LRRC1 (Leucine Rich Repeat Containing 1)

In the murine model, MDSCs were significantly increased in MIF-expressing PDAC tumors, as were CD74+ M-MDSCs per M-MDSC, confirming in vivo interaction between CD74 and MIF. MDSCs play a crucial role in creating an immunosuppressive TME in PDAC; the MIF-CD74 axis drives interactions between MDSCs and CAFs.

LRRC15-CAR T cells exert anti-osteosarcoma activity while maintaining a positive safety profile. These promising findings support clinical translation of LRRC15-CAR T cells for patients with osteosarcoma and potentially other LRRC15-positive solid tumors.

Finally, development of a bispecific antibody targeting LRRC15 and TGF-β enabled effective downregulation of LRRC15 expression in CAFs and limited tumor progression in mice. This study highlights LRRC15 as a promising therapeutic target and provides insights into CAF-directed cancer treatment strategies.

By integrating recent advancements in genomics, proteomics, single-cell sequencing, and clinical translational research, this article comprehensively elucidates the multifaceted mechanisms of LRRC15 in tumor initiation, metastasis, immune regulation, and therapy resistance. It also discusses current research limitations and future directions, aiming to provide multidimensional theoretical and practical insights for precision oncology.

Further mechanism studies showed that LRRC1 enhances PDK1 stability by promoting its deubiquitination via USP7, thereby increasing AKT1 phosphorylation levels and activating the AKT/GSK3β/β-catenin/VEGFA signaling pathway, ultimately accelerating tumor angiogenesis in HCC. These findings demonstrated a novel role of LRRC1 in tumor angiogenesis, opening up new avenues for future research and treatment development.

Decision curve and calibration curve analyses further confirmed its significant clinical net benefit and good consistency. These four identified DEGs (SULF1, CXCL8, LRRC19, and PBLD) may contribute to the treatment of CRC as a new therapeutic target and provide valuable biomarkers for cancer metastasis research.The four identified DEGs were combined with machine learning to construct a CRC diagnostic model with high clinical application value.

LRRC15 expression is a marker of poorer prognosis in patients with CC, suggesting that LRRC15 represents a potential therapeutic strategy for CC.

Lymph node MSCs in DLBCL patients exhibit unique biological behavior and gene expression profiles, which may be closely related to clinical chemotherapy resistance.

Furthermore, the combination of TAVO423 in combination with other solid tumor cell targeting modalities such as 5-fluorouracil (5-FU), anti-PD-L1 monoclonal antibody, a PD-L1 × CD3 bispecific T-cell engager (TCE), and a CD318-targeting antibody-drug conjugate (ADC) all demonstrated enhanced tumor growth inhibition (TGI) values of 49-67% as compared to the respective monotherapy TGI values of 1-28%...Conclusions. These findings demonstrated the broad potential of the modular AbEn platform for targeted HA degradation to overcome barrier entry in stromal HA-rich solid tumors.

In a syngeneic tumor model, administration of [177Lu]Lu-DUNP19 significantly potentiated checkpoint-blockade therapy, yielding durable complete responses. Together, these results demonstrate that radio-theranostic targeting of LRRC15 with DUNP19 is a compelling precision medicine platform for image-guided diagnosis, eradication, and reprogramming of LRRC15+ tumor tissue that drives immuno-resistance and disease aggressiveness in a wide range of currently untreatable malignancies.

This study describes attempts to identify HuNoV proteinaceous attachment factors from the diarrheal sample. Findings from this study will aid in understanding of HuNoV infection in humans, enrichment of GII.4 HuNoV from various environments and construction of cell lines for HuNoV cultivation in vitro.

Mechanistically, LRRC15 exerted these effects by activating the PI3K/AKT/mTOR signaling cascade. LRRC15 regulates autophagy-induced proliferation and other biological activities of breast cancer cells through the PI3K/AKT/mTOR signaling pathway.