title: [Inhibitory effects of celecoxib combined with octreotide on growth of multidrug resistant human gastric cancer cell line SGC7901/ADR].
abstract: OBJECTIVE
  Both cyclooxygenase-2 (COX-2) inhibitor and octreotide can inhibit growth of tumor cells. This study was to investigate inhibitory effects of COX-2 inhibitor celecoxib alone, and celecoxib combined with octreotide on growth of multidrug resistant human gastric cancer cell line SGC7901/ADR.
  
  
  METHODS
  Experimental groups:(1)celecoxib (1 x 10(-4)-1 x 10(-8) mol/L); (2)octreotide (1 x 10(-5)-1 x 10(-9) mol/L); (3)celecoxib (1 x 10(-4)-1 x 10(-8) mol/L) combined with octreotide (1 x 10-6 mol/L);(4)control group (RPMI-1640 medium without serum). The effects of all treatments on SGC7901 cells, and SGC7901/ADR cells were observed. Cell proliferation was measured by (3)H-thymidine incorporation into DNA. The expression of proliferating cell nuclear antigen (PCNA) was detected by immunocytochemistry. Cell apoptosis was measured by TdT-mediated dUTP nick end-labeling assay (TUNEL) and flow cytometry.
  
  
  RESULTS
  (3)H-thymidine incorporation into SGC7901/ADR cells treated with celecoxib [(471.3+/-79.7) cpm] was significantly lower than that of control group [(917.5+/-130.8) cpm](P< 0.05). When combined with octreotide, celecoxib presented lower (3)H-thymidine incorporation [(220.0+/-19.7)cpm] than it alone with a 53.3% decrease. The concentration of celecoxib in combination group negatively related to synthesis of DNA in SGC7901/ADR cells (r=0.996,P< 0.001). The expression of PCNA in either celecoxib group or combination group markedly decreased. The apoptosis rates of SGC7901/ADR cells induced by celecoxib alone, and combination treatment were 32.9%, and 52.5%.
  
  
  CONCLUSIONS
  Celecoxib combined with octreotide may enhance inhibition of growth of multidrug resistant human gastric cancer cells. The mechanism may be related with inhibiting DNA synthesis, and inducing apoptosis.
authors.affiliation: Division of Peptides Related with Human Diseases, Key Laboratory of Biotherapy of Human Diseases, Ministry of Education,West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
authors.forename: Wen-Bin
authors.initials: WB
authors.lastname: Zheng
authors.forename: Chun-Hui
authors.initials: CH
authors.lastname: Wang
authors.forename: Ou
authors.initials: O
authors.lastname: Qiang
authors.forename: Cheng-Wei
authors.initials: CW
authors.lastname: Tang
mesh_terms: D018931:Antineoplastic Agents, Hormonal / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D000068579:Celecoxib; D045744:Cell Line, Tumor; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D004273:DNA, Neoplasm / Q000096:biosynthesis; D018432:Drug Resistance, Multiple; D019008:Drug Resistance, Neoplasm; D004357:Drug Synergism; D006801:Humans; D015282:Octreotide / Q000494:pharmacology*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011720:Pyrazoles / Q000494:pharmacology*; D013274:Stomach Neoplasms / Q000378:metabolism / Q000473:pathology*; D013449:Sulfonamides / Q000494:pharmacology*
chemical_list: D018931:Antineoplastic Agents, Hormonal; D016861:Cyclooxygenase Inhibitors; D004273:DNA, Neoplasm; D018809:Proliferating Cell Nuclear Antigen; D011720:Pyrazoles; D013449:Sulfonamides; D000068579:Celecoxib; D015282:Octreotide