MCAM (Melanoma Cell Adhesion Molecule)

CD146+ hPDL-MSCs do not always show higher levels of immunomediator expression. Further research is necessary to isolate hPDL-MSC subpopulations with optimal potential for therapeutic applications.

EVs enriched in platelet (CD49e) and endothelial (CD31) markers were associated with corticosteroid response, whereas EVs enriched with endothelial (CD105 and CD146) and B lymphocyte (CD19) markers were associated with mortality. Overall, EVs enriched in endothelial and monocyte markers may represent a candidate non-invasive tool for predicting corticosteroid response and mortality in AH, aiding risk stratification and early identification of non-responders for timely transplant evaluation.

They also wish to apologize to the readership of the Journal for any inconvenience caused. [Molecular Medicine Reports 12: 3432‑3438, 2015; DOI: 10.3892/mmr.2015.3815].

The CD73+CD39+CD146+ cell subset showed self-renewal and multipotency abilities and was located in perivascular areas of BM. Such cell subset was also reported in single and dual-mobilized leukopaks.

Our findings underscore the pivotal role of CD146+ CAFs in shaping an immunosuppressive microenvironment and highlight CD146+ CAFs and COL4A1 as promising candidates for targeted therapy in gastric cancer.

Elevated levels of soluble MCAM have been linked to poor outcomes in various malignancies and can influence tumor microenvironments. This review synthesizes current understanding of MCAM's multifunctional roles, its bidirectional influence in health and disease, and its potential as a therapeutic target in cancer.

Additionally, the transcription factor myocyte enhancer factor 2 C (MEF2C) was found to bind to the promoters of PDGFA, PDGFB, ANGPT1, and ANGPT2, initiating their transcription. Knockdown of MEF2C inhibited the pro-angiogenic activity of MCAM+ myCAFs both in vitro and in vivo MCAM+ myCAFs promote the transcription of pro-angiogenic factors through MEF2C, thereby enhancing angiogenesis and promoting tumor growth in solid-type ACC.

However, bevacizumab (Bev) shows limited therapeutic effects on NSCLC BrM...Targeting CD146 by imaprelimab or AXL by bemcentinib exhibits more effective anti-angiogenic effects than Bev for BrM in vivo. These findings provide novel anti-vascular strategies for BrM. CD146+ BrM-CSCs promotes high vascularization of lung cancer brain metastases through dual enhancement of VEGF/VEFGR, which suggests that targeting CD146 is a novel anti-vascular strategy for BrM.

CD146+ MSCs show stronger ARDS therapeutic potential than CD146- MSCs via pro-angiogenic/immunomodulatory traits. Nuclear factor kappa B/cyclooxygenase 2 activation aids epithelial repair, highlighting CD146+ MSCs as promising targets.

Paradoxically, exosomes also mediate treatment resistance through intercellular transfer of resistant phenotypes, particularly in imatinib-resistant CML and chemoresistant AML, revealing both challenges and therapeutic targets. Clinical translation faces significant hurdles, including standardization of isolation protocols, optimization of cargo loading, scalable manufacturing, and regulatory framework development. The convergence of enhanced biological understanding, technological innovation, and evolving regulatory landscapes positions exosome-based strategies to revolutionize leukemia management through precision diagnostics and targeted therapies with reduced systemic toxicity.

Immunohistochemistry confirmed cerebral endothelial localization of MCAM and SCARB1 in GBM, in addition to nonvascular patterning within the GBM, suggesting these receptors may be targets that could be exploited for drug delivery. The present study identified changes to BBB markers of paracellular permeability, as well as active and receptor-mediated transcellular transport that could present novel avenues to consider to enhance the permeability and GBM access of current and future therapeutics.

P-gp and CD146 represent complementary markers of endothelial identity in gliomas and may serve as histopathological indicators of BBB integrity and tumor vascular remodeling. Their combined evaluation offers a novel insight into the BBB-BBTB transition and may support microvascular phenotyping as an adjunct criterion for glioma grading.