title: Oral inoculation of probiotics Lactobacillus acidophilus NCFM suppresses tumour growth both in segmental orthotopic colon cancer and extra-intestinal tissue.
abstract: Modulation of the cellular response by the administration of probiotic bacteria may be an effective strategy for preventing or inhibiting tumour growth. We orally pre-inoculated mice with probiotics Lactobacillus acidophilus NCFM (La) for 14 d. Subcutaneous dorsal-flank tumours and segmental orthotopic colon cancers were implanted into mice using CT-26 murine colon adenocarcinoma cells. On day 28 after tumour initiation, the lamina propria of the colon, mesenteric lymph nodes (MLN) and spleen were harvested and purified for flow cytometry and mRNA analyses. We demonstrated that La pre-inoculation reduced tumour volume growth by 50·3 %, compared with untreated mice at 28 d after tumour implants (2465·5 (SEM 1290·4) v. 4950·9 (SEM 1689·3) mm³, P<0·001). Inoculation with La reduced the severity of colonic carcinogenesis caused by CT-26 cells, such as level of colonic involvement and structural abnormality of epithelial/crypt damage. Moreover, La enhanced apoptosis of CT-26 cells both in dorsal-flank tumour and segmental orthotopic colon cancer, and the mean counts of apoptotic body were higher in mice pre-inoculated with La (P<0·05) compared with untreated mice. La pre-inoculation down-regulated the CXCR4 mRNA expressions in the colon, MLN and extra-intestinal tissue, compared with untreated mice (P<0·05). In addition, La pre-inoculation reduced the mean fluorescence index of MHC class I (H-2Dd, -Kd and -Ld) in flow cytometry analysis. Taken together, these findings suggest that probiotics La may play a role in attenuating tumour growth during CT-26 cell carcinogenesis. The down-regulated expression of CXCR4 mRNA and MHC class I, as well as increasing apoptosis in tumour tissue, indicated that La may be associated with modulating the cellular response triggered by colon carcinogenesis.
authors: Department of Pediatrics, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Chang Gung Children's Hospital, 12L, 5 Fu-Hsing Street, Kwei-Shan, Taoyuan 333, Taiwan, ROC.
authors: Chien-Chang
authors: CC
authors: Chen
authors: Wei-Chuan
authors: WC
authors: Lin
authors: Man-Shan
authors: MS
authors: Kong
authors: Hai Ning
authors: HN
authors: Shi
authors: W Allan
authors: WA
authors: Walker
authors: Chun-Yen
authors: CY
authors: Lin
authors: Ching-Tai
authors: CT
authors: Huang
authors: Yung-Chang
authors: YC
authors: Lin
authors: Shih-Ming
authors: SM
authors: Jung
authors: Tzou-Yien
authors: TY
authors: Lin
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control* / Q000556:secondary; D000818:Animals; D016588:Anticarcinogenic Agents / Q000627:therapeutic use*; D017209:Apoptosis; D045744:Cell Line, Tumor; D003110:Colonic Neoplasms / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D005805:Genes, MHC Class I; D007779:Lactobacillus acidophilus; D008207:Lymphatic Metastasis / Q000473:pathology / Q000517:prevention & control; D051379:Mice; D008807:Mice, Inbred BALB C; D009363:Neoplasm Proteins / Q000235:genetics / Q000378:metabolism; D009368:Neoplasm Transplantation; D019936:Probiotics / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D019718:Receptors, CXCR4 / Q000235:genetics / Q000378:metabolism; D013160:Splenic Neoplasms / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control / Q000556:secondary
chemical_list: D016588:Anticarcinogenic Agents; C514936:CXCR4 protein, mouse; D009363:Neoplasm Proteins; D012333:RNA, Messenger; D019718:Receptors, CXCR4