title: [Mechanisms of antimicrobial peptide cathelicidin secreted by non-tumorous cells for lung tumor growth].
abstract: OBJECTIVE
  To investigate the effect of antimicrobial peptide cathelicidin secreted by non-tumorous cells in lung tumor growth.
  
  
  METHODS
  CRAMP(-/-) mice and WT mice were used to establish a lung cancer model via tail vein injection of Lewis lung carcinoma cells (LLC1). Lung was weighted and tumor number on the lung surface was counted. Kaplan-Meier (K-M) survival curve was used to analyze survival rate of mice. Expression of cathelicidin, Ki-67 and CD68 in the tumor tissue was measured by immunohistochemical analysis. BALF cells were stained with Diff Quik and percentages of leukocyte types were determined by light microscopy.
  
  
  RESULTS
  Cathelicidin was high expression in inflammatory cells of tumor tissue, whereas weak expression in tumor cells. The lung weight and number of tumor in CRAMP-/- mice were (0.25±0.04)g and (9.60± 2.25), respectively, which were significantly lower than those of WT mice (0.65±0.05) g and (23.40± 2.68). The difference was statistically significant (t=6.07, 3.95, all P<0.05). And Kaplan-Meier survival analysis showed median survival time of CRAMP-/- mice was 49(46-51)d, which was longer than 34(28-39) d of WT mice (χ2=12.00, P<0.05). And the positive rate of Ki-67 tumor cells was significant reduced from (35.80±2.96)% in WT mice to (18.80±2.38)% in CRAMP-/- groups (t=4.48, P<0.05). The total cell number as well as the number of lymphocytes, neutrophils, and macrophages in BALFs of CRAMP-/- mice were (4.72±0.86)×10(4), (0.08±0.02)×10(4), (0.05±0.02)×10(4) and (4.60±0.84)×10(4), respectively, while of WT mice were (16.18±1.61)×10(4), (0.32±0.05)×10(4), (0.20±0.05)×10(4) and (15.66±1.57)×10(4). All of them had significant difference (t=6.28, 4.39, 3.00, 6.20, all P<0.05). In addition, the infiltration of macrophages into lung tumors was decreased in CRAMP-/- mice compared to WT mice, from (15.53±2.28)/high power field to (6.77±3.12)/high power field (t=3.41, P<0.05).
  
  
  CONCLUSIONS
  Non-tumor cells secreted cathelicidin promotes tumor cell proliferation and lung tumor growth. Recruitment of inflammatory cells such as macrophages into the tumor microenvironment may be the main mechanism of action.
authors.affiliation: Department of Clinical Laboratory, Tongji Hospital, University of Tongji, Shanghai 200065, China.
authors.forename: Yiwen
authors.initials: Y
authors.lastname: Yao
authors.affiliation: Department of Clinical Laboratory, Tongji Hospital, University of Tongji, Shanghai 200065, China.
authors.forename: Junlu
authors.initials: J
authors.lastname: Wu
authors.affiliation: Department of Clinical Laboratory, Tongji Hospital, University of Tongji, Shanghai 200065, China.
authors.forename: Wenqiang
authors.initials: W
authors.lastname: Quan
authors.affiliation: Department of Clinical Laboratory, Tongji Hospital, University of Tongji, Shanghai 200065, China.
authors.forename: Haiying
authors.initials: H
authors.lastname: Wan
authors.affiliation: Department of Clinical Laboratory, Tongji Hospital, University of Tongji, Shanghai 200065, China; Email: 186ld@163.com.
authors.forename: Dong
authors.initials: D
authors.lastname: Li
mesh_terms: D000818:Animals; D000890:Anti-Infective Agents; D023181:Antimicrobial Cationic Peptides; D018827:Carcinoma, Lewis Lung; D054804:Cathelicidins; D018450:Disease Progression; D053208:Kaplan-Meier Estimate; D008168:Lung; D008175:Lung Neoplasms; D008264:Macrophages; D051379:Mice; D009504:Neutrophils
chemical_list: D000890:Anti-Infective Agents; D023181:Antimicrobial Cationic Peptides; D054804:Cathelicidins