ArticleJournal of cancer research updates2012
PAX3-FKHR regulates the expression of pleiotrophin to mediate motility in alveolar rhabdomyosarcoma cells.
Article in Journal of cancer research updates, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
More than 80% of the aggressive alveolar rhabdomyosarcoma (ARMSs) harbor a PAX3-FKHR fusion transcription factor, which regulates cell motility and promotes metastasis. Our hypothesis is that PAX3-FKHR regulates cell motility by regulating the expression of its transcriptional targets that are also its downstream effectors, which if identified, may lead to novel therapeutic approaches for treating ARMS. Here we report that PAX3-FKHR regulates the expression of pleiotrophin (PTN) by binding specifically to a paired-box domain binding-site in the PTN promoter, indicating that PTN is a transcriptional target of PAX3-FKHR. Significantly, we show that PTN regulates ARMS cell motility. Taken together, we have identified PTN as a novel transcriptional target of PAX3-FKHR that promotes ARMS cell motility. PTN may be a novel therapeutic target for the treatment of ARMS.
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Registered trials
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