The aims of the study are to explore the effect of ursolic acid (UA) on the growth of gastric cancer cell line BGC-803 and hepatocellular cancer cell H22 xenograft and to understand the mechanism. UA inhibits growth of BGC-803 cells in vitro in dose-dependent and time-dependent manner. Treated with UA in vivo, tumor cells can be arrested to G0/G1 stage. The apoptotic rate was significantly increased in tumor cells treated with UA both in vitro and in vivo. DNA fragmentation was found in BGC-803 cells exposed to UA. UA activated caspase-3, -8, and -9 and down regulated expression of Bcl-2 in BGC-803 cells. The expression of caspase-3 and -8 was elevated in tumor cells from xenograft treated with UA. ¹⁸F-FLT PET-CT imaging confirmed tumor model and UA effectiveness. Our results indicated that UA inhibits growth of tumor cells both in vitro and in vivo by decreasing proliferation of cells and inducing apoptosis.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116524 | PMC |
http://dx.doi.org/10.1155/2011/419343 | DOI Listing |
Hepatology
January 2025
Hepatic Surgery Centre, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, People's Republic of China.
Background And Aims: Immune checkpoint inhibitors (ICIs) have revolutionized systemic hepatocellular carcinoma (HCC) treatment. Nevertheless, numerous patients are refractory to ICIs therapy. It is currently unknown whether diet therapies such as short-term starvation (STS) combined with ICIs can be used to treat HCC.
View Article and Find Full Text PDFNeuro Oncol
January 2025
Department of Medicine, Division of Experimental Medicine, McGill University.
Background: Glioblastoma is an aggressive brain cancer with a 5-year survival rate of 5-10%. Current therapeutic options are limited, due in part to drug exclusion by the blood-brain barrier, restricting access of targeted drugs to the tumor. The receptor for the type 1 insulin-like growth factor (IGF-1R) was identified as a therapeutic target in glioblastoma.
View Article and Find Full Text PDFAn Acad Bras Cienc
January 2025
Universidade Federal de Pernambuco, Departamento de Histologia e Embriologia, Av. Prof. Moraes Rego, 1235, Cidade Universitária, 50760-420 Recife, PE, Brazil.
Matrix metalloproteinases (MMP) have been identified as biomarkers for several diseases, including cancer. The increase in the expression of these enzymes has been related to greater tumor aggressiveness. MMP-26 is expressed constitutively in the endometrium and some cancer cells of epithelial origin.
View Article and Find Full Text PDFJ Appl Oral Sci
January 2025
Ningde Hospital Affiliated to Ningde Normal University, Department of Stomatology, Fujian, China.
Objective: This study aimed to investigate the role of transmembrane emp24 domain-containing protein 2 (TMED2) in oral squamous cell carcinoma (OSCC).
Methodology: A bioinformatics analysis was first conducted to explore TMED2 expression in OSCC and its relation with overall survival. The analysis results were further verified by assessing TMED2 expression levels in human normal oral keratinocyte cells and human OSCC cell lines using quantitative real-time polymerase chain reaction and the Western blot.
Brief Bioinform
November 2024
Department of Neurosurgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100730, China.
This study aimed to investigate the genetic association between glioblastoma (GBM) and unsupervised deep learning-derived imaging phenotypes (UDIPs). We employed a combination of genome-wide association study (GWAS) data, single-nucleus RNA sequencing (snRNA-seq), and scPagwas (pathway-based polygenic regression framework) methods to explore the genetic links between UDIPs and GBM. Two-sample Mendelian randomization analyses were conducted to identify causal relationships between UDIPs and GBM.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!