RNASE1 (Ribonuclease A Family Member 1)

WWOX2 serves as a tumor suppressor, whereas FUT1 functions as a promoter of malignancy. The interplay between tumor inducers and suppressors may serve as a survival mechanism for cancer cells, a subject that has received limited research attention.

However, given the small, male-only cohort, these findings should be regarded as preliminary and will require validation in larger, sex-balanced cohorts, including patients with benign or inflammatory head and neck conditions, to confirm disease specificity. Altogether, our data underscores the translational promise of urinary proteogenomics in HNSCC management.

This investigation marks the initial systematic characterization of a new MDSCs gene signature in breast cancer, alongside the establishment of an MDSCs-associated marker scoring framework with multi-aspect clinical translation capability, thereby linking MDSCs fundamental biology to precision oncology in this cancer type.

Here, we investigated the mechanistic role of eRNA and its interplay with TNF-α signaling in cardiac I/R injury, and evaluated the therapeutic potential of RNase1 and cyclosporine-A (CsA)...These findings identify eRNA as both a biomarker and pathogenic mediator of myocardial I/R injury, and support a dual-targeted strategy using RNase1 and CsA to interrupt the TNF-α/TNFR1-driven inflammatory and mitochondrial death pathways. Targeting both upstream inflammatory and downstream mitochondrial mechanisms represents a promising cardioprotective intervention for acute myocardial infarction.

Finally, a promising RNASE1 target among the most significantly upregulated mRNAs upon RNASE1 depletion is DKK1 (Dickkopf inhibitor 1) which is upregulated in CRC and negatively regulated by RNASE1. Collectively, this initial characterization of endogenous RNASE1 uncovers a function of RNASE1 in inhibition of gene expression and CRC cell proliferation.

Notably, among the nine RDAA-positive NSCLC patients who accepted ALK inhibitor treatment, five achieved objective response including two who experienced complete response (CR). Together, the current study identifies RDAA as an oncogenic driver and proposes an effective targeted therapy strategy for non-mutated NSCLC patients.

We identified 10 M2-like TAM-related prognostic signature genes for BRCA, providing potential therapeutic targets for the treatment of the cancer.

Overall, the study supports the immunosuppressive role of RNase1 in cancer of negatively regulating STAT1 to impair CD8+ T-cell cytotoxicity. Targeting the RNase1-STAT1 interaction could prevent CD8+ T-cell dysfunction in RNase1-highly expressing cancer patients.

We showed that the engineered GnRH-hpRNase1 can specifically target the GnRH receptor-expressing cells and inhibit their proliferation through inducing apoptosis. Owing to its promising anti-tumor activity, the fusion enzyme can be further examined on GnRH-R-expressing tumor xenografts to evaluate its anti-tumor effects in vivo.

Inhibition of ROS1 with lorlatinib suppressed sperm maturation and male fertility reversibly. Future exploration of molecules that specifically target ROS1 and the ROS1 pathway in the epididymis may lead to the development of safe and reversible male contraceptives.

We built and validated the value of NRRS. This contributes to deepening our view of NETosis and potentially provides new strategies for GC treatment.

This study demonstrates the potential of radiogenomics, combining CT and ST, for identifying diagnostic and therapeutic targets for HGSOC, marking a step towards personalized medicine.