Association of HOMER1 rs2290639 with suicide attempts in Hong Kong Chinese and the potentially functional role of this polymorphism

نویسندگان

  • Shitao Rao
  • Marco H. B. Lam
  • Venus S. Y. Yeung
  • Yun Kwok Wing
  • Mary Miu Yee Waye
چکیده

OBJECTIVE Animal evidence and genetic studies suggest that HOMER1 (homer homolog 1) is involved in the etiology of suicidal behavior and major depression disorder (MDD). However, most of genetic studies were performed in Caucasians and the potentially functional role of associated polymorphisms in HOMER1 was seldom reported. The purpose of this study was to investigate the association of a HOMER1 polymorphism rs2290639 with suicide attempts (SA) and MDD in Hong Kong Chinese, and then briefly elucidate the potentially functional role of the associated polymorphism. METHODS NEO personality inventory, impulsiveness and depression rating scales were completed by the subjects. The association studies of HOMER1 rs2290639 with SA or MDD were performed by case-control association studies. The bioinformatics analyses were adapted to predict potential transcription factors binding sites for the associated polymorphism. RESULTS The association studies and meta-analysis suggested that the HOMER1 rs2290639 was significantly associated with susceptibility to SA but seemed not to be associated with MDD in Hong Kong Chinese. This polymorphism might affect the transcription of the HOMER1 gene through interacting with a reliable transcription factor as found by three of four bioinformatics tools. In addition, close correlations between impulsiveness and NEO personality five factors were found in SA and MDD patients, which provide a possible way to assess the impulsiveness of patients through subjects' personality profiles for Hong Kong Chinese. CONCLUSIONS The HOMER1 rs2290639 polymorphism was significantly associated with susceptibility to SA in Hong Kong Chinese affected by psychiatric disorders, which might be explained by the potentially functional role of this polymorphism.

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عنوان ژورنال:

دوره 5  شماره 

صفحات  -

تاریخ انتشار 2016