Interest in cancer metabolism has increased in recent years. The pentose phosphate pathway (PPP) is a major glucose catabolism pathway that directs glucose flux to its oxidative branch and leads to the production of a reduced form of nicotinamide adenine dinucleotide phosphate and nucleic acid. The PPP serves a vital role in regulating cancer cell growth and involves many enzymes. The aim of the present review was to describe the recent discoveries associated with the deregulatory mechanisms of the PPP and glycolysis in malignant tumors, particularly in hepatocellular carcinoma, breast and lung cancer. Contents 1. Introduction 2. Glucose in the PPP 3. Glucose breakdown through glycolysis in the PPP 4. PPP in malignant tumors 5. Perspectives
We demonstrate a systematic visualization of the unique photophysical and fluorescence anisotropic properties of polyfluorene coplanar conformation (β-conformation) using time-resolved scanning confocal fluorescence imaging (FLIM) and fluorescence anisotropy imaging microscopy (FAIM) measurements. We observe inhomogeneous morphologies and fluorescence decay profiles at various micrometer-sized regions within all types of polyfluorene β-conformational spin-coated films. Poly(9,9-dioctylfluorene-2,7-diyl) (PFO) and poly[4-(octyloxy)-9,9-diphenylfluoren-2,7-diyl]-co-[5-(octyloxy)-9,9-diphenylfluoren-2,7-diyl] (PODPF) β-domains both have shorter lifetime than those of the glassy conformation for the longer effective conjugated length and rigid chain structures. Besides, β-conformational regions have larger fluorescence anisotropy for the low molecular rotational motion and high chain orientation, while the low anisotropy in glassy conformational regions shows more rotational freedom of the chain and efficient energy migration from amorphous regions to β-conformation as a whole. Finally, ultrastable ASE threshold in the PODPF β-conformational films also confirms its potential application in organic lasers. In this regard, FLIM and FAIM measurements provide an effective platform to explore the fundamental photophysical process of conformational transitions in conjugated polymer.
Pancreatic ductal adenocarcinoma (PDAC) is a malignancy with a poor prognosis and low survival rates. PDAC is characterized by a fibroinflammatory tumor microenvironment enriched by abundant fibroblasts and a variety of immune cells, contributing to its aggressiveness. Neutrophils are essential infiltrating immune cells in the PDAC microenvironment. Recent studies have identified several cellular mechanisms by which neutrophils are recruited to tumor lesion and promote tumorigenesis. This review summarizes the current understanding of the interplay between neutrophils, tumor cells, and other components in the PDAC tumor microenvironment. The prognosis and therapeutic implications of neutrophils in PDAC are also discussed.
Loss of KDM6A promotes pancreatic cancer progression and metastasis and delays pancreatic tissue recovery from pancreatitis. Mechanistically, a noncanonical p38-dependent activin A pathway likely mediates KDM6A function.BACKGROUND & AIMS: Inactivating mutations of KDM6A, a histone demethylase, were frequently found in pancreatic ductal adenocarcinoma (PDAC). We investigated the role of KDM6A in PDAC development.
METHODS:We performed a pancreatic tissue microarray analysis of KDM6A Q8
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