TAGLN (Transgelin)

We identified several novel plasma proteins for VTE that reflect biological processes outside established VTE pathophysiology, including extracellular matrix regulation, immunity, immune-vascular endothelium interactions, and vascular senescence. Results may provide new modifiable targets to improve VTE risk stratification, prevention, or treatment.

Furthermore, TAGLN emerged as a strong predictive biomarker of dasatinib response, with functional studies confirming its role in modulating drug sensitivity. Altogether, these findings support the clinical utility of basal markers for TNBC stratification and highlight a targeted treatment opportunity for tB-TNBC patients.

In summary, we demonstrate that protein profiling of EVs in relation to osimertinib refractoriness has the potential to identify possible biomarkers that can indicate osimertinib treatment resistance, for example, CSPG4, HSPG2, TAGLN, TNC, THBS1, ANXA1 and CD73/NT5E. Studies in expanded cohorts should be conducted to further validate these putative osimertinib biomarkers.

Our findings suggest that the expression levels of serglycin, ILK, ESD, and PLPD1 may play a significant role in the development of LAC. This information can be valuable for identifying potential treatment targets for lung cancer.

Clinically, TAGLN exhibits progressive overexpression from normal epithelium to primary tumors and metastatic lesions. These findings establish TAGLN as a stiffness-responsive regulator of ECM remodeling and EMT, driving colorectal cancer metastasis and serving as a potential therapeutic target.

In patients post-KTx, elevated serum POSTN is an independent predictor of new-onset malignancy. Further prospective evaluation is warranted.

Our findings highlight the functional heterogeneity of myCAFs and identify TAGLN-expressing myCAFs as critical mediators of tumour progression, providing evidence that targeting stromal TAGLN may represent a promising therapeutic strategy for PDAC.

The drug prediction analysis identified potential therapeutic agents, including agarose, clofibrate, ascorbic acid (vitamin C), 6-aminohexanoic acid, and tetracycline...These findings offer valuable insights into the molecular pathogenesis of OS and highlight novel opportunities for the development of targeted therapeutic strategies. Nevertheless, further functional investigations, large-scale cohort studies, and clinical trials are warranted to substantiate the causal relationships, assess therapeutic efficacy, and establish safety profiles, thereby advancing the prospects for clinical translation.

Immunofluorescent double staining was used to examine the co-expression of CD31 in α-SMA-positive CAFs to identify whether the endothelial-to-mesenchymal transition (EndoMT) is involved in the origin, and obvious colocalization was observed. Visium and Visium HD spatial transcriptomics further revealed endothelial cells (ECs) exhibited remarkable co-expression of CAF-specific marker genes and revealed inferred developmental trajectories to CAFs; molecular determinants, including TIMP1, IGFBP7, THBS2, CD74, COL4A1, COL4A2, AEBP1, S100A6, KCTD12, CALD1, IGHG1, SERPINE1, MCL1, MGP, GSTP1, TAGLN, THBS1, and CTGF, were positively correlated with the spatial developmental trajectories of ECs to CAFs; and CTGF exhibited extensive interactions with other common positively correlated molecular determinants and was a highly connected node in the interaction network. ECs that undergo EndoMT may be one of the potential cellular and mechanical origins of CAFs in HCC, and the development of EndoMT may be associated with CTGF.

In a system of two overlaying scaffolds, cells also retained the viability and expression of smooth muscle contractility markers. The developed approach can be used for three-dimensional myometrium modeling to study the pathogenesis of myometrium-associated diseases.

Our work innovates novel methods of studying EndMT by developing a flexible and cost-effective protein-stamp fabrication and image analysis pipeline. This pipeline can be used by researchers to study the endothelial cell chirality in response to EndMT induction.

Across 324 non-AD controls aged 24-108 years, aging is associated with declines in gene expression associated with translation, proteostasis, and mitochondrial function and increases in those linked to oligodendrocyte and myelination programs (for example M4; hub CNTN2; key driver MOBP); in a 65+ subset, neuronal and protein-folding modules show the strongest decrements with reduced glial gene expression upregulatio. Our results indicate that late-life aging involves increased glial responses and neuronal/proteostasis suppression, whereas AD is also associated with immune- vascular-ECM activation and suppression of neuronal programs.