ArticlePloS one2008
ICAM-2 expression mediates a membrane-actin link, confers a nonmetastatic phenotype and reflects favorable tumor stage or histology in neuroblastoma.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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.
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.
Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Dysregulation of the inside-out signaling pathway in CNS-infiltrated pediatric T-cell acute lymphoblastic leukemia.Research square · 2026Article
- Article
- Tumor cells escape immunosurveillance by hampering LFA-1.Frontiers in immunology · 2025Review
- Intercellular adhesion molecule 2 as a novel prospective tumor suppressor induced by ERG promotes ubiquitination-mediated radixin degradation to inhibit gastric cancer tumorigenicity and metastasis.Journal of translational medicine · 2023Article
- Article
- Review
- The immune system in cancer metastasis: friend or foe?Journal for immunotherapy of cancer · 2017Review
- Protein glycosylation in cancers and its potential therapeutic applications in neuroblastoma.Journal of hematology & oncology · 2016Review
- Identification and characterization of the intercellular adhesion molecule-2 gene as a novel p53 target.Oncotarget · 2016Article
- ICAM-2 confers a non-metastatic phenotype in neuroblastoma cells by interaction with α-actinin.Oncogene · 2015Article
- The role of ICAM-2 in neuroblastoma.Oncoscience · 2015Article
- Article
- Investigation of intercellular adhesion molecules (ICAMs) gene expressions in patients with Barrett's esophagus.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Glycobiology of neuroblastoma: impact on tumor behavior, prognosis, and therapeutic strategies.Frontiers in oncology · 2014Review
- N-glycosylation of ICAM-2 is required for ICAM-2-mediated complete suppression of metastatic potential of SK-N-AS neuroblastoma cells.BMC cancer · 2013Article
- Intercellular adhesion molecule-2 is involved in apical ectoplasmic specialization dynamics during spermatogenesis in the rat.The Journal of endocrinology · 2013Article
- Differential secretome analysis reveals CST6 as a suppressor of breast cancer bone metastasis.Cell research · 2012Article
- CASZ1, a candidate tumor-suppressor gene, suppresses neuroblastoma tumor growth through reprogramming gene expression.Cell death and differentiation · 2011Article
- Metastatic canine mammary carcinomas can be identified by a gene expression profile that partly overlaps with human breast cancer profiles.BMC cancer · 2010Article
- Intercellular adhesion molecules (ICAMs) and spermatogenesis.Human reproduction updateReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The actin cytoskeleton is a primary determinant of tumor cell motility and metastatic potential. Motility and metastasis are thought to be regulated, in large part, by the interaction of membrane proteins with cytoplasmic linker proteins and of these linker proteins, in turn, with actin. However, complete membrane-to-actin linkages have been difficult to identify. We used co-immunoprecipitation and competitive peptide assays to show that intercellular adhesion molecule-2 (ICAM-2)/alpha-actinin/actin may comprise such a linkage in neuroblastoma cells. ICAM-2 expression limited the motility of these cells and redistributed actin fibers in vitro, and suppressed development of disseminated tumors in an in vivo model of metastatic neuroblastoma. Consistent with these observations, immunohistochemical analysis demonstrated ICAM-2 expression in primary neuroblastoma tumors exhibiting features that are associated with limited metastatic disease and more favorable clinical outcome. In neuroblastoma cell lines, ICAM-2 expression did not affect AKT activation, tumorigenic potential or chemosensitivity, as has been reported for some types of transfected cells. The observed ICAM-2-mediated suppression of metastatic phenotype is a novel function for this protein, and the interaction of ICAM-2/alpha-actinin/actin represents the first complete membrane-linker protein-actin linkage to impact tumor cell motility in vitro and metastatic potential in an in vivo model. Current work focuses on identifying specific protein domains critical to the regulation of neuroblastoma cell motility and metastasis and on determining if these domains represent exploitable therapeutic targets.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.