Evidence map›Paper›PMID 26067567›Full record

ArticleViruses2015

Lentiviral Vector Mediated Claudin1 Silencing Inhibits Epithelial to Mesenchymal Transition in Breast Cancer Cells.

Xianqi Zhao, Yanan Zou, Qingqing Gu, Guannan Zhao, Horace Gray, Lawrence M Pfeffer, Junming Yue

Open access · goldAbstract read
In one paragraph

Article in Viruses, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  19. CLDN1 Increases Drug Resistance of Non-Small Cell Lung Cancer by Activating Autophagy via Up-Regulation of ULK1 Phosphorylation.Medical science monitor : international medical journal of experimental and clinical research · 2017
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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

7 authors at 2 institutions in 2 countries.

Xianqi ZhaoDepartment of Medicine, Harbin Medical University, Harbin 150086, China. ynzou@sina.com.
Yanan ZouDepartment of Medicine, Harbin Medical University, Harbin 150086, China. yzou4@uthsc.edu.
Qingqing GuDepartment of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA. qgu4@uthsc.edu.
Guannan ZhaoDepartment of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA. gzhao4@uthsc.edu.
Horace GrayDepartment of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA. horacegray1991@yahoo.com.
Lawrence M PfefferDepartment of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA. lpfeffer@uthsc.edu.
Junming YueDepartment of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA. jyue@uthsc.edu.
University of Tennessee Health Science Center · USHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer has a high incidence and mortality rate worldwide. Several viral vectors including lentiviral, adenoviral and adeno-associated viral vectors have been used in gene therapy for various forms of human cancer, and have shown promising effects in controlling tumor development. Claudin1 (CLDN1) is a member of the tetraspan transmembrane protein family that plays a major role in tight junctions and is associated with tumor metastasis. However, the role of CLDN1 in breast cancer is largely unexplored. In this study, we tested the therapeutic potential of silencing CLDN1 expression in two breast cancer (MDA-MB-231 and MCF7) cell lines using lentiviral vector mediated RNA interference. We found that a CLDN1 short hairpin (shRNA) construct efficiently silenced CLDN1 expression in both breast cancer cell lines, and CLDN1 knockdown resulted in reduced cell proliferation, survival, migration and invasion. Furthermore, silencing CLDN1 inhibited epithelial to mesenchymal transition (EMT) by upregulating the epithelial cell marker, E-cadherin, and downregulating mesenchymal markers, smooth muscle cell alpha-actin (SMA) and Snai2. Our data demonstrated that lentiviral vector mediated CLDN1 RNA interference has great potential in breast cancer gene therapy by inhibiting EMT and controlling tumor cell growth.

Indexed as

Gene SilencingAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCell MovementCell ProliferationCell SurvivalClaudin-1Epithelial CellsEpithelial-Mesenchymal TransitionFemaleGenetic VectorsHumansLentivirusModels, BiologicalRNA InterferenceAntineoplastic AgentsClaudin-1CLDN1 protein, humanRNA, Small Interferingbreast cancerCLDN1epithelial to mesenchymal transition

Identifiers

PMID26067567
PMCPMC4488722
OpenAlexW1520568004

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.