The controversial role of CD151 in different solid tumors: promoter or suppressor?Gao, Liu, Cao
et alCancer Cell Int (2025) 25 (1), 110
Abstract: As a member of the tetraspanin superfamily, CD151 plays a pivotal role in tumorigenesis, progression, and metastasis. CD151 is involved in various cellular processes, including cell-cell junction, signal transduction, epithelial-mesenchymal transition (EMT), cancer stem cell maintenance (CSCs), angiogenesis, and exosome regulation. Therefore, CD151 is a potential target for tumor therapy and may be valuable in tumor diagnosis and prognosis. Notably, while CD151 predominantly functions as an oncogene in most cancers, it can also exhibit tumor-suppressive roles in specific contexts, indicating that its function is context-dependent. Additionally, CD151 plays a significant role in modulating the immune microenvironment. For instance, CD151 supports the proliferation, activation, and migration of T cells. The CD151 peptide may function as a tumor vaccination by stimulating CD8 + IFNγ + lymphocytes and inducing cytotoxic effects. Thus, the function of CD151 in tumors is intricate and warrants further investigation. In this review, we discuss the diagnostic and prognostic potential of CD151, as well as its regulatory roles in solid cancers, including those of the digestive system, lung, breast, prostate, and gynecological tissues. Basic experiments and clinical data demonstrate the beneficial and detrimental effects of CD151 in malignancies and offer a path forward for future investigation.© 2025. The Author(s).
Trichomonas vaginalis adhesion protein 33 (TvAP33) promotes HPV infection by upregulating the expression of HPV membrane receptor moleculesSheng, Zhou, Zhang
et alActa Trop (2025) 264, 107578
Abstract: An increasing number of studies have identified Trichomonas vaginalis (T. vaginalis) as a risk factor for human papillomavirus (HPV) infection, yet experimental data and the mechanisms involved are still lacking. Wild-type and T. vaginalis adhesion protein 33 (TvAP33) knockdown T. vaginalis were used to infect HaCaT cells and the vaginal tissue of mice, while HaCaT cells were also transfected to overexpress TvAP33. The effects of TvAP33 on the expression of HPV membrane receptor molecules and HPV infection were assessed. Infection of HaCaT cells with low expression of HPV membrane receptor molecules by T. vaginalis with reduced TvAP33 expression was conducted to analyze whether TvAP33 influences HPV infection through HPV membrane receptor molecules. In this study, we found that T. vaginalis significantly enhances HPV invasion into HaCaT cells and the mouse vagina while also increases the expression of HPV receptor molecules CD151 and HSPG2. Reducing the expression of TvAP33 led to a significant decrease in both HPV invasion rate and CD151/HSPG2 expression. Conversely, overexpressing TvAP33 in HaCaT cells resulted in a notable increase in HPV invasion and CD151/HSPG2 expression. Additionally, the simultaneous reduction of TvAP33 expression in T. vaginalis and CD151/HSPG2 expression in HaCaT cells further decreased HPV invasion rates. These findings suggest that TvAP33 promotes HPV infection by upregulating CD151 and HSPG2 expression. This study not only confirms, through both in vivo and in vitro experiments, that T. vaginalis facilitates HPV infection but also explores the mechanism by which TvAP33 enhances HPV infection by regulating HPV receptor expression. These results provide a theoretical basis for understanding the mechanisms of T. vaginalis co-infection with HPV.Copyright © 2025 Elsevier B.V. All rights reserved.
Mosaic loss of Y chromosome and mortality after coronary angiographyWeyrich, Zewinger, Sarakpi
et alEur Heart J (2025)
Abstract: Acquired somatic mutations emerged as important drivers of adverse cardiovascular disease outcomes. Recently, mosaic loss of Y chromosome (LOY) in haematopoietic cells was identified to induce diffuse cardiac fibrosis in male mice. The aim of the present study was to determine the association between LOY and cardiovascular mortality in patients undergoing coronary angiography.LOY was quantified in 1698 male participants of the LURIC study, who underwent coronary angiography, and its association with all-cause and cardiovascular mortality was determined. Furthermore, the interaction between LOY and inherited genetic susceptibility for cardiac fibrosis was assessed.The frequency of LOY steeply increased in male participants of LURIC at the age of 60 years. Loss of Y chromosome > 17% was associated with significantly higher all-cause [hazard ratio (HR) 1.41, 95% confidence interval (CI) 1.09-1.82] and cardiovascular mortality (HR 1.49, 95% CI 1.09-2.03), which was driven by a higher risk for fatal myocardial infarction (HR 2.65, 95% CI 1.46-4.81). Loss of Y chromosome > 17% was associated with a profibrotic and proinflammatory plasma protein expression profile as characterized by higher plasma levels of osteoprotegerin, matrix metalloproteinase-12, growth differentiation factor 15, heparin-binding EGF-like growth factor, and resistin. Genetic predisposition for lower myocardial fibrosis attenuated the association between LOY and cardiovascular mortality. Genome-wide methylation analyses identified differential methylation in 298 genes including ACTB, RPS5, WDR1, CD151, and ARAP1. Single-cell RNA sequencing further confirmed differential gene expression of 37 of these genes in LOY in peripheral blood mononuclear cells comprising a set of fibrosis-regulating genes including RPS5. RPS5 silencing in macrophages induced a paracrine induction of collagen expression in cardiac fibroblasts documenting a functional role in vitro.LOY represents an important independent risk factor for cardiovascular mortality in male patients with coronary artery disease. Targeting LOY may represent a sex-specific personalized medicine approach.© The Author(s) 2025. Published by Oxford University Press on behalf of the European Society of Cardiology.
Molecular responses of Mytilus coruscus hemocytes to lipopolysaccharide and peptidoglycan as revealed by 4D-DIA based quantitative proteomics analysisXiao, Song, Yang
et alFish Shellfish Immunol (2025) 158, 110143
Abstract: Mytilus are sessile filter feeders that live in close contact with numerous marine microorganisms. Hemocytes, the immunocompetent cells of Mytilus, participate in the immune response in a very efficient manner. Lipopolysaccharide (LPS) and peptidoglycan (PGN) follow specific microbe/pathogen-associated molecular patterns (MAMPs or PAMPs) and are involved in immune stimulation in host cells. This study evaluated the molecular profiles and reactions at protein level of Mytilus hemocytes after stimulation with LPS and PGN. Mytilus coruscus was challenged in vivo with LPS and PGN. The hemocytes were collected after 48 h and analyzed for quantitative proteomics, cell subpopulations, and the free amino acid composition. 4D-DIA technology-based proteomic analysis revealed different protein profiles, as well as different responses at protein level, under either the LPS or PGN challenge. C-type lectins, collagens, and CD151 protein were highly upregulated in LPS-challenged mussels, while phospholipase A2 and dCMP deaminase were highly upregulated in PGN-challenged mussels. Moreover, LPS challenge disrupted dsRNA-mediated translation and stimulated energy-related metabolism, while PGN challenge stimulated proteins involved in the inflammatory response and suppressed amino acid metabolism. In addition, the LPS and PGN challenges differed in their effects on the free amino acid composition and granulocytes ratio of the hemocytes. These findings highlight the different strategies employed by mussel hemocytes in response to different MAMPs, providing insights into the effects of LPS and PGN on Mytilus.Copyright © 2025 Elsevier Ltd. All rights reserved.
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