Clinics and research in hepatology and gastroenterology · 2012
Reduced expression of PTEN and increased PTEN phosphorylation at residue Ser380 in gastric cancer tissues: a novel mechanism of PTEN inactivation.
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Yang Zhen, Yuan Xiao-Gang, Chen Jiang, Luo Shi-Wen, Luo Zhi-Jun, Lu Nong-Hua
Аннотация
AIM: PTEN is a tumor suppressor gene in different cancers. This study was to determine the protein expression of PTEN and phosphorylation of PTEN (p-PTEN) at residue Ser380 in different histology specimens of gastric tissues.
METHODS: A total of 179tissue specimens of normal gastric mucosa, chronic gastritis, intestinal metaplasia, dysplasia, and gastric cancer were recruited for immunohistochemical analysis of PTEN and p-PTEN expression. Four gastric cancer AGS, MKN-45, MKN-28, and SGC-7901 cell lines and a non-cancerous gastric GES-1 cell line were used to detect expression of PTEN and p-PTEN protein using Western blot.
RESULTS: Expression level of PTEN protein was significantly decreased in gastric cancer tissues compared to normal gastric mucosa, chronic gastritis, intestinal metaplasia and dysplasia (P<0.05). In contrast, p-PTEN protein level was significantly increased in intestinal metaplasia, dysplasia and gastric cancer compared to normal gastric mucosa and chronic gastritis (P<0.05). However, there was no any association of PTEN and p-PTEN expression with clinicopathological characteristics from gastric cancer patients. Moreover, the ratio of p-PTEN and PTEN was higher in gastric cancer cell lines than that of the non-malignant cells.
CONCLUSIONS: This study demonstrated that aberrant expression of PTEN and p-PTEN at residue Ser380 was early event that could contribute to gastric carcinogenesis, and that PTEN phosphorylation at residue Ser380 could be a mechanism for PTEN inactivation.
METHODS: A total of 179tissue specimens of normal gastric mucosa, chronic gastritis, intestinal metaplasia, dysplasia, and gastric cancer were recruited for immunohistochemical analysis of PTEN and p-PTEN expression. Four gastric cancer AGS, MKN-45, MKN-28, and SGC-7901 cell lines and a non-cancerous gastric GES-1 cell line were used to detect expression of PTEN and p-PTEN protein using Western blot.
RESULTS: Expression level of PTEN protein was significantly decreased in gastric cancer tissues compared to normal gastric mucosa, chronic gastritis, intestinal metaplasia and dysplasia (P<0.05). In contrast, p-PTEN protein level was significantly increased in intestinal metaplasia, dysplasia and gastric cancer compared to normal gastric mucosa and chronic gastritis (P<0.05). However, there was no any association of PTEN and p-PTEN expression with clinicopathological characteristics from gastric cancer patients. Moreover, the ratio of p-PTEN and PTEN was higher in gastric cancer cell lines than that of the non-malignant cells.
CONCLUSIONS: This study demonstrated that aberrant expression of PTEN and p-PTEN at residue Ser380 was early event that could contribute to gastric carcinogenesis, and that PTEN phosphorylation at residue Ser380 could be a mechanism for PTEN inactivation.