title: Knockdown of S100P by lentiviral-mediated RNAi promotes apoptosis and suppresses the colony-formation ability of gastric cancer cells.
abstract: S100P is a putative candidate oncogene in several types of human tumors. However, expression of S100P, its potential role and its clinical significance in gastric cancer remain unclear. In the present study, S100P expression was examined by immunohistochemistry using a tissue microarray. Positive staining for S100P was noted in 77.1% of the cases while 22.9% were negative. In two gastric cancer cell lines, MGC-803 and SGC-7901, S100P expression was knocked down by a lentiviral short hairpin delivery system. The RNA interference-mediated downregulation of S100P expression markedly promoted cell apoptosis and inhibited cell colony-formation ability of the gastric cancer cells. In addition, knockdown of S100P significantly regulated the expression of 12 apoptosis-associated genes with a >1.5-fold change compared with the negative control. Among them, FOS, DDIT3 and FN1 were significantly upregulated, while FASLG, DAPK1, CTNNB1 and CASP2 were notably downregulated following S100P silencing. These results suggest that S100P acts as an oncogenic factor in gastric cancer and is a potential molecular target for gastric cancer gene therapy.
authors.affiliation: Department of General Surgery, Zhongda Hospital, Southeast University, Gulou, Nanjing, Jiangsu 210009, P.R. China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Zhang
authors.affiliation: Department of General Surgery, Zhongda Hospital, Southeast University, Gulou, Nanjing, Jiangsu 210009, P.R. China.
authors.forename: Haolin
authors.initials: H
authors.lastname: Hu
authors.affiliation: Department of General Surgery, Zhongda Hospital, Southeast University, Gulou, Nanjing, Jiangsu 210009, P.R. China.
authors.forename: Xin
authors.initials: X
authors.lastname: Shi
authors.affiliation: Department of General Surgery, Zhongda Hospital, Southeast University, Gulou, Nanjing, Jiangsu 210009, P.R. China.
authors.forename: Wenhao
authors.initials: W
authors.lastname: Tang
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis / Q000235:genetics*; D002135:Calcium-Binding Proteins / Q000235:genetics*; D053143:Caspase 2 / Q000096:biosynthesis; D000068579:Celecoxib; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology; D003546:Cysteine Endopeptidases / Q000096:biosynthesis; D064550:Death-Associated Protein Kinases / Q000096:biosynthesis; D015536:Down-Regulation; D053222:Fas Ligand Protein / Q000096:biosynthesis; D005260:Female; D005353:Fibronectins / Q000096:biosynthesis; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008297:Male; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000235:genetics*; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis; D011720:Pyrazoles / Q000494:pharmacology; D034622:RNA Interference; D034741:RNA, Small Interfering; D013270:Stomach / Q000473:pathology; D013274:Stomach Neoplasms / Q000235:genetics*; D013449:Sulfonamides / Q000494:pharmacology; D051742:Transcription Factor CHOP / Q000096:biosynthesis; D014410:Tumor Stem Cell Assay; D015854:Up-Regulation; D055815:Young Adult; D051176:beta Catenin / Q000096:biosynthesis
chemical_list: C495270:CTNNB1 protein, human; D002135:Calcium-Binding Proteins; D052246:Cyclooxygenase 2 Inhibitors; C497249:DDIT3 protein, human; C505661:FASLG protein, human; C067625:FN1 protein, human; D053222:Fas Ligand Protein; D005353:Fibronectins; D009363:Neoplasm Proteins; D016760:Proto-Oncogene Proteins c-fos; D011720:Pyrazoles; D034741:RNA, Small Interfering; C103003:S100P protein, human; D013449:Sulfonamides; D051176:beta Catenin; D051742:Transcription Factor CHOP; C579096:DAPK1 protein, human; D064550:Death-Associated Protein Kinases; C490360:CASP2 protein, human; D053143:Caspase 2; D003546:Cysteine Endopeptidases; D000068579:Celecoxib