Evidence map›Paper›PMID 19724263›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2010

Multiple functions of the 37/67-kd laminin receptor make it a suitable target for novel cancer gene therapy.

Jonathan Scheiman, Jen-Chieh Tseng, Yun Zheng, Daniel Meruelo

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

38 citing papers in PubMed, 80 citations in OpenAlex.

  1. Gene Therapy Strategies for Uveal Melanoma: Adeno-associated Virus Delivery Challenges and Translational Opportunities.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
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  9. LRP1B: A Giant Lost in Cancer Translation.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  10. Src Mediates Epigallocatechin-3-Molecules (Basel, Switzerland) · 2020
    Article
  11. Article
  12. Review
  13. Article
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  18. Review
  19. Article
  20. A novel biomarker C6orf106 promotes the malignant progression of breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
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

4 authors at 1 institution in 1 country.

Jonathan ScheimanNYU Cancer Institute and the NYU Gene Therapy Center, NYU School of Medicine, New York, New York 10016, USA.
Jen-Chieh Tseng
Yun Zheng
Daniel Meruelo
NYU Langone Health · US

Funding

Sindbis Vectors For Advanced Pancreatic Cancer TherapyR01CA100687 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI MERUELO, DANIEL · 2004 to 2008
$1.5M
NCI NIH HHS CA100687NCI NIH HHS R01 CA100687
6 · The paper itself

Abstract

The 37/67-kd laminin receptor, LAMR, is a multifunctional protein that associates with the 40S ribosomal subunit and also localizes to the cell membrane to interact with the extracellular matrix. LAMR is overexpressed in many types of cancer, playing important roles in tumor-cell migration and invasion. Here, we show that LAMR is also vital for tumor-cell proliferation, survival, and protein translation. Small-interfering RNA (siRNA)-mediated reduction in expression of LAMR leads to G1 phase cell-cycle arrest in vitro by altering cyclins A2/B1, cyclin-dependent kinases (CDKs) 1/2, Survivin, and p21 expression levels. In vivo, reduction in LAMR expression results in inhibition of HT1080 cells to develop tumors. We also found that LAMR's ribosomal functions are critical for translation as reduction in LAMR expression leads to a dramatic decrease in newly synthesized proteins. Further, cells with lower expression of LAMR have fewer 40S subunits and 80S monosomes, causing an increase in free 60S ribosomal subunits. These results indicate that LAMR is able to regulate tumor development in many ways; further enhancing its potential as a target for gene therapy. To test this, we developed a novel Sindbis/Lenti pseudotype vector carrying short-hairpin RNA (shRNA) designed against lamr. This pseudotype vector effectively reduces LAMR expression and specifically targets tumors in vivo. Treatment of tumor-bearing severe combine immunodeficient (SCID) mice with this pseudotype vector significantly inhibits tumor growth. Thus, we show that LAMR can be used as a target in novel therapy for tumor reduction and elimination.

Indexed as

AnimalsBlotting, WesternCell CycleCell LineCell Line, TumorCell ProliferationCyclin-Dependent KinasesFemaleGenetic TherapyHumansMiceMice, SCIDNeoplasmsReceptors, LamininRibosome Subunits, Small, EukaryoticRNA, Small InterferingCyclin-Dependent KinasesReceptors, LamininRNA, Small Interfering

Identifiers

PMID19724263
PMCPMC2839218
OpenAlexW2033632216

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.