Evidence map›Paper›PMID 23070870›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2013

Aerosol delivery of lentivirus-mediated O-glycosylation mutant osteopontin suppresses lung tumorigenesis in K-ras (LA1) mice.

Arash Minai-Tehrani, Seung-Hee Chang, Jung-Taek Kwon, Soon-Kyung Hwang, Ji-Eun Kim, Ji-Young Shin, Kyeong-Nam Yu, Sung-Jin Park, Hu-Lin Jiang, Ji-Hye Kim and 7 more

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

2 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Role of osteopontin in the pathophysiology of cancer.Matrix biology : journal of the International Society for Matrix Biology · 2014
    Review
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

17 authors at 5 institutions in 2 countries.

Arash Minai-TehraniLaboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul, South Korea.
Seung-Hee Chang
Jung-Taek Kwon
Soon-Kyung Hwang
Ji-Eun Kim
Ji-Young Shin
Kyeong-Nam Yu
Sung-Jin Park
Hu-Lin Jiang
Ji-Hye Kim
Seong-Ho Hong
Bitna Kang
Duyeoul Kim
Chan-Hee Chae
Kee-Ho Lee
George R Beck
Myung-Haing Cho
Seoul National University · KRAdvanced Institute of Convergence Technology · KREmory University · USKorea Institute of Radiological and Medical Sciences · KRSeoul National University of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteopontin (OPN) is a secreted glycophosphoprotein that has been implicated in the regulation of cancer development. The function of OPN is primarily regulated through post-translational modification such as glycosylation. As yet, however, the relationship between OPN glycosylation and lung cancer development has not been investigated. In this study, we addressed this issue by studying the effect of a triple mutant (TM) of OPN, which is mutated at three O-glycosylation sites, on lung cancer development in K-ras (LA1) mice, a murine model for human non-small cell lung cancer.

methodsAerosolized lentivirus-based OPN TM was delivered into the lungs of K-ras (LA1) mice using a nose-only-inhalation chamber 3 times/wk for 4 wks. Subsequently, the effects of repeated delivery of OPN TM on lung tumorigenesis and its concomitant OPN-mediated signaling pathways were investigated.

resultsAerosol-delivered OPN TM inhibited lung tumorigenesis. In addition, the OPN-mediated Akt signaling pathway was inhibited. OPN TM also decreased NF-κB activity and the phosphorylation of 4E-BP1, while facilitating apoptosis in the lungs of K-ras (LA1) mice.

conclusionsOur results show that aerosol delivery of OPN TM successfully suppresses lung cancer development in the K-ras (LA1) mouse model and, therefore, warrant its further investigation as a possible therapeutic strategy for non-small cell lung cancer.

Indexed as

MutationAdaptor Proteins, Signal TransducingAerosolsAnimalsApoptosisBlotting, WesternCarrier ProteinsCell Cycle ProteinsCell Line, TumorCell Transformation, NeoplasticEukaryotic Initiation FactorsGenetic TherapyGene Transfer TechniquesGlycosylationLentivirusLung NeoplasmsAdaptor Proteins, Signal TransducingAerosolsAkt1 protein, mouseCarrier ProteinsCell Cycle ProteinsEif4ebp1 protein, mouseEukaryotic Initiation FactorsHras protein, mouseN-AcetylgalactosaminyltransferasesNF-kappa BOsteopontinPhosphoproteinsPolypeptide N-acetylgalactosaminyltransferaseProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)

Identifiers

PMID23070870
PMCPMC13012684
OpenAlexW1989399375

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.