RORC (RAR Related Orphan Receptor C)

Drug sensitivity analysis indicates that the RORC gene is responsive to agents such as VX-680, MG-132, and Sunitinib. Cell biology experiments have confirmed that RORC overexpression significantly diminishes the proliferation, invasion, and migration capabilities of gastric cancer cells. Integrating bioinformatics and cell biology experiments suggests that RORC, a gene associated with rhythm regulation, acts as a tumor suppressor gene that is underexpressed in gastric cancer, thereby serving as a potential biomarker and therapeutic target for this malignancy.

Ili-A inhibited RORC expression, increased malondialdehyde (MDA) content, suppressed glutathione (GSH) production, released free Fe2+, increased reactive oxygen species (ROS), activated the ferroptosis pathway, enhanced enzalutamide sensitivity, and inhibited CRPC cell proliferation. Furthermore, ili-A enhances the interaction between ROR-γ and GPX4.

Spatial imaging analysis of GBM tissues showed that all specimens were positive for both MAIT cells and TANs, and localized enrichment of TANs. These findings revealed an immunosuppressive role of MAIT cells in GBM and highlighted the MAIT-TAN axis as a potential novel therapeutic target to modulate GBM's immunosuppressive tumor microenvironment.

Pharmacological blockade of RORγ/γt with digoxin significantly reduced LC development in two mouse models: a KrasG12D-driven genetic model and a urethane-induced chemical model...Additionally, TCGA analysis revealed that elevated RORC expression is associated with an altered tumor microenvironment (TME) and poorer prognosis in patients with lung adenocarcinoma (LUAD). These findings highlight the therapeutic potential of targeting RORγt to reduce pro-tumor inflammation and propose a strategy for LC treatment.

Furthermore, RORC is also associated with multiple drug resistance, especially docetaxel and paclitaxel. IHC revealed that RORC and candidate gene CDC6 were valuable predictive biomarkers for prognosis. The six-gene signature provides valuable insights into the biological status of HCC patients and is a robust tool for clinical application.

RORc-expressing cells negatively regulate B cell responses and facilitate the pro-tumorigenic functions of hepatic TLSs.

The observed alterations in MAIT cell activity could potentially impact disease prognosis, particularly in colorectal cancer. This study provides new insights into the dynamics of MAIT cell responses at mucosal barriers, highlighting possible therapeutic targets for modulating MAIT cell functions in aging and disease.

Conversely, ligation of PD-1 suppressed Il17a and Rorc gene expression and IL-17A production by purified Vγ4 γδ T cells stimulated via the TCR, but not with IL-1β and IL-23. Our study demonstrates that PD-1 regulates TCR-activated CD27- Vγ4 γδ T cells, but that cytokine-activated IL-17A producing γδ T cells escape the regulatory effects of the PD-1-PD-L1 pathway.

The hypoxic microenvironment in thymoma may be a driver of TAMG by increasing HIF1A. These findings may lead to new therapeutic approaches targeting HIF1A in the development of TAMG.

Th22, Th17, Th1, and Th2 subsets may play an essential role in BC patients. Th22, Th17, Th1, and Th2 cells may have potential significance to be used as clinical markers in BC patients with different molecular classification. Th22 cells may have potential value in BC patients' outcomes prediction, providing clinical value.

In the two validation cohorts, 1-year AUCs were also >0.70, and the model could well distinguish high-risk and low-risk subgroups. The above results may provide guidance for developing novel treatment and prognostic strategies in ESCC patients.

We performed single-cell RNA sequencing (scRNA-seq) of sorted CD4 + T cells from BM mononuclear cells (BMMCs) of healthy donor (HD), patients with monoclonal gammopathy of undetermined significance (MGUS), smoldering MM (SMM), and MM at diagnosis, and patients with or without minimal residual disease (MRD) after treatment with bortezomib/thalidomide/dexamethasone (VTD). We identified 17 clusters of BM CD4 T cells by scRNA-seq,, which were subdivide into classical CD4 T subsets; naïve (CCR7 + SELL + HNRNPLL - ), central memory (CCR7+SELL+HNRNPLL+), tissue-resident memory T (TRM, CD69 high KLF3 - S1PR1 - ), Th1 (TBX21 + CXCR3 + IFNG + ), Th2 (GATA3 + CCR4 high ), Th17(RORC + CCR6 high ), cytotoxic T (GZMB + PRF1 + GNLY + NKG7 + ) and regulatory T cells (Tregs, FOXP3 + CTLA4 + ). Notably, the frequency of cytotoxic T was increased in MM patients at diagnosis compared with HD, while the frequency of cytotoxic T was significantly reduced after VTD in both patients with or without MRD. Interestingly, frequency of activated Tregs (HLA- DR high CTLA4 high ) among total Tregs was increased in MM at diagnosis compared with HD.