Adv Sci (Weinh). 2026 Apr 3:e17640. doi: 10.1002/advs.202517640. Online ahead of print.

ABSTRACT

The embryonic coelomic mesothelium acts as a critical progenitor hub during mammalian organogenesis, undergoing epithelial-to-mesenchymal transition (EMT) to drive vascular growth and parenchymal development in visceral organs. A prominent example is the epicardium, which plays an essential role during heart development. The principles of gene regulation in the coelomic mesothelium remain poorly defined. Specifically, it is unclear how cis-regulatory elements, including enhancers, orchestrate the spatiotemporal patterns of gene expression required for mesothelial identity and function. Here, a multi-omic approach was used to identify trans- and cis-regulatory elements that regulate mesothelial gene expression in three organs: heart, lung, and pancreas. This analysis uncovers a cardiac-specific regulatory circuit in which the transcription factor (TF) TBX20 selectively activates epicardial enhancers to orchestrate essential developmental programs. In contrast, TF MAF orchestrates pan-mesothelial gene expression via conserved CREs, which are absent in non-mesothelial lineages. Our integrated genomic analysis reveals MAF as a central custodian of mesothelial identity, a role underscored by its negative correlation with EMT, evolutionary conservation, and dynamic regulatory activity throughout development. Our work establishes a foundational blueprint of the gene regulatory landscape governing the coelomic mesothelium, defining both conserved principles and organ-specific mechanisms of spatiotemporal gene expression during early mammalian development.

PMID:41933934 | DOI:10.1002/advs.202517640

Future Sci OA. 2026 Dec;12(1):2653101. doi: 10.1080/20565623.2026.2653101. Epub 2026 Apr 3.

ABSTRACT

BACKGROUND: Clarification of the molecular mechanism of malignant tumor progression, identification of the key signaling pathways and molecules involved in the processes of invasion and metastasis, and identification of new targets and strategies for effective tumor treatment are extremely important for scientific research and clinical application prospects.

METHODS: Based on large-sample data mining, we first evaluated the expression and mutation profiles of SPRR family genes across cancers and then focused on the molecular functions of SPRR2D across cancers.

RESULTS: Multi-omics experiments revealed that SPRR2D is significantly overexpressed in various tumors, especially in LUSC. ROC curve analysis revealed that SPRR2D demonstrated significant diagnostic efficacy across cancers. Cox regression analysis revealed that the expression of SPRR2D was associated with the survival time of patients with various tumors. Moreover, the expression of SPRR2D is closely related to tumor immune infiltration. GDSC data analysis revealed that the expression levels of SPRR1A, SPRR1B, SPRR2A, SPRR3, and SPRR2D are negatively correlated with the sensitivity to gefitinib, trametinib, bosutinib, afatinib, lapatinib, and erlotinib.

CONCLUSIONS: From a multi-omics perspective, it was revealed that SPRR2D plays a significant role in regulating tumorigenesis and drug sensitivity in tumors.

PMID:41933926 | PMC:PMC13051589 | DOI:10.1080/20565623.2026.2653101