2012Chin J PancreatolRequires access

Heterogeneous PTEN inhibits ASPC-1 cell proliferation, invasion and metastasis

Hongyu Li, Xu Liu, Chunyan Wu, Jiajun Zhao, Xiaozhong Guo

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Abstract

Objective To investigate the effects of heterogeneous phosphatase and tensinhomologue deleted on chromosome ten (PTEN) on cell cycles,proliferation,invasion,tumorigenicity,metastasis and the expressions of vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR)proteins in human pancreas cancer cell line ( ASPC-1 ).Methods ASPC-1 cells was transfected with plasmid pE-PTEN containing PTEN,and empty plasmid pE-PTEN transfection was used as control,then ASPC-1-pE-PTEN (A-pE-P) cell and ASPC-1-pE (A-pE) cell was obtained.The expression of PTEN mRNA was determined by RT-PCR. PTEN,VEGF and EGFR proteins were measured by cell immunohistochemical method.Clone formation assay was used to observe the numbers of clone.Transwell was used to test the invasion ability of cells.The growths of tumor were detected by nude mice subcutaneous injection of cancer cells in vivo.Results Compared with ASPC-1,the expressions of PTEN mRNA of A-pE-P increased by 179.3%,and the expressions of PTEN protein were also significantly increased.The expressions of VEGF protein were significantly decreased.The expressions of EGFR protein were not significantly changed.Number of G2/M phase cells was significantly increased from (26.81 ± 1.03)% to (31.5 ± 1.76)% (P <0.05).The numbers of clone was decreased by 28% (P <0.05).The number of penetrating cells was decreased[(46.3 ±6.6) vs (63.8 ±7.5) per high power field,P <0.05].The tumor volumes were significantly reduced [(142.4 ±30.9) vs (202.7 ±43.6) mm3,P <0.05].The tumor inhibitory rate was 42.4%.The distant metastases were significantly reduced [(2.0 ±0.7) vs (5.0 ± 1.3),P <0.01 ].Conclusions Heterogeneous PTEN can not only inhibit the proliferation,invasion and metantasis of ASPC-1 cells,arrest the cell growth at G2/M phase,but also decrease the expressions of VEGF. Key words: Pancreatic neoplasms;  Gene, tumor suppressor;  Transfection;  Phosphatase and tensinhomology deleted on chromosome ten

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Objective To investigate the effects of heterogeneous phosphatase and tensinhomologue deleted on chromosome ten (PTEN) on cell cycles,proliferation,invasion,tumorigenicity,metastasis and the expressions of vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR)proteins in human pancreas cancer cell line ( ASPC-1 ).Methods ASPC-1 cells was transfected with plasmid pE-PTEN containing PTEN,and empty plasmid pE-PTEN transfection was used as control,then ASPC-1-pE-PTEN (A-pE-P) cell and ASPC-1-pE (A-pE) cell was obtained.The expression of PTEN mRNA was determined by RT-PCR. PTEN,VEGF and EGFR proteins were measured by cell immunohistochemical method.Clone formation assay was used to observe the numbers of clone.Transwell was used to test the invasion ability of cells.The growths of tumor were detected by nude mice subcutaneous injection of cancer cells in vivo.Results Compared with ASPC-1,the expressions of PTEN mRNA of A-pE-P increased by 179.3%,and the expressions of PTEN protein were also significantly increased.The expressions of VEGF protein were significantly decreased.The expressions of EGFR protein were not significantly changed.Number of G2/M phase cells was significantly increased from (26.81 ± 1.03)% to (31.5 ± 1.76)% (P <0.05).The numbers of clone was decreased by 28% (P <0.05).The number of penetrating cells was decreased[(46.3 ±6.6) vs (63.8 ±7.5) per high power field,P <0.05].The tumor volumes were significantly reduced [(142.4 ±30.9) vs (202.7 ±43.6) mm3,P <0.05].The tumor inhibitory rate was 42.4%.The distant metastases were significantly reduced [(2.0 ±0.7) vs (5.0 ± 1.3),P <0.01 ].Conclusions Heterogeneous PTEN can not only inhibit the proliferation,invasion and metantasis of ASPC-1 cells,arrest the cell growth at G2/M phase,but also decrease the expressions of VEGF. Key words: Pancreatic neoplasms;  Gene, tumor suppressor;  Transfection;  Phosphatase and tensinhomology deleted on chromosome ten

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Available abstract

Objective To investigate the effects of heterogeneous phosphatase and tensinhomologue deleted on chromosome ten (PTEN) on cell cycles,proliferation,invasion,tumorigenicity,metastasis and the expressions of vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR)proteins in human pancreas cancer cell line ( ASPC-1 ).Methods ASPC-1 cells was transfected with plasmid pE-PTEN containing PTEN,and empty plasmid pE-PTEN transfection was used as control,then ASPC-1-pE-PTEN (A-pE-P) cell and ASPC-1-pE (A-pE) cell was obtained.The expression of PTEN mRNA was determined by RT-PCR. PTEN,VEGF and EGFR proteins were measured by cell immunohistochemical method.Clone formation assay was used to observe the numbers of clone.Transwell was used to test the invasion ability of cells.The growths of tumor were detected by nude mice subcutaneous injection of cancer cells in vivo.Results Compared with ASPC-1,the expressions of PTEN mRNA of A-pE-P increased by 179.3%,and the expressions of PTEN protein were also significantly increased.The expressions of VEGF protein were significantly decreased.The expressions of EGFR protein were not significantly changed.Number of G2/M phase cells was significantly increased from (26.81 ± 1.03)% to (31.5 ± 1.76)% (P <0.05).The numbers of clone was decreased by 28% (P <0.05).The number of penetrating cells was decreased[(46.3 ±6.6) vs (63.8 ±7.5) per high power field,P <0.05].The tumor volumes were significantly reduced [(142.4 ±30.9) vs (202.7 ±43.6) mm3,P <0.05].The tumor inhibitory rate was 42.4%.The distant metastases were significantly reduced [(2.0 ±0.7) vs (5.0 ± 1.3),P <0.01 ].Conclusions Heterogeneous PTEN can not only inhibit the proliferation,invasion and metantasis of ASPC-1 cells,arrest the cell growth at G2/M phase,but also decrease the expressions of VEGF. Key words: Pancreatic neoplasms;  Gene, tumor suppressor;  Transfection;  Phosphatase and tensinhomology deleted on chromosome ten

Key concepts: PTEN, Transfection, Metastasis, clone (Java method), Cancer research, Cell growth, Cell, Biology

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