Quercetin is involved in several biological activities including inhibition of cell growth and induction of apoptosis in cancer cells. However, it is unclear and unknown whether quercetin influences cell maturation. We examined the effect of quercetin on the growth and differentiation of human preadipocyte cells AML-I. Induced growth arrest of AML-I by quercetin was accompanied by the appearance of characteristics of apoptosis under the adipogenic stimulation by annexin V-fluorescein isothiocyanate staining method. A decrease of nuclear factor-kappaB and the antiapoptotic protein Mcl-1 and an increase of the proapoptotic protein Bad were observed in time-dependent fashion in the quercetin-treated cells compared with the vehicle-treated cells by Western blot analysis. Structure-related flavonoids, including rutin (quercetin-3-O-rutinoside) and quercitrin (quercetin-3-O-rhamnoside), did not have any cytotoxic effect on AML-I. Interestingly, exposure of AML-I to quercetin for 6 days increased the amount of cytoplasmic lipid droplets as well as the expression of fatty acid synthase and peroxisome proliferator-activated receptor gamma proteins. These results suggested that apoptosis induced by quercetin was not linked to adipogenic conversion of preadipocytes.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.metabol.2007.07.008 | DOI Listing |
Sci Rep
December 2024
Princess Margaret Cancer Centre, University Health Network, Toronto, Canada.
Despite decades of improvements in cytotoxic therapy, the current standard of care for locally advanced pancreatic cancer (LAPC) provides, on average, only a few months of survival benefit. Stereotactic Body Radiation Therapy (SBRT), a technique that accurately delivers high doses of radiation to tumors in fewer fractions, has emerged as a promising therapy to improve local control of LAPC; however, its effects on the tumor microenvironment and hypoxia remain poorly understood. To explore how SBRT affects pancreatic tumors, we combined an orthotopic mouse model of pancreatic cancer with an intravital microscopy platform to visualize changes to the in vivo tumor microenvironment in real-time.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Life Sciences, College of Life Sciences, National Chung Hsing University, Kuo Kuang Rd., Taichung, 402, Taiwan.
Hepatocellular carcinoma (HCC) constitutes 90% of liver cancer cases and ranks as the third leading cause of cancer-related mortality, necessitating urgent development of alternative therapies. Lactoferrin (LF), a natural iron-binding glycoprotein with reported anticancer effects, is investigated for its potential in liver cancer treatment, an area with limited existing studies. This study focuses on evaluating LF's anti-liver cancer effects on HCC cells and assessing the preventive efficacy of oral LF administration in a murine model.
View Article and Find Full Text PDFEur J Pharmacol
December 2024
The School of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou, 510006, PR China. Electronic address:
Glioblastoma multiforme (GBM) is a highly heterogeneous and aggressive brain tumor, which presents significant challenges for treatment in clinical settings. Phosphodiesterase 4 (PDE4) inhibitors can prevent the degradation of cAMP and have been used as a potential targeted therapeutic approach for different cancer types. However, its clinical use is restricted by the side effects such as nausea and vomiting.
View Article and Find Full Text PDFInt J Biol Macromol
December 2024
BioLab, Instituto Universitario de Bio-Orgánica "Antonio González", University of La Laguna, La Laguna, Spain.
Glycosylation patterns represent an important signature of cancer cells that can be decoded by glycan-binding proteins, i.e., lectins.
View Article and Find Full Text PDFBiomed Pharmacother
December 2024
Department of Pharmacy, College of Pharmacy, Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan, Gyeonggi-do 15588, Republic of Korea. Electronic address:
Colorectal malignancies associated with KRAS and TP53 mutations led us to investigate the effects of combination therapy targeting KRAS, MEK1, or PLK1 in colorectal cancer. MEK1 is downstream of RAS in the MAPK pathway, whereas PLK1 is a mitotic kinase of the cell cycle activated by MAPK and regulated by p53. Bioinformatics analysis revealed that patients with colorectal cancer had a high expression of MAP2K1 and PLK1.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!