Correlation of several forms of folic acid with endometrial cancer: cross-sectional data from the National Health and Nutrition Examination Surveys (NHANES) 2011-2018.

OBJECTIVE: Endometrial cancer (EC) is a common malignancy of the female reproductive system and although most patients have a good prognosis, 20-30% of patients with advanced disease have a poor prognosis. There are currently no reliable biomarkers for early diagnosis and effective prognostic improvement of the disease. The purpose of this study was to explore the correlation between different forms of folic acid and endometrial cancer. METHODS: This study included 8809 female subjects aged ≥ 20 years in the NHANES database from 2011 to 2018, including 8738 non-oncology patients and 71 EC patients. Selection bias was reduced using 1:1 propensity score matching (PSM) method. Restricted cubic spline (RCS) was plotted to explore the non-linear relationship between different forms of folic acid and EC. RESULT: Using data from the NHANES database from 2011 to 2018, the association between folic acid and the risk of developing EC was assessed. The results of the 1:1 ratio propensity score matching (PSM) showed 68 each for EC patients and non-oncology participants. Total serum folate, 5-methyltetrahydrofolate (5-methylTHF), 5-formyltetrahydrofolate (5-formylTHF), tetrahydrofolate (THF) and 5,10-methylenetetrahydrofolate (5,10-methenylTHF) were significantly correlated with EC (p < 0.05). In addition, the RCS showed a significant non-linear correlation between THF and 5,10-formyl THF and the risk of developing EC. CONCLUSION: The results of this study showed that changes in serum total folate, 5-methylTHF, 5-formylTHF, THF and 5,10-methenylTHF were related to EC.

S100A16 Regulates HeLa Cell through the Phosphatidylinositol 3 Kinase (PI3K)/AKT Signaling Pathway.

BACKGROUND S100 calcium-binding protein A16 (S100A16) is closely related to the onset and progression of tumors. MATERIAL AND METHODS In the research, the mainly purpose was to investigate the effect of S100A16 on the proliferation ability, invasion, and angiogenesis of HeLa cells. An adenoviral vector overexpressing S100A16 (Ad-S100A16) was constructed and transfected into HeLa cells, forming a stable cells line of overexpression. The effect of S100A16 on the proliferative capacity of HeLa cells was evaluated by a Cell Counting Kit-8 (CCK-8) assay. Cell migration capacity was determined by a Transwell migration assay. Changes in matrix metalloproteinase-2 (MMP-2), MMP-9, E-cadherin, and vimentin expression were evaluated by a cell-based immunofluorescence assay. The effect of S100A16 on angiogenesis was verified by knockout experiment. RESULTS Overexpression of S100A16 significantly enhanced the proliferative and migratory capacities of HeLa cells (P<0.05), upregulated expression of matrix MMP-2, MMP-9, vimentin, phosphatidylinositol 3 kinase, and phosphorylated protein kinase B, and downregulated expression of E-cadherin. Vascular endothelial growth factor expression increased, phosphatase and tensin homolog expression decreased, and angiogenesis was positively correlated with S100A16 expression. These effects were largely mediated by the activation of the phosphatidylinositol 3 kinase/protein kinase B pathways. CONCLUSIONS S100A16 could promote the proliferation, migration, and tumor angiogenesis of HeLa cells by regulating the phosphatidylinositol 3 kinase/protein kinase B signaling pathways.