Details

Autor(en) / Beteiligte

• Yang, Xue-Xi
• Sun, Jing-Zhe
• Li, Fen-Xia
• Wu, Ying-Song
• Du, Hong-Yan
• Zhu, Wei
• Li, Xiang-Hong
• Li, Ming

Titel

Aberrant methylation and downregulation of sall3 in human hepatocellular carcinoma

Ist Teil von

• World journal of gastroenterology : WJG, 2012-06, Vol.18 (21), p.2719-2726

Ort / Verlag

United States: Baishideng Publishing Group Co., Limited

Erscheinungsjahr

2012

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• AIM： To investigated whether sall3 transcription was regulated by promoter CpG island hypermethylation in hepatocellular carcinoma （HCC）. METHODS： The cell lines Huh7, HepG2, SK-HEP1, SM-MC7721, Bel7402, QGY7703 and a cohort of 38 HCC tissue specimens and corresponding nontumorous tissues were subjected to analysis for sall3 promoter CpG island methylation and mRNA transcription. sall3 promoter CpG island methylation levels were determined using the MassARRAY platform and mRNA transcription levels of the gene were detected by quantitative realtime polymerase chain reaction.RESULTS： The levels of sall3 mRNA were decreased by more than twofold in 33 of 38 tumor tissues compared to adjacent noncancerous tissues. Among these 33 tumor tissues with lower levels of sall3 mRNA, 24 showed higher levels of methylation. Based on these results, we hypothesized that the decrease in sall3 mRNA transcription level was likely due to promoter CpG island hypermethylation. Changes in sall3 mRNA transcription and promoter CpG island methylation were determined in the above six cell lines after treatment with 0, 0.1, 0.5 and 2.5 mmol 5-aza-2-deoxycytidine, a demethylating agent. Promoter CpG island methylation levels de- creased in a dose-dependent manner in all six cell lines, while the mRNA transcription level increased dose-dependently in Huh7, HepG2, SK-HEP1 and SMMC7721 cells and irregularly in Bel7402 and QGY7703 cells. CONCLUSION： These results indicated that promoter CpG island hypermethylation contributes to the downregulation of sall3 mRNA transcription in HCC.