作者: Seung-Kyoon Kim , Hae-Ran Jang , Jeong-Hwan Kim , Seung-Moo Noh , Kyu-Sang Song
DOI: 10.1016/J.BBRC.2006.08.128
关键词: Gastric mucosa 、 Cancer cell 、 Tumor progression 、 Epigenetics 、 Biology 、 DNA methylation 、 Cell growth 、 Molecular biology 、 Metastasis 、 Cancer
摘要: Recent finding has shown that LIMS2 (also known as PINCH2) functions a natural regulator of the LIMS1-ILK-parvin complex formation and is associated with cell spreading migration via integrins at focal adhesions. Here, we report for first time epigenetic silencing in gastric tumors. Downregulation was detected 91% (10 11) cancer lines by real-time quantitative RT-PCR 80% (8 10) LIMS2-downregulated were CpG island hypermethylation 5'-upstream region LIMS2. Furthermore, restored its non-expressing after treatment 5-Aza-dC and/or trichostatin A. Loss expression also 53% (51 96) primary This decrease level significantly correlated an increase hypermethylation. In addition, methylation status any normal-appearing tissues gradually increased age-dependent manner, suggesting positive mucosa can be due to 'field cancerization effect' early event carcinogenesis. Moreover, transient transfection LIMS2-siRNA stimulated cells but had no effects on growth. These results suggest frequent inactivation alteration may important tumor progression events, such invasion metastasis. Thus, useful molecular biomarker therapeutic target increasing activity cancer.