The current study aimed to explore the effect of homocysteine (Hcy) on the viability and migration ability of human umbilical vein endothelial cells (HUVECs), as well as to examine the underlying mechanism. The association between the expression level of Hcy and lower extremity deep vein thrombosis (DVT) was detected in clinical samples collected from patients. In addition, the effect of Hcy on the viability and migration ability of HUVECs was detected by cell counting kit-8 and Transwell assays, respectively, while vascular endothelial growth factor (VEGF) expression was measured in order to verify the effect of Hcy on VEGF. The results indicated that the serum Hcy levels in DVT patients were significantly increased. experiments also confirmed that Hcy was able to significantly inhibit the viability and migration ability of HUVECs, and downregulate the expression of VEGF in these cells. Furthermore, the inhibitory effect of Hcy on HUVEC viability and migration ability was achieved by downregulating the expression of VEGF using small interfering RNA transfection. In conclusion, Hcy inhibited the viability and migration ability of HUVECs by downregulating the expression of VEGF. This may underlie the high incidence of DVT in patients with hyperhomocysteinemia.
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http://dx.doi.org/10.3892/etm.2019.8043 | DOI Listing |
Open Life Sci
December 2024
Department of Pathology, Harbin Medical University Cancer Hospital, No. 150, Haping Road, Harbin, Heilongjiang, 150081, China.
To investigate the biological role of MFAP5 in endometrial cancer (EC). HEC-1-A and Ishikawa cells overexpressing MFAP5 were created. Cell proliferation, apoptosis, migration, and invasion were evaluated using CCK8, colony formation, flow cytometry, and transwell assays.
View Article and Find Full Text PDFCancer Med
January 2025
Department of Gastroenterology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, People's Republic of China.
Background: The toxicity and drug resistance associated with oxaliplatin (L-OHP) limit its long-term use for colorectal cancer (CRC) patients. p53 mutation is a common genetic trait of CRC. PRIMA-1 (APR-246, eprenetapopt) restores the DNA-binding capacity of different mutant P53 proteins.
View Article and Find Full Text PDFAnticancer Agents Med Chem
January 2025
Department of Chemistry, College of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi Arabia.
Background: Cucurbitacin E glucoside (CEG), a prominent constituent of Cucurbitaceae plants, exhibits notable effects on cancer cell behavior, including inhibition of invasion and migration, achieved through mechanisms such as apoptosis induction, autophagy, cell cycle arrest, and disruption of the actin cytoskeleton.
Objective: Melanoma, the fastest-growing malignancy among young individuals in the United States and the predominant cancer among young adults aged 25 to 29, poses a significant health threat. This study aims to elucidate the apoptotic mechanism of CEG against the melanoma cancer cell line (A375).
Curr Cancer Drug Targets
January 2025
Laboratory of Translational Medicine in Microvascular Regulation, Medical Research Center, Institute of Microvascular Medicine, Medical Research Center, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong, China.
Background: Over 50% of lung adenocarcinoma patients have high levels of complement factor H (CFH) expression. Previous studies have reported that CFH inhibits the migration of endothelial cells. In this study, we investigated the mechanism by which CFH affects lung adenocarcinoma development via phosphorylation of STAT3.
View Article and Find Full Text PDFArab J Gastroenterol
January 2025
Fourth Oncology Department, Anyang Tumor Hospital, Anyang City, Henan Province 455000, China. Electronic address:
Background And Study Aims: Nicotinamide N-methyltransferase (NNMT) is aberrantly expressed in tumors and is implicated in the progression and chemoresistance of cancers. This project attempts to explore the specific molecular mechanism by which NNMT enhances 5-fluorouracil (5-FU) resistance in gastric cancer (GC).
Materials And Methods: By bioinformatics analysis, the expression of NNMT in GC was analyzed and its relationship with patients' prognoses was examined.
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