Abstract. Th1 antigen-specific T cells secrete interferon-γ, which is able to kill antigen-specific cancer cells and is helpful for cancer vaccines. The aim of the present study was to explore whether B16 cell lysates plus polyinosinic-cytidylic acid (poly I:C) can effectively inhibit the progression of melanoma in an animal model. In the present study, C57BL/6 mice were divided into three groups, with each group containing more than six mice. The groups of mice were immunized twice with B16 cell lysates plus poly I:C, B16 cell lysates, or phosphate-buffered saline only, respectively. The in vivo results demonstrated that splenocytes from the mice immunized with B16 cell lysates plus poly I:C contained higher percentages of CD3 + CD8 + T lymphocytes and CD3 + CD4 + T lymphocytes, which were detected by a fluorescence-activated cell sorter, and produced higher levels of antigen-specific splenocyte proliferation activity, as detected by MTT assay. The splenocytes from the mice immunized with B16 cell lysates in combination with poly I:C produced higher levels of interferon-γ, as detected by quantitative polymerase chain reaction and ELISA, as well as cytotoxic T lymphocyte activity when stimulated in vitro with B16 lysates. Additionally, subcutaneous immunization of the C57BL/6 mice with B16 cell lysates plus poly I:C conferred greater protection against tumor-forming B16 melanoma cells than that of the mice immunized with injection of B16 cell lysate alone. In conclusion, the cancer vaccine of B16 cell lysates plus poly I:C exerts potently protective effects that polarize responses toward Th1 and elicit antitumor immunity. IntroductionMalignant melanoma is a serious disease arising from melanocytes which threatens human health in China and worldwide (1,2). The incidence and mortality rate of malignant melanoma continues to increase at a higher rate than that of any other type of malignancy (3,4). Although melanoma is curable if detected at an early localized stage, metastatic malignant melanoma has already become a therapeutic challenge (5). Hundreds of patients with advanced stage III or IV melanoma, particularly those with metastatic disease, have participated in studies of immunological therapy having failed on chemotherapy (6). Thus, ways to prevent and treat malignant melanoma using immunological methods are urgently required. Vaccination has been used for centuries, causing mortality due to infectious disease in humans to profoundly decrease, but a number of serious global diseases with no effective vaccines remain, including acquired immunodeficiency syndrome, influenza, malaria and cancer. It is harder to produce effective immune responses when using vaccines as a treatment for cancer, compared with when using preventive cancer vaccines (7,8). The cancer vaccine for cervical tumors is the first vaccine to prevent human cancer. With the success of the cervical cancer vaccine, an increasing number of researchers have been working to identify novel and effective cancer vaccines. Thus, the aim of the present ...

Necrotizing enterocolitis (NEC) is the most common life‐threatening gastrointestinal disease encountered in the premature infant. It has been shown that the intercellular reactive oxygen species (ROS) generation activated by lipopolysaccharide involved in the nuclear factor kappa B (NF‐κB) activation and pathogenesis of NEC. Here, we report that an antioxidant peptide from tuna backbone protein (APTBP) reduces the inflammatory cytokines transcription and release. APTBP directly scavenges the free radical through 1,1‐diphenyl‐2‐picrylhydrazyl (DPPH) and 2‐phenyl‐4,4,5,5‐tetramethylimidazoline‐1‐oxyl 3‐oxide (PTIO) assay. In addition, APTBP reduces the intracellular ROS level, exhibiting an antioxidant activity within cells. Remarkably, gavage with APTBP attenuates the phenotype of NEC in the mice model. Mechanically, the NF‐κB activation, together with the expression of inflammatory cytokines are decreased significantly when intracellular ROS are eliminated by APTBP. Therefore, our findings demonstrated that an antioxidant peptide, APTBP, ameliorates inflammation in NEC through attenuating ROS–NF‐κB axis.

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The acquisition of metastasis potential is a critical point for malignant tumors. Melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24) is a potential tumor suppress gene and frequently down-regulated in malignant tumors. It has been implicated that overexpression of MDA-7 led to proliferation inhibition in many types of human tumor. Invasion is an important process which is potential to promote tumor metastasis. However, the role and potential molecular mechanism of mda-7/IL-24 to inhibit the invasion of human melanoma cancer is not fully clear. In this report, we identified a solid role for mda-7/IL-24 in invasion inhibition of human melanoma cancer LiBr cells, including decreasing of adhesion and invasion in vitro, blocking cell cycle, down-regulating the expression of ICAM-1, MMP-2/9, CDK1, the phosphorylation of ERK and Akt, NF-κB and AP-1 transcription activity. Meanwhile, there was an increased expression of PTEN in mda-7/IL-24 over-expression LiBr cells. Our results demonstrated that mda-7/IL-24 is a potential invasion suppress gene, which inhibits the invasion of LiBr cells by the down-regulation of ICAM-1, MMP-2/9, PTEN, and CDK1 expression. The molecular pathways involved were the MAPK/ERK, PI3K-Akt, NF-κB, and AP-1. These findings suggest that mda-7/IL-24 may be used as a possible therapeutic strategy for human melanoma cancer.