title: The therapeutic function of the chemokine RANTES on the H22 hepatoma ascites model.
abstract: This study aimed at analyzing the therapeutic function of the chemokine RANTES on the H22 hepatoma ascites model and preliminarily explore the mechanism of RANTES in malignant ascites to provide an important reference for applying chemokines in anti-tumor therapy. The murine H22 hepatoma ascites model was used. Three treatment groups were analyzed: a RANTES treatment group, an IL-2 control group, and an NS control group. Two regimens of early treatment and late treatment were designed, and the therapeutic effect of RANTES on malignant ascites was studied by measuring changes in mouse body weight and abdominal circumference and observing the survival time. The expression of TNF-α, IFN-γ, TGF-β1, and MCP-1 in mouse ascites was detected by ELISA, and the chemotactic function of RANTES on B lymphocytes and T lymphocytes was analyzed by flow cytometry. In the early and late treatment regimens, RANTES could effectively inhibit the increase in mouse body weight and abdominal circumference in the murine H22 hepatoma ascites model. The secretion of TNF-α and IFN-γ, which had anti-tumor effects, was higher in the RANTES treatment group than in the control groups (P < 0.05), whereas the secretion of TGF-β1 and MCP-1, which promoted tumor growth, invasion, and metastasis, was lower than in the control groups (P < 0.05). RANTES had chemotactic effects on CD4(+) and CD8(+) T lymphocytes; therefore, the percentage of CD3, CD4, and CD8 in the mouse ascites in the RANTES treatment group was significantly higher than in the NS control and IL-2 treatment groups, and the CD4/CD8 ratio was also significantly higher. RANTES can effectively inhibit the increase in body weight and abdominal circumference and significantly extend survival time in mice in the H22 hepatoma ascites model.
authors.affiliation: Department of Breast Oncology, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Hexi District, Tianjin, China.
authors.forename: Chunfang
authors.initials: C
authors.lastname: Hao
authors.forename: Yehui
authors.initials: Y
authors.lastname: Shi
authors.forename: Jinpu
authors.initials: J
authors.lastname: Yu
authors.forename: Xueqing
authors.initials: X
authors.lastname: Wei
authors.forename: Shufen
authors.initials: S
authors.lastname: Li
authors.forename: Zhongsheng
authors.initials: Z
authors.lastname: Tong
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D001201:Ascites / Q000188:drug therapy* / Q000473:pathology; D018932:Chemokine CCL2 / Q000378:metabolism; D018946:Chemokine CCL5 / Q000627:therapeutic use*; D005260:Female; D007371:Interferon-gamma / Q000378:metabolism; D007376:Interleukin-2 / Q000627:therapeutic use*; D008114:Liver Neoplasms, Experimental / Q000188:drug therapy* / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D047368:Tumor Burden / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015430:Weight Gain / Q000187:drug effects; D023041:Xenograft Model Antitumor Assays
chemical_list: D015703:Antigens, CD; D000970:Antineoplastic Agents; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D018946:Chemokine CCL5; D007376:Interleukin-2; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma