title: RASAL1 influences the proliferation and invasion of gastric cancer cells by regulating the RAS/ERK signaling pathway.
abstract: The aim of this study was to investigate the biological characteristics of the RASAL1 gene in a well-differentiated gastric cancer cell line MKN-28 and a poorly differentiated gastric cancer cell line BGC-823 cells, using RNA interference and gene transfection technology, respectively. MKN-28 cells were transfected with the shRNA of RASAL1 and BGC-823 cells were transfected with the pcDNA 3.1 plasmid vector containing RASAL1. RT-PCR and western blotting were then used to detect the expression of RASAL1 mRNA and protein. The activities of RAS and extracellular signal-regulated kinase 1/2 were analyzed by the pull-down method and western blotting. The proliferate capacity, apoptosis rate, invasive and migratory potentials of MKN-28 or BGC-823 cells were also measured by Cell Counting Kit-8 cell proliferation assay, propidium iodide/Annexin V staining coupled with flow cytometry, and transwell chamber assays, respectively. Measurement of RASAL1 mRNA and protein expression in two cells revealed successful transfection of the shRNA of RASAL1 and RASAL1-pcDNA3.1 plasmid into these two cells. Moreover, decreased expression of RASAL1 in MKN-28 cells resulted in increased expression of RAS-GTP and p-ERK1/2. Interestingly, decreased expression of RASAL1 inhibited apoptosis and facilitated cell proliferation, invasion and migration. The increased expression of RASAL1 in BGC-823 cells caused declined expression of RAS-GTP and p-ERK1/2, as well as promoted apoptosis and restrained cell proliferation, invasion and migration. The down-regulation of RASAL1 promoted the proliferation, invasion and migration of gastric cancer MKN-28 cells, and up-regulation of RASAL1 inhibited the proliferation, invasion and migration of BGC-823 gastric cancer cells by regulating the RAS/ERK signaling pathway. Thus, our results suggest that RASAL1 may play an important role as a tumor suppressor gene in gastric cancer.
authors: Department of Gastroenterology, Zhongda Hospital, Southeast University, Nanjing, 210009, Jiangsu, People's Republic of China, njchenhong66@163.com.
authors: Hong
authors: H
authors: Chen
authors: Zheng-Yuan
authors: ZY
authors: Cheng
authors: Ying
authors: Y
authors: Pan
authors: Zhi
authors: Z
authors: Wang
authors: Yang
authors: Y
authors: Liu
authors: Jin-Qi
authors: JQ
authors: Zhang
mesh_terms: D049109:Cell Proliferation / Q000235:genetics*; D020690:GTPase-Activating Proteins / Q000502:physiology*; D006801:Humans; D020935:MAP Kinase Signaling System / Q000235:genetics* / Q000502:physiology*; D009361:Neoplasm Invasiveness / Q000235:genetics; D013274:Stomach Neoplasms / Q000235:genetics* / Q000473:pathology*; D014407:Tumor Cells, Cultured; D018631:ras Proteins / Q000235:genetics / Q000502:physiology
chemical_list: D020690:GTPase-Activating Proteins; C580923:RASAL1 protein, human; D018631:ras Proteins