Evidence map›Paper›PMID 25973065›Full record

ArticleInternational journal of clinical and experimental pathology2015

RNAi-mediated silencing of praline-rich gene causes growth reduction in human lung cancer cells.

Qingbo Zhao

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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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

1 author at 1 institution in 1 country.

Qingbo ZhaoDepartment of Emergency, 324 Hospital of The Chinese People's Liberation Army Chongqing 400020, China.
First People's Hospital of Chongqing · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer ranks among one of the most frequent causes of cancer death in the world. Here, we investigated PRR11, one novel gene, with no functional annotation, was found to be over-expressed in lung cancer patients suggesting its potential implication in tumorigenesis. Furthermore, high PRR11 levels predict shorter survival of lung cancer patients. In this study, we investigated the therapeutic potential of PRR11 in lung cancer using the technique of RNA silencing via small interfering RNA (siRNA). Synthetic siRNA duplexes against PRR11 were introduced into 3 lung cancer cell lines, which subsequently resulted in a significant depletion in PRR11 expression in the cells. We found that the targeted depletion of PRR11 caused a dramatic cell cycle arrest followed by massive apoptotic cell death, and eventually resulted in a significant decrease in growth and viability of all 2 lung cancer cell lines. In summary, our study strongly suggests that PRR11 may serve as a potential therapeutic target in human lung cancer.

Indexed as

Cell ProliferationRNA InterferenceApoptosisCell Cycle CheckpointsCell Line, TumorGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLung NeoplasmsProteinsRNA, Small InterferingTime FactorsTransfectionProteinsPRR11 protein, humanRNA, Small Interferingcell growthLung cancerPRR11 depletionRNAi

Identifiers

PMID25973065
PMCPMC4396257
OpenAlexW2413328493

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.