Evidence map›Paper›PMID 21660043›Full record

ArticleLeukemia2011

Cooperative roles for emmprin and LYVE-1 in the regulation of chemoresistance for primary effusion lymphoma.

Z Qin, L Dai, M Bratoeva, M G Slomiany, B P Toole, C Parsons

Abstract read
In one paragraph

Article in Leukemia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Infection of human induced pluripotent stem cells by an oncogenic herpesvirus.Frontiers in cellular and infection microbiology · 2025
    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

6 authors at 3 institutions in 2 countries.

Z QinDepartment of Medicine, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
L Dai
M Bratoeva
M G Slomiany
B P Toole
C Parsons
Medical University of South Carolina · USMUSC Hollings Cancer Center · USTongji University · CN

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
THE ROLE OF THE RNA BINDING PROTEIN LA IN ORAL TUMOR BIOLOGYP20RR017696 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SOMMER, GUNHILD · 2002 to 2011
$20.7M
PERTURBATION OF HYALURONAN FUNCTION IN CANCERR01CA082867 · NCI · TUFTS UNIVERSITY BOSTON · PI TOOLE, BRYAN P · 1999 to 2010
$2.1M
Inhibition of Tumor Progression by Hyaluronan OligomersR01CA073839 · NCI · TUFTS UNIVERSITY BOSTON · PI TOOLE, BRYAN P · 1997 to 2008
$1.8M
Regulation of the Tumor Microenvironment by KSHVR01CA142362 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI PARSONS, CHRISTOPHER H · 2010 to 2014
$1.4M
NCI NIH HHS P30 CA138313NCI NIH HHS P30-CA138313NCI NIH HHS R01 CA073839NCI NIH HHS R01-CA073839NCI NIH HHS R01 CA082867NCI NIH HHS R01-CA082867NCI NIH HHS R01 CA142362NCI NIH HHS R01-CA142362NCRR NIH HHS P20 RR017696NCRR NIH HHS P20-RR017696
6 · The paper itself

Abstract

The Kaposi's sarcoma-associated herpesvirus is the causative agent of primary effusion lymphoma (PEL), for which cytotoxic chemotherapy represents the standard of care. The high mortality associated with PEL may be explained in part by resistance of these tumors to chemotherapy. The membrane-bound glycoprotein emmprin (CD147) enhances chemoresistance in tumors through effects on transporter expression, trafficking and interactions. Interactions between hyaluronan and hyaluronan receptors on the cell surface also facilitate emmprin-mediated chemoresistance. Whether emmprin or hyaluronan-receptor interactions regulate chemotherapeutic resistance for virus-associated malignancies is unknown. Using human PEL tumor cells, we found that PEL sensitivity to chemotherapy is directly proportional to expression of emmprin, the lymphatic vessel endothelial hyaluronan receptor-1 (LYVE-1) and a drug transporter known as the breast cancer resistance protein/ABCG2 (BCRP), and that emmprin, LYVE-1 and BCRP interact with each other and colocalize on the PEL cell surface. In addition, we found that emmprin induces chemoresistance in PEL cells through upregulation of BCRP expression, and RNA interference targeting of emmprin, LYVE-1 or BCRP enhances PEL cell apoptosis induced by chemotherapy. Finally, disruption of hyaluronan-receptor interactions using small hyaluronan oligosaccharides reduces expression of emmprin and BCRP while sensitizing PEL cells to chemotherapy. Collectively, these data support interdependent roles for emmprin, LYVE-1 and BCRP in chemotherapeutic resistance for PEL.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsBase SequenceBasiginCell Line, TumorDNA PrimersFlow CytometryFluorescent Antibody TechniqueHumansLymphoma, Primary EffusionReal-Time Polymerase Chain ReactionRNA InterferenceVesicular Transport ProteinsAntineoplastic AgentsBasiginBSG protein, humanDNA PrimersLYVE1 protein, humanVesicular Transport Proteins

Identifiers

PMID21660043
PMCPMC3683648
OpenAlexW2066150200

What OpenQuestion holds

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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.