COLEC11 (Collectin Subfamily Member 11)

Notably, CALCB is already under development as a therapeutic target for migraines, lending credibility to the promising drug development prospects for TBC1D17. Future studies are needed to confirm the causal role of TBC1D17 and explore the underlying mechanisms in migraine.

These findings provide crucial new insights into fibroblast heterogeneity within CRC liver metastases. We characterize PRELP+ CAFs as a specialized, terminally differentiated fibroblast population that contributes to immunosuppression and tumor progression, highlighting them as a potential therapeutic target for inhibiting metastatic advancement.

Further, EGFR and TGF-βRII were found to be abundantly expressed in renal fibroblasts, and molecular docking analysis along with immunofluorescence/confocal microscopy confirmed CL-11's interaction with these receptors. Our findings provide strong evidence that CL-11 plays a critical role in renal fibroblast proliferation and activation via engagement with EGFR and TGF-βRII, shedding light on the mechanisms by which CL-11 stimulates cellular activation and proliferation.

Circulating FAP reflects age-independent, fibrotic ovarian aging, offering stromal-specific information not captured by conventional hormonal markers. This study provides the first clinical validation of FAP as a biomarker for ovarian stromal aging, holding potential for improved reproductive risk assessment.

Overall, our study provides the first single-cell analysis of the cellular and molecular differences between PL and LM in CRNELM patients. We identified distinct cell subsets and receptor-ligand interactions that may drive TME discrepancies and support metastatic tumor growth. These insights highlight potential therapeutic targets and inform strategies for better managing CRNELM patients.

This study provides evidence of a causal relationship between AD and CRC, suggesting that shared genetic and inflammatory pathways may underlie both conditions. The identification of COLEC11 as a potential link between AD and CRC offers new avenues for research and therapeutic interventions. These findings contribute to a deeper understanding of the interplay between neurodegenerative and oncologic diseases, highlighting the importance of exploring common pathogenic mechanisms.

In short, 3 biomarkers with good diagnostic efficacy were identified, providing a new perspective of therapeutic targets for liver metastasis in COAD.

The inflammatory response in IHS is primarily induced by myeloid cells. COLEC11 can reduce the infiltration level of this group of cells, and myeloid inflammatory cells may be a novel target for ICC treatment. We developed a novel nomogram that could effectively predict the inflammatory state of patients with ICC, which will be useful for guiding individualized treatment plans.

Finally, our in vitro experiments proved that ANGPTL2CAFs and SPP1macrophages promote the metastasis of CRC cells. Our study selected four characteristic genes of LM-CRC and identified ANGPTL2CAFs and SPP1macrophages subtypes as metastasis accelerators of CRC which provided a potential therapeutic target for LM-CRC.

CL-11 also had direct stimulatory effects on human tumor cell proliferation in melanoma and several other types of cancer cells in vitro. Overall, our findings provide the first evidence to our knowledge that CL-11 is a key tumor growth-promoting protein and a promising therapeutic target in tumor growth.