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Methylation of PTCH1a gene in a subset of gastric cancers

World Journal of Gastroenterology 2009年第30期15卷 3799-3806页

作者： Peng Du Hai-Rong Ye Jun Gao Wei Chen Zhong-Chuan Wang Hong-Hua Jiang Ji Xu Ji-We Zhang Jian-Cheng Zhang Long Cui Department of Surgery Shanghai Xinhua Hospital Shanghai Jiao Tong University School of Medicine 1665 Kong Jiang Road Shanghai 200092 China Department of Anesthesiology Shanghai Xinhua Hospital Shanghai Jiao Tong University School of Medicine 1665 Kong Jiang Road Shanghai 200092 China Department of Gastroenterology Changhai Hospital Second Military Medical University Shanghai 200433 China Division of Ship Hygiene Navy Medical Research Institute Shanghai 200433 China

AIM： To establish if PTCHla transcriptional regulation region （TRR） is methylated in gastric cancer and its influence in gastric tumorigenesis.METHODS： The CpG islands in PTCHla TRR were analyzed by Methyl Primer Express v1.0 software. The region from -643 to -355 bp （the transcription initiation site of PTCHla was designated as 0） that contained 19 CpG sites was chosen for bisulfitesequencing PCR （BSP） and methylation-specific PCR （MSP） detection. The gastric cancer cell line AGS was treated with 5-aza-2′-deoxycytidine （5-Aza-dC; 1 μmol/L） for 3 d. Alterations in PTCHla TRR methylation in treated AGS cells was measured through BSP clone sequences, and their PTCH1 expression was measured by quantitative RT-PCR. The cell cycle and apoptosis were observed with flow cytometry through propidium iodide （PI） staining or annexin V/PI double staining. The prevalence of PTCHla TRR methylation was investigated in 170 gastric cancer tissue samples and the adjacent normal tissues by MSP. The correlation of PTCH1a TRR methylation with PTCH1 expression or with patients＇ clinical features was analyzed.RESULTS： Methylation of PTCHla TRR was observed in AGS ceils and a subset of gastric cancer tissues （32%, 55/170）, while no methylation amplification products were observed in any normal tissues by MSP. The methylation of PTCH1α TRR was correlated negatively with PTCH1 expression （Spearman＇s r = -0.380, P = 0.000）. However, methylation of PTCHla TRR was not related to the gastric cancer patients＇ clinical features, such as sex, age of onset, clinical stage, lymph node metastasis or histological grade. The methylation of PTCHla TRR in AGS cells was almost converted to non-methylation after 5-Aza-dC treatment, which increased PTCH1 expression （5.3 ± 2.5 times; n = 3） and apoptosis rate （3.0 ± 0.26 times; P 〈 0.05; n = 3）.CONCLUSION： Methylation of PTCH1α TRR is present in a subset of gastric cancers and correlated negatively with PTCH1 expression. This may be an early event in gast

关键词： Carcinogenesis Methylation Hedgehogsignaling pathway Methylation PTCH1 stomachneoplasms

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Apoptotic effect of Epigallocatechin-3-gallate on the human gastric cancer cell line MKN45 via activation of the mitochondrial pathway

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World Journal of Gastroenterology 2007年第31期13卷 4255-4259页

作者： Zhi-Hua Ran Qi xu Jin-Lu Tong Shu-Dong Xiao Departmentof Gastroenterology Renji Hospital Shanghai Jiao TongUniversity School of Medicine Shanghai Institute of DigestiveDisease Shanghai 200001 China

To investigate whether Epigallocatechin-3-gallate （EGCG） can induce apoptosis of the gastric cancer cell line MKN45 and its apoptotic ***： To determine this, apoptotic rates of MKN45 cells after EGCG treatment with or without caspase-3 inhibitor were evaluated by Annexin V-FITC ＋ PI staining The influence of EGCG on the activity of caspase-3 in the MKN45 cells was determined by ELISA. By Rhodamine123 staining, the membrane potential change of the mitochondrion was also investigated, and mRNAs and protein expression of the bcl-2 family were analyzed by RT-PCR and Western ***： EGCG can induce apoptosis of MKN45 cells in time- and dose-dependent manner. Eight hours after EGCG treatment, the activity of caspase-3 in the MKN45 increased, especially 12 h after treatment. The mitochondrial membrane potential was significantly weakened 4 h after EGCG insult. The mRNA and protein expression levels of pro-apoptotic members, such as Bax, Bid and Bad, were upregulated gradually as treated time increased. Moreover, the mRNA and protein expression levels of anti-apoptotic members, such as Bcl-xL and Bcl-2, were inhibited. CONCLUSION： These data support that EGCG can induce apoptosis of the human gastric cancer cell line MKN45, and the effect is in a time- and dose-dependent manner. The apoptotic pathway triggered by EGCG in MKN45 is mitochondrial-dependent.

关键词： Epigallocatechin-3-gallate stomachneoplasms Bcl-2 Apoptosis

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