Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related deaths among cancer patients. Vascular endothelial growth factor A (VEGFA) is involved in regulating biological processes, such as angiogenesis and vascular permeability, and is very closely related to the pathogenesis of various tumours, especially vascular-rich, solid tumours. Clinical data of patients with HCC and other tumours were analysed through public databases, such as the TCGA database, Gene Expression Omnibus database, Human Protein Atlas database, STRING, Tumour Immune Estimation Resource and Kaplan-Meier Plotter. The tumour tissues and adjacent normal tissues of patients with HCC from Hunan Provincial People's Hospital were collected to verify the expression of VEGFA by immunohistochemistry, immunofluorescence, Western blotting and qPCR. VEGFA expression is elevated in multiple tumour types and correlates with the prognosis of tumour patients. VEGFA is involved in regulating the tumour microenvironment and immune cell function in tumour development. Inhibition of VEGFA reduces proliferation, invasion, and migration and promotes apoptosis in HCC cells. VEGFA is a potential predictive biomarker for the diagnosis and prognosis of HCC.
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http://dx.doi.org/10.1111/jcmm.17678 | DOI Listing |
Cell Death Differ
January 2025
Department of Pathology and International Institutes of Medicine, The Fourth Affiliated Hospital (Yiwu), Zhejiang University School of Medicine, Hangzhou, 310058, China.
Cancer stem cells (CSCs) typically reside in perivascular niches, but whether endothelial cells of blood vessels influence the stemness of cancer cells remains poorly understood. This study revealed that endothelial cell-specific GLTSCR1 deletion promotes colorectal cancer (CRC) tumorigenesis and metastasis by increasing cancer cell stemness. Mechanistically, knocking down GLTSCR1 induces the transformation of endothelial cells into tip cells by regulating the expression of Neuropilin-1 (NRP1), thereby increasing the direct contact and interaction between endothelial cells and tumour cells.
View Article and Find Full Text PDFEur J Pharmacol
January 2025
Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
Colorectal cancer (CRC) is a significant global health challenge, marked by varying incidence and mortality rates across different regions. The pathogenesis of CRC involves multiple stages, including initiation, promotion, progression, and metastasis, influenced by genetic and epigenetic factors. The chaperone protein glucose-regulated protein 78 (GRP78), crucial in regulating the unfolded protein response (UPR) during endoplasmic reticulum (ER) stress, plays a pivotal role in CRC pathogenesis.
View Article and Find Full Text PDFObjectives: This study explores the relationship between obesity, endothelial dysfunction, and the critical role of oxidative stress biomarkers in subclinical atherosclerosis.
Design & Methods: The study included 114 adolescents aged 12-17 years from Juiz de Fora, Brazil, divided into 40 individuals with obesity and 74 controls. Physical and biochemical assessments were conducted, including measurements of Brachial Flow-Mediated Dilation (BFMD), Carotid Intima-Media Thickness (IMT), and oxidative biomarkers such as nitrite, nitrate, and 8-isoprostane.
Introduction: In recent years, intravitreal injections (IVT) of vascular endothelial growth factor (VEGF) inhibitors have become the standard of care for several macular disorders. Frequently, the therapeutic course requires numerous injections, posing a burden on patients. Non-adherence to treatment may result in reduced visual outcomes, therefore understanding and addressing the underlying causes is imperative.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2025
Department of Ultrasonography, Fuwai Yunnan Hospital, Chinese Academy of Medical, Sciences/Affiliated Cardiovascular Hospital of Kunming Medical University, Kunming, 650102, China. Electronic address:
Pulmonary arterial hypertension (PAH) is a syndrome characterized by increased pulmonary vascular resistance and elevated pulmonary artery pressure, ultimately leading to right heart failure and even death. Increasing evidence implicates the fat mass and obesity-associated protein (FTO) in various metabolic and inflammatory pathways; however, its role in pulmonary endothelial function and PAH remains largely unexplored. In this study, we examined the effects of endothelial cell-specific FTO knockout on PAH development.
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