Malaria importation and local vector susceptibility to imported Plasmodium vivax infection are a continuing risk along the China–Myanmar border. Malaria transmission has been prevented in 3 border villages in Tengchong County, Yunnan Province, China, by use of active fever surveillance, integrated vector control measures, and intensified surveillance and response.

The role of myeloid differentiation factor 88 (MyD88) in malignant tumors is largely unknown. Therefore, in this study, we aimed to examine the function and underlying mechanism of MyD88 in colorectal carcinoma in vitro using SW480 and HCT116 cell lines and in vivo using a nude mouse model. SW480 and HCT116 cells were infected with a lentiviral-based effective MyD88 siRNA virus. CCK-8 and colony formation assay were used to assess cell proliferation. Transwell and scratch assays were used to test the migration of colorectal cancer cells, and the Transwell assay was further used to analyze the invasiveness of colorectal cancer cells. Western blotting was performed to analyze the underlying mechanism of MyD88 regulation. In vitro experiments demonstrated that silencing MyD88 in SW480 and HCT116 cells markedly suppressed growth and invasion. Furthermore, MyD88 knockdown affected the MyD88-NF-κB/AP-1 signaling pathways in SW480 and HCT116 cells. In vivo, MyD88 knockdown inhibited tumor growth in a HCT116 cell subcutaneous nude model. We found that knockdown of the MyD88 gene can affect proliferation, invasion, and migration of colorectal cancer cells. We further verified that MyD88 knockdown can reduce the activity of NF-κB and AP-1 pathways. These results show that MyD88 gene plays an important role in promoting colorectal cancer, and thus can be exploited as a potential diagnostic and prognostic biomarker for colorectal cancer.

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BACKGROUND: Malaria control programs have achieved remarkable success during the past decade. Nonetheless, sensitive and affordable methods for active screening of malaria parasites in low-transmission settings remain urgently needed.

Background/Aim: Inflammation may play a role in cancer initiation and progression. The molecular mechanisms by which inflammation causes colorectal cancer, remains unclear. The present study investigated a signaling pathway that affects inflammation in colorectal cancer. Materials and Methods: SW480 cells, HCT116 cells, and cells with knockdown of myeloid differentiation 88 (MyD88), and forced expression of MyD88 were treated with lipopolysaccharide (LPS; 1 μg/ml). Inflammation-related mRNA expression was analyzed by the quantitative reverse transcription polymerase chain reaction and inflammatory cytokines were detected by western blotting. The enzymelinked immunosorbent assay (ELISA) was used to quantify inflammation-related cytokines in colorectal cancer cells. Cancer cell properties were evaluated using the woundhealing assay, transwell migration assay, transwell invasion assay, colony-formation assay, and CCK-8 assay. Results: LPS up-regulated mRNA and protein levels of inflammatory factors in colorectal cancer cells. Knockdown of MyD88 inhibited LPS-induced mRNA expression and inflammatory protein expression in colorectal cancer cells. Similarly, silencing of MyD88 expression suppressed LPS-induced changes in the biological behavior of colorectal cancer cells. Silencing of MyD88 expression down-regulated expression of proteins of the LPS/nuclear factor kappa-light-chainenhancer of activated B-cells (NF-ĸB)/mitogen-activated protein kinase (MAPK) signaling pathway. Restoration of the expression of MyD88 reversed the effects in LPS-treated HCT116 cells. Conclusion: MyD88-regulated LPS/NF-ĸB/MAPK signaling pathway affects the inflammatory and biological behavior of LPS-induced colorectal cancer cells. Colorectal cancer is the fourth leading cause of cancerrelated death in the world and the fifth in China, with increasing incidence and mortality (1, 2). For more than two centuries, it has been known that inflammation and coexist. Some studies have indicated that inflammation promotes the progression of cancer (3-5). Long-term microbial infection may cause colorectal mucosa metaplasia, atypical hyperplasia and carcinoma in situ, finally leading to colorectal cancer (6, 7). However, the mechanisms by which inflammation promotes cancer progression remain unclear. Lipopolysaccharide (LPS) is present in the cell wall of Gram-negative bacteria (6, 7). Gram-negative bacterial infection leads to release of LPS in colorectal tumors in situ. Previous studies have reported that LPS can promote cell migration, invasion and the epithelial-mesenchymal transition and contribute to the progression of cancer (8-10). LPS may contribute to metastasis by accelerating cell 409 This article is freely accessible online.

Colorectal cancer (CRC) is the third most common cancer in the world and the second leading cause of cancer-related deaths worldwide. 1 Surgical resection is still the most important treatment method for improving the 5-year survival rate of patients with CRC.However, 50% of patients with CRC eventually experience relapse and metastasis, shortening the patients' survival and affecting their

Background. The drug resistance and the immune suppression in the tumor microenvironment are important factors affecting tumor progression. Reversing drug resistance and changing tumor suppression microenvironment are ideal ways to inhibit tumor progression. Objective. The aim of the study is to verify antitumor immune response of probiotics in patients with colorectal carcinoma and to explore its mechanism. Methods. To detect the tumor samples of 122 patients with colorectal carcinoma after surgery, analyze the effect of probiotics on enhancing tumor-infiltrating CD8+T cells to inhibit colorectal carcinoma, and further verify the mechanism of probiotics on enhancing the antitumor immune response of CD8+T cells through animal experiments. Results. The results of immunohistochemistry showed that the proportion of CD8+T cells in the patients treated with probiotics before surgery was increased significantly than that in other patients (P=0.033). The results of flow cytometry also showed that the proportion of CD8+T cells in the probiotics group was higher than that in the nonprobiotics group (P=0.029). Kaplan-Meier survival estimates also showed that the CD8+T cells, TNM stage, pathology grade, lymphatic metastasis, and probiotic treatment were significantly associated with the progression-free survival (PFS) (χ2=9.684, P=0.002 for CD8+T cells; χ2=5.878, P=0.015 for TNM stage; χ2=7.398, P=0.004 for pathology grade; χ2=8.847, P=0.003 for Lymphatic metastasis; and χ2=4.622, P=0.032 for the group (group A was treated with probiotics before surgery; group B was not treated with probiotics)). The experimental results in mice showed that probiotics could inhibit tumor growth and increase the proportion of CD8+T cells in mice; the difference was statistically significant (P=0.037). It was also found that probiotic feeding could upregulate the expression of T-cell immunoglobulin mucin receptor 1(TIM-1) in CD8+T cells of mice and also found that probiotic feeding could downregulate the expression of programmed cell death protein 1 (PD-1) in CD8+T cells of mice, compared with the nonfeeding group; the difference was statistically significant (P=0.045 for TIM-1 and P=0.02 for PD-1, respectively). In order to further understand the functional status of CD8+T cells, we analyzed interferon-gamma (IFN-γ)+ T cells and tumor necrosis factor-α (TNF-α)+CD8+T cells by flow cytometry. The results showed that the proportion of IFN-γ+ T cells and TNF-α+CD8+T cells significantly increased after probiotic treatment, compared with the nonprobiotic treatment group; the difference was statistically significant (P=0.040 for IFN-γ+ T cells and P=0.014 for TNF-α+CD8+T, respectively). Conclusions. Probiotics can enhance the antitumor immune response of CD8+T cells. It can play a synergistic antitumor role. On the one hand, its mechanism is through regulating intestinal flora, and on the other hand, through regulating the antitumor immune function of CD8+T cells.