Search

Hepatocellular carcinoma (HCC) is a highly aggressive malignant tumor with a poor prognosis. This research aimed to investigate the role of F13B in HCC and its underlying mechanisms. Through comprehensive bioinformatics analysis of the GSE120123 and The Cancer Genome Atlas (TCGA)-Liver hepatocellular carcinoma (LIHC) datasets, we identified 220 overlapping prognosis-related genes. Eight key genes, including the previously unreported CCDC170 and F13B in HCC, were identified through Least Absolute Shrinkage and Selection Operator (LASSO)-Cox regression analysis. F13B emerged as a significant prognostic factor in HCC, warranting further investigation in subsequent analyses. In vitro experiments showed that F13B expression was notably reduced in HCC cell lines and tissues, particularly in Huh-7 and SMMC-7721 cells. Overexpression of F13B inhibited cell invasion, migration, and proliferation, while its knockdown produced the opposite effect. A lactate dehydrogenase (LDH) activity assay in human umbilical vein endothelial cells (HUVECs) demonstrated that F13B overexpression reduced vascular endothelial growth factor (VEGF)-induced cytotoxicity, whereas knockdown increased it. Further analysis revealed that F13B negatively regulates VEGFA expression, affecting HUVEC proliferation. In HUVECs, F13B overexpression reversed VEGF-induced upregulation of key angiogenesis markers, including phospho-VEGF receptor 2 (p-VEGFR2), matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), as well as AKT/mTOR signaling proteins, phospho-Akt (p-AKT), and phospho-mTOR (p-mTOR). Additionally, F13B negatively regulated VEGFA and hypoxia-inducible factor 1 A (HIF1A) under hypoxic conditions, counteracting the hypoxia-induced increase in cell viability. These findings suggest that F13B regulates angiogenesis through the HIF-1α/VEGF pathway and plays a crucial role in HCC progression. Our results highlight the potential of F13B as a therapeutic target in HCC, providing novel insights into the molecular mechanisms of HCC and its prognostic significance.

Background & Aims. Small nuclear ribonucleoprotein U1 subunit 70 (SNRNP70) as one of the components of the U1 small nuclear ribonucleoprotein (snRNP) is rarely reported in cancers. This study aims to estimate the application potential of SNRNP70 in hepatocellular carcinoma (HCC) clinical practice. Methods. Based on the TCGA database and cohort of HCC patients, we investigated the expression patterns and prognostic value of SNRNP70 in HCC. Then, the combination of SNRNP70 and alpha-fetoprotein (AFP) in 278 HCC cases was analyzed. Next, western blotting and immunohistochemistry were used to detect the expression of SNRNP70 in nucleus and cytoplasm. Finally, Cell Counting Kit-8 (CCK-8) and scratch wound healing assays were used to detect the effect of SNRNP70 on the proliferation and migration of HCC cells. Results. SNRNP70 was highly expressed in HCC. Its expression was increasingly high during the progression of HCC and was positively related to immune infiltration cells. Higher SNRNP70 expression indicated a poor outcome of HCC patients. In addition, nuclear SNRNP70/AFP combination could be a prognostic biomarker for overall survival and recurrence. Cell experiments confirmed that knockdown of SNRNP70 inhibited the proliferation and migration of HCC cells. Conclusion. SNRNP70 may be a new biomarker for HCC progression and HCC diagnosis as well as prognosis. SNRNP70 combined with serum AFP may indicate the prognosis and recurrence status of HCC patients after operation. [ABSTRACT FROM AUTHOR]

In the present work, adhesion has been incorporated in a model for receding contact between an elastic layer and a half plane under flat and parabolic punches. Based on the JKR model for adhesion and with the help of integral transformation, solution of the problem may be reduced to a system of singular integral equations. A numerical scheme has been proposed and verified. The effect of adhesion on contact size and the stresses has been demonstrated. [ABSTRACT FROM AUTHOR]

IntroductionSclerotherapy is a commonly utilized treatment approach for venous malformations. Absolute ethanol is renowned for its remarkable efficacy as a potent sclerosants, but it is potentially associated with severe complications. Foam sclerotherapy is considered superior to liquid sclerotherapy owing to its heightened efficacy and diminished incidence of complications. Thus, our objective was to devise an ethanol foam sclerosant that delivers exceptional efficacy while mitigating complications.MethodsIn the first set of experiments, we identified the suitable range of ethanol concentrations for sclerotherapy through human umbilical vein endothelial cell proliferation assays and blood clotting experiments. Next, the surfactants polysorbate 80, egg yolk lecithin, and hyaluronic acid were added to create stable ethanol foam, with their ratios meticulously optimized.ResultsThe optimal concentration range of ethanol was determined to be 30–60%. Eventually, a 48% ethanol foam was successfully produced with excellent stability. Other than ethanol, the formulation included 5 × 10−3 g/mL polysorbate 80, 10−2 g/mL egg yolk lecithin, and 0.04 mL/mL hyaluronic acid.DiscussionThe novel ethanol foam produced here could be a promising candidate for the treatment of venous malformations.