Evidence map›Paper›PMID 27463802›Full record

ArticlePLoS pathogens2016

KSHV-Mediated Regulation of Par3 and SNAIL Contributes to B-Cell Proliferation.

Hem C Jha, Zhiguo Sun, Santosh K Upadhyay, Darine W El-Naccache, Rajnish K Singh, Sushil K Sahu, Erle S Robertson

RetractedOpen access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 15% 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, 33 citations in OpenAlex.

  1. Article
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  7. Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022
    Review
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  20. Cellular responses to human cytomegalovirus infection: Induction of a mesenchymal-to-epithelial transition (MET) phenotype.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Hem C JhaDepartment of Otorhinolaryngology-Head and Neck Cancer, and Tumor Virology Program and Tumor Virology Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Zhiguo SunDepartment of Otorhinolaryngology-Head and Neck Cancer, and Tumor Virology Program and Tumor Virology Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Santosh K UpadhyayDepartment of Otorhinolaryngology-Head and Neck Cancer, and Tumor Virology Program and Tumor Virology Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Darine W El-NaccacheDepartment of Otorhinolaryngology-Head and Neck Cancer, and Tumor Virology Program and Tumor Virology Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Rajnish K SinghDepartment of Otorhinolaryngology-Head and Neck Cancer, and Tumor Virology Program and Tumor Virology Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Sushil K SahuDepartment of Otorhinolaryngology-Head and Neck Cancer, and Tumor Virology Program and Tumor Virology Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Erle S RobertsonDepartment of Otorhinolaryngology-Head and Neck Cancer, and Tumor Virology Program and Tumor Virology Program, Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
University of Pennsylvania · US

Funding

TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Ken Hashigiwa Cadwell · 1997 to 2026
$32.5M
Role of LANA-RBP-jk During Early KSHV InfectionP01CA174439 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2013 to 2018
$8.7M
Genome Persistence of KSHVR01CA171979 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2013 to 2017
$1.5M
EBV Antigen and Cell Cycle RegulationR01CA137894 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2009 to 2013
$1.4M
KSHV genome modification in KS tissueR01CA177423 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2013 to 2015
$594k
NCI NIH HHS P01 CA174439NCI NIH HHS R01 CA137894NCI NIH HHS R01 CA171979NCI NIH HHS R01 CA177423NIDDK NIH HHS P30 DK050306
6 · The paper itself

Abstract

Studies have suggested that Epithelial-Mesenchymal Transition (EMT) and transformation is an important step in progression to cancer. Par3 (partitioning-defective protein) is a crucial factor in regulating epithelial cell polarity. However, the mechanism by which the latency associated nuclear antigen (LANA) encoded by Kaposi's Sarcoma associated herpesvirus (KSHV) regulates Par3 and EMTs markers (Epithelial-Mesenchymal Transition) during viral-mediated B-cell oncogenesis has not been fully explored. Moreover, several studies have demonstrated a crucial role for EMT markers during B-cell malignancies. In this study, we demonstrate that Par3 is significantly up-regulated in KSHV-infected primary B-cells. Further, Par3 interacted with LANA in KSHV positive and LANA expressing cells which led to translocation of Par3 from the cell periphery to a predominantly nuclear signal. Par3 knockdown led to reduced cell proliferation and increased apoptotic induction. Levels of SNAIL was elevated, and E-cadherin was reduced in the presence of LANA or Par3. Interestingly, KSHV infection in primary B-cells led to enhancement of SNAIL and down-regulation of E-cadherin in a temporal manner. Importantly, knockdown of SNAIL, a major EMT regulator, in KSHV cells resulted in reduced expression of LANA, Par3, and enhanced E-cadherin. Also, SNAIL bound to the promoter region of p21 and can regulate its activity. Further a SNAIL inhibitor diminished NF-kB signaling through upregulation of Caspase3 in KSHV positive cells in vitro. This was also supported by upregulation of SNAIL and Par3 in BC-3 transplanted NOD-SCID mice which has potential as a therapeutic target for KSHV-associated B-cell lymphomas.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntigens, ViralBlotting, WesternB-LymphocytesCell Cycle ProteinsCell Transformation, ViralEpithelial-Mesenchymal TransitionFemaleFluorescent Antibody TechniqueGene Expression RegulationHerpesviridae InfectionsHerpesvirus 8, HumanHumansImmunohistochemistryImmunoprecipitationAdaptor Proteins, Signal TransducingAntigens, ViralCell Cycle Proteinslatency-associated nuclear antigenMembrane ProteinsNuclear ProteinsPARD3 protein, humanSnail Family Transcription Factors

Identifiers

PMID27463802
PMCPMC4963126
OpenAlexW2487722884

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.