S100A4 (S100 calcium binding protein A4)

Moreover, intratumoral hypoxia induces the secretion of Treg-derived extracellular vesicle (EV)-S100a4, which serves as a transcriptional corepressor to impede γδ T cell activation in an epigenetic manner. Overall, these results demonstrate that sex-specific differences in Tregs from HCC are related to the ability of androgen-dependent Ccl2 secretion to enable immune evasion through the suppression of γδ T cell activity.

Using CRISPR/Cas9 to generate S100a4 gene knockout mice, imiquimod was continuously applied to the back skin to induce the psoriasis disease model...Our findings suggest a potential pathogenic role for S100A4 in psoriasis and highlight previously uncharacterized cell-specific transcriptional landscapes and regulatory mechanisms. Our results provide novel insights into the complex pathology of psoriasis and could offer important clues for the development of new targeted therapeutic strategies.

CA1 and SMPDL3A proteins are promising novel specific biomarkers for the early diagnosis of CRC. However, larger prospective trials are necessary to validate their clinical utility.

Our findings provide new insights into the metabolic and immunological mechanisms underlying SOC, and highlight potential targets for therapeutic interventions.

This study reveals the distinct origins and functional heterogeneity of intestinal ILC subsets in CRC. The enrichment of bone marrow-derived ILC2s in TLSs, where they likely support B cell maturation, is associated with improved prognosis and favourable immunotherapy response, which may serve as biomarkers for survival and therapeutic efficacy in CRC.

[This retracts the article on p. 2209 in vol. 7, PMID: 29218245.].

Additionally, TNX05II was significantly resistant to α-glucosidase degradation. This study suggests a possible key structure-target relationship underlying TNX05's antitumor activity, providing a molecular basis for the antitumor mechanism of Arisaema polysaccharides.

This leads to a compensatory increase in ICAM1 levels, ultimately resulting in the promotion of epithelial-to-mesenchymal transition (EMT) in TNBC cells and an increase in tumor metastasis. In summary, our findings highlight the crucial role of XLH-36 in TNBC metastasis, which could be exploited in the development of therapeutic and diagnostic strategies for TNBC patients.

The NRG-based risk model can effectively predict the survival outcomes and immune profiles of DLBCL patients, offering a novel perspective on the link between NRGs and DLBCL.

Notably, many transcripts with METTL2A-mediated m3C sites are upregulated upon METTL2A knockdown. We reveal the transcriptome-wide presence of m3C sites in poly(A) RNA and suggest their potential roles in regulating gene expression.

Both Gli-1 siRNA and GANT61 (an inhibitor of Gli-1) could abrogate the increased TNBC trans-endothelial migration through TNFα-treated ECs. We demonstrated that DM might promote TNBC metastasis via activating the TNFα/Gli-1 axis initiated vascular endothelial mesenchymal-like phenotype.

Moreover, RP11-54O7.17 delivered via liposome demonstrated significant anti-TNBC efficacy in an in vivo model without observing significant systemic toxicity. This study elucidates the regulatory role and molecular mechanism of RP11-54O7.17 in TNBC, which provides a strong scientific basis and potential therapeutic targets for the development of novel SE-lncRNA-based therapeutic strategies.