Zhiwang Song1, Chan Feng1, Yonglin Lu1, Yun Lin2, Chunyan Dong3. 1. Department of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, People's Republic of China. 2. Department of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, People's Republic of China. Electronic address: ylin96@sina.com. 3. Department of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, People's Republic of China. Electronic address: cydong_tongji@sina.com.
Abstract
PURPOSE: To investigate the expression, clinical significance, biological function, and the potential mechanism of PHGDH in pancreatic cancer. METHODS: The expression of PHGDH in human pancreatic cancer tissues and corresponding adjacent normal tissues were analyzed through immunohistochemistry staining. Simultaneously, the association between the PHGDH expression and the clinicopathological parameters and OS and DFS was evaluated. Human pancreatic cancer cell line BxPC-3 and SW1990 were selected to investigate the effect of PHGDH knockdown on cell proliferation, migration, and invasion. In addition, we performed western blot to assess the expression of cyclin B1, and cyclin D1, MMP-2, and MMP-9 protein. RESULTS: Our results suggested that the expression of PHGDH is increased in pancreatic cancer compared with adjacent normal tissues and the increased expression of PHGDH is associated with tumor size, lymph node metastasis, and TNM state of pancreatic cancer patients. Moreover, the expression of PHGDH is an independent prognostic indicator for pancreatic cancer patients. In addition, we found that knockdown of PHGDH in pancreatic cancer cells inhibits the cell proliferation, migration, and invasion abilities by down-regulating the expression of cyclin B1, and cyclin D1, MMP-2, and MMP-9. CONCLUSIONS: Our data indicated that the expression of PHGDH is increased in pancreatic cancer and is an independent molecular prognostic factor for pancreatic cancer patients. In addition, PHGDH controls cell proliferation, migration and invasion abilities. Therefore, PHGDH could serve as an important prognostic indicator and therapeutic target for pancreatic cancer.
PURPOSE: To investigate the expression, clinical significance, biological function, and the potential mechanism of PHGDH in pancreatic cancer. METHODS: The expression of PHGDH in humanpancreatic cancer tissues and corresponding adjacent normal tissues were analyzed through immunohistochemistry staining. Simultaneously, the association between the PHGDH expression and the clinicopathological parameters and OS and DFS was evaluated. Humanpancreatic cancer cell line BxPC-3 and SW1990 were selected to investigate the effect of PHGDH knockdown on cell proliferation, migration, and invasion. In addition, we performed western blot to assess the expression of cyclin B1, and cyclin D1, MMP-2, and MMP-9 protein. RESULTS: Our results suggested that the expression of PHGDH is increased in pancreatic cancer compared with adjacent normal tissues and the increased expression of PHGDH is associated with tumor size, lymph node metastasis, and TNM state of pancreatic cancerpatients. Moreover, the expression of PHGDH is an independent prognostic indicator for pancreatic cancerpatients. In addition, we found that knockdown of PHGDH in pancreatic cancer cells inhibits the cell proliferation, migration, and invasion abilities by down-regulating the expression of cyclin B1, and cyclin D1, MMP-2, and MMP-9. CONCLUSIONS: Our data indicated that the expression of PHGDH is increased in pancreatic cancer and is an independent molecular prognostic factor for pancreatic cancerpatients. In addition, PHGDH controls cell proliferation, migration and invasion abilities. Therefore, PHGDH could serve as an important prognostic indicator and therapeutic target for pancreatic cancer.
Authors: Sha Yao; Luogen Peng; Omar Elakad; Stefan Küffer; Marc Hinterthaner; Bernhard C Danner; Alexander von Hammerstein-Equord; Philipp Ströbel; Hanibal Bohnenberger Journal: Transl Lung Cancer Res Date: 2021-06