Abstract
Abstract Semaphorins are a family of axon guidance molecules, which signal through their co-receptors neuropilins and plexins to subserve various functions in the nervous system, the immune system and during organogenesis. Contrary to their role in development, accumulating evidence suggests the pro- and anti-tumorigenic functions of semaphorins and plexins in different cancer types. Similar to other semaphorins, semaphorin 5A (Sema5A) has recently been implicated in various cancers, though its functions remain ambiguous. Our former study revealed the suppressive effect of Sema5A in glioma cell migration and invasion. Analysis of human glioma specimens revealed a marked down-regulation of Sema5A protein expression in high grade glioblastomas, which are highly infiltrative. Here, we provide evidence that forced expression of Sema5A inhbits glioma cell proliferation by disrupting the cell cycle. Taken together, these findings suggest a tumor suppressor function of Sema5A in glioma. Interestingly, real-time quantitative PCR analysis revealed no significant difference in Sema5A mRNA levels across different grades of glioma. Analysis of Sema5A gene in human glioma specimens detected no mutations but the presence of various alternatively spliced variants that could potentially lead to premature truncation of Sema5A protein. Notably, the predominant Sema5A splice variant is expressed at almost equal level as the wild-type counterpart in the glioma specimens analysed. Ectopic expression of this truncated isoform in fact results in an unstable protein that is targeted for proteasomal degradation. These findings reinforce our hypothesis that reduced Sema5A protein levels in glioblastomas could compromise its suppressive effects in glioma progression. Citation Format: Fathima Rifkhana Shah Jahan, Alan Yiu Wah Lee. Genetic analysis of semaphorin 5A and plexin-B3 in human glioma. [abstract]. In: Proceedings of the Third AACR International Conference on Frontiers in Basic Cancer Research; Sep 18-22, 2013; National Harbor, MD. Philadelphia (PA): AACR; Cancer Res 2013;73(19 Suppl):Abstract nr A53.
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