Conjugated drug delivery has gained immense interest due to the possibility of overcoming the resistance of cancer cells to a specific drug when treated using it for a period of time. In the present study, CS/Pd nanocomposite has been prepared using cost effective chemical reduction method and has been used for the delivery of curcumin (CUR) and 5-Fluorouracil (5-FU) separately and in a conjugated form. The prepared nanocomposite before and after drug encapsulation have been studied using various characterization techniques. The release of drugs from the nanocomposite with respect to time has been analyzed and the release kinetics has also been studied. The release profile is mostly seen to adhere to zero order kinetics which represents the constant release of drugs from drug delivery system. This is the most favored release kinetic as this leads to the prolonged release of the drug, thus leading to a reduction in the number of doses administered. The cytotoxicity of the drug loaded nanocomposites on colon cancer cells has been studied, which shows the effectiveness of the composite system towards successfully inhibiting the growth of cancer cells.
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http://dx.doi.org/10.1016/j.msec.2017.03.058 | DOI Listing |
Mol Aspects Med
January 2025
Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran; Department of Epidemiology, West Kazakhstan Marat Ospanov Medical University, Aktobe, Kazakhstan; Department of Natural Sciences, West Kazakhstan Marat Ospanov Medical University, Aktobe, Kazakhstan. Electronic address:
Microplastics (MPs) are known as substantial environmental and health threats because of their pervasive existence and potential function in human diseases. This study is the first research in which a comprehensive analysis of various impacts of MPs on cancer cells is performed through pharmacological and in silico approaches. Moreover, our results demonstrate that MPs have both promotive and suppressive impacts on cancer cells, changing some of the important features of these kinds of cells including cellular viability, migration, metastasis, and apoptosis.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
January 2025
Department of Pathology and Pathophysiology, School of Medicine, Jinan University, Guangzhou, China.
Metastasis is a major cause of poor prognosis of pancreatic cancer. Exosomes (Exos) regulate cancer progression by modulating macrophage polarization. This study aimed to investigate the effects of cancer-associated fibroblast (CAF)-released Exos on macrophage polarization in pancreatic cancer and the molecular mechanisms.
View Article and Find Full Text PDFCell Rep
January 2025
Department of Biochemistry, University of Utah, Salt Lake City, UT 84112, USA; Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, USA. Electronic address:
Tumor cells must optimize metabolite acquisition between synthesis and uptake from a microenvironment characterized by hypoxia, lactate accumulation, and depletion of many amino acids, including arginine. We performed a metabolism-focused functional screen using CRISPR-Cas9 to identify pathways and factors that enable tumor growth in an arginine-depleted environment. Our screen identified the SLC-family transporter SLC7A5 as required for growth, and we hypothesized that this protein functions as a high-affinity citrulline transporter.
View Article and Find Full Text PDFFEBS J
January 2025
Université d'Angers, Inserm, CNRS, CRCI2NA, ICO, Angers, France.
Senescence is a tumor suppressor mechanism triggered by oncogene expression and chemotherapy treatment. It orchestrates a definitive cessation of cell proliferation through the activation of the p53-p21 and p16-Rb pathways, coupled with the compaction of proliferative genes within heterochromatin regions. Some cancer cells have the ability to elude this proliferative arrest but the signaling pathways involved in circumventing senescence remain to be characterized.
View Article and Find Full Text PDFAngiogenesis
January 2025
Department of Pharmacology & Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA.
Reduction-oxidation factor-1 or apurinic/apyrimidinic endonuclease 1 (Ref-1/APE1) is a crucial redox-sensitive activator of transcription factors such as NF-κB, HIF-1α, STAT-3 and others. It could contribute to key features of ocular neovascularization including inflammation and angiogenesis; these underlie diseases like neovascular age-related macular degeneration (nAMD). We previously revealed a role for Ref-1 in the growth of ocular endothelial cells and in choroidal neovascularization (CNV).
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