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.
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.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.