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LYG1 exerts antitumor function through promoting the activation, proliferation, and function of CD4+ T cells.

ABSTRACT: Identification of novel stimulatory cytokines with antitumor function would have great value in tumor immunotherapy investigations. Here, we report LYG1 (Lysozyme G-like 1) identified through the strategy of Immunogenomics as a novel classical secretory protein with tumor-inhibiting function. LYG1 recombinant protein (rhLYG1) could significantly suppress the growth of B16 tumors in WT B6 mice, but not in SCID-beige mice, Rag1-/- mice, CD4+- or CD8+ T cell-deleted mice. It could increase the number of CD4+ and CD8+ T cells in tumor-infiltrating lymphocytes, tumor-draining lymph nodes, and spleens, and promote IFN? production by T cells in tumor-bearing mice. In vitro experiments demonstrated that rhLYG1 could directly enhance IFN? secretion by CD4+ T cells, but not CD8+ T cells. Moreover, it could promote the activation, proliferation, and IFN? production of tumor antigen-specific CD4+ T cells. The tumor-inhibiting effect of LYG1 was eliminated in Ifng-/- mice. Furthermore, LYG1 deficiency accelerated B16 and LLC1 tumor growth and inhibited the function of T cells. In summary, our findings reveal a tumor-inhibiting role for LYG1 through promoting the activation, proliferation, and function of CD4+ T cells in antitumor immune responses, offering implications for novel tumor immunotherapy.

SUBMITTER: Liu H

PROVIDER: S-EPMC5414861 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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LYG1 exerts antitumor function through promoting the activation, proliferation, and function of CD4+ T cells.

Liu Huihui H Zhang Yanfei Y Liu Zhengyang Z Wang Pingzhang P Mo Xiaoning X Fu Weiwei W Liu Wanchang W Cheng Yingying Y Han Wenling W

Oncoimmunology 20170307 4

Identification of novel stimulatory cytokines with antitumor function would have great value in tumor immunotherapy investigations. Here, we report LYG1 (Lysozyme G-like 1) identified through the strategy of Immunogenomics as a novel classical secretory protein with tumor-inhibiting function. LYG1 recombinant protein (rhLYG1) could significantly suppress the growth of B16 tumors in WT B6 mice, but not in SCID-beige mice, Rag1-/- mice, CD4+- or CD8+ T cell- ...[more]

PMID: 28507796

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Project description:BackgroundTo observe and explore the effect of metformin on the migration and proliferation of bladder cancer T24 and 5637 cells in vitro.MethodsBladder cancer T24 and 5637 cell lines were cultured in vitro, and were divided into group A (blank control group) and group B (metformin group: 5, 10, 15, and 20 mmol/L); both groups were plated on 6-well plates at the same time. Culture in 24-well plates was used for wound healing assays and in 96-well plates for Transwell migration and invasion, and Cell Counting Kit-8 proliferation experiments. We observed and detected the cell migration and proliferation ability of each group at 48 h, and calculated the cell migration area and survival rate. Flow cytometry was used to detect cell apoptosis in the groups. The apoptosis-related proteins, cleaved-caspase 3, cleaved-PARP, and the PI3K/AKT/mTOR signaling pathway member proteins PI3K, phosphorylated (p)-PI3K, AKT, p-AKT, mTOR, and p-mTOR were detected using western blotting.ResultsAfter 48 h of treatment with different concentrations of metformin, the cell migration and proliferation capabilities were significantly lower than those in the blank control group. The proliferation and migration abilities of T24 and 5637 cells decreased in a metformin concentration-dependent manner (P < 0.05). The apoptosis rate under different concentrations of metformin, as detected by flow cytometry, showed a significantly higher rate in the metformin group than in the control group (P < 0.05). Compared with that in the control group, the level of cleaved-caspase 3 and cleaved-PARP protein in the metformin group was increased in each treatment group, and the levels of p-mTOR, p-AKT, and p-PI3K decreased significantly compared with those in the control group (P < 0.05).ConclusionMetformin inhibited bladder cancer T24 and 5637 cell migration and proliferation, and induced their apoptosis. The mechanism might involve inhibition of the activation of the PI3K/AKT/mTOR signaling pathway.

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LYG1 exerts antitumor function through promoting the activation, proliferation, and function of CD4+ T cells.

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LYG1 exerts antitumor function through promoting the activation, proliferation, and function of CD4<sup>+</sup> T cells.

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