCell ProliferationCell Transformation, NeoplasticHumansMiceMice, NudePrognosisProportional Hazards ModelsCIAPIN1 protein, humanIntracellular Signaling Peptides and Proteins

Identifiers

PMID22677939
OpenAlexW2073708081

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.