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This document discusses the role of noncoding RNAs (ncRNAs) in cancer. NcRNAs are RNA molecules that do not code for proteins but instead regulate gene expression and participate in cellular processes. Dysregulated ncRNAs are involved in various human diseases, including cancer. The document highlights several studies on the molecular mechanisms and clinical implications of ncRNAs in different types of cancer, including head and neck cancer, colorectal cancer, and triple-negative breast cancer. The studies explore the functions, expression patterns, and potential therapeutic applications of ncRNAs in cancer. The document emphasizes the importance of understanding ncRNAs for the development of refined treatment strategies and identifies ncRNAs as potential prognostic indicators, biomarkers, and therapeutic targets for cancer. [Extracted from the article]

This article explores the role of a circular RNA called circLIPH in the progression of pancreatic cancer. The study reveals that circLIPH is increased in pancreatic tumor tissue and is associated with tumor size and stage. It also demonstrates that circLIPH promotes the growth, migration, and invasion of pancreatic cancer cells. The researchers identify miR-769-3p as a target of circLIPH and show that circLIPH increases the expression of GOLM1, a gene involved in cancer progression. These findings suggest that circLIPH could potentially be used as a biomarker and therapeutic target for pancreatic cancer. The study further investigates the role of circLIPH in pancreatic cancer progression and finds that overexpression of miR-769-3p inhibits the growth, proliferation, migration, and invasion of pancreatic cancer cells. Conversely, treatment with a miR-769-3p inhibitor has the opposite effects. The target genes of miR-769-3p are enriched in the mTOR signaling pathway. Additionally, circLIPH is found to promote pancreatic cancer progression by enhancing glycolysis in cancer cells. In vivo experiments demonstrate that si-circLIPH effectively reduces circLIPH expression and suppresses tumor growth. These findings suggest that circLIPH may activate the miR-769-3p/GOLM1/PI3K/AKT/mTOR axis to promote pancreatic cancer progression. [Extracted from the article]

Abstract: The two membrane transporters Slc23a1 and Slc23a2 mediate ascorbic acid uptake into cells. We recently determined the key role of Slc23a1 in renal re-absorption of ascorbic acid in a [...]

Long noncoding RNAs (lncRNAs) play a critical role in the immune regulation and tumor microenvironment of pancreatic cancer (PaCa). To construct a novel immune-related prognostic risk model for PaCa and evaluate the prognostic prediction of lncRNAs, essential immune-related lncRNAs (IRlncRNAs) were identified by Pearson correlation analysis of differentially expressed immune-related genes (IRGs) and IRlncRNAs in PaCa from The Cancer Genome Atlas (TCGA) and GTEx databases. Least absolute shrinkage and selection operator (LASSO) regression was also applied to construct a prognostic risk model of IRlncRNAs, and gene set enrichment analysis (GSEA) was further applied for functional annotation for these IRlncRNAs. A total of 148 IRlncRNAs were identified in PaCa to construct a prognostic risk model. Among them, lncRNA LINC02325, FNDC1-AS1, and ZEB2-AS1 were significantly upregulated in 69 pairs of PaCa tissues by qRT-PCR. ROC analyses showed that LINC02325 (AUC = 0.80), FNDC1-AS1 (AUC = 0.76), and ZEB2-AS1 (AUC = 0.75) had a good predictive effect on 5-year survival prognosis. We demonstrated that high expression levels of ZEB2-AS1 and LINC02325 were not only positively associated with tumor size and CA199, but elevated levels of ZEB2-AS1 and FNDC1-AS1 were also positively correlated with tumor stage. GSEA further revealed that immune-related pathways were mainly enriched in the high-risk groups. Several immune-related algorithms demonstrated that four IRlncRNAs were related to immune infiltration, immune checkpoints, and immune-related functions. Thus, the prognostic risk model based on IRlncRNAs in Paca indicates that the four IRlncRNA signatures may serve as predictors of survival and potential predictive biomarkers of the pancreatic tumor immune response. [ABSTRACT FROM AUTHOR]

Levels of the necessary nutrient vitamin C (ascorbate) are tightly regulated by intestinal absorption, tissue accumulation, and renal reabsorption and excretion. Ascorbate levels are controlled in part by regulation of transport through at least 2 sodium-dependent transporters: Slc23a1 and Slc23a2 (also known as Svct1 and Svct2, respectively). Previous work indicates that Slc23a2 is essential for viability in mice, but the roles of Slc23a1 for viability and in adult physiology have not been determined. To investigate the contributions of Slc23a1 to plasma and tissue ascorbate concentrations in vivo, we generated [Slc23a1.sup.[-/-]] mice. Compared with wild-type mice, [Slc23a1.sup.[-/-]] mice increased ascorbate fractional excretion up to 18-fold. Hepatic portal ascorbate accumulation was nearly abolished, whereas intestinal absorption was marginally affected. Both heterozygous and knockout pups born to [Slc23a1.sup.[-/-]] dams exhibited approximately 45% perinatal mortality, and this was associated with lower plasma ascorbate concentrations in dams and pups. Perinatal mortality of [Slc23a1.sup.[-/-]] pups born to [Slc23a1.sup.[-/-]] dams was prevented by ascorbate supplementation during pregnancy. Taken together, these data indicate that ascorbate provided by the dam influenced perinatal survival. Although [Slc23a1.sup.[-/-]] mice lost as much as 70% of their ascorbate body stores in urine daily, we observed an unanticipated compensatory increase in ascorbate synthesis. These findings indicate a key role for Slc23a1 in renal ascorbate absorption and perinatal survival and reveal regulation of vitamin C biosynthesis in mice., Introduction Vitamin C (ascorbate) is synthesized by most mammals. Humans lack the terminal enzyme gulonolactone oxidase in the synthesis pathway and rely on dietary intake for ascorbate (1). Ascorbate is [...]

The role of diet in diurnal control of hexose transporter mRNA and protein expression was investigated in a rat model. Total mRNA from jejunum was isolated and quantitated by Northern blotting. The levels of SGLT-1, GLUT-2 and GLUT-5 mRNA varied during a 24-hr. period. Rats fed a 60% fructose-enriched diet showed an increase in GLUT-5 mRNA and protein levels and this increase was sustained after the 24-hr. period, whereas GLUT-2 and SGLT-1 mRNA showed no changes during fructose feeding. Data indicate that diet mediates the level of hexose transporter expression in the intestine.