NR1D1 (Nuclear Receptor Subfamily 1 Group D Member 1)

These findings support the concept that the efficacy of anticancer therapies can be enhanced by targeting the metabolic adaptations that tumor cells rely on for survival. Combining sorafenib with agents like SR9009, that disrupt metabolic homeostasis, may offer a promising strategy for treating advanced HCC.

A mechanistic pharmacokinetic-pharmacodynamic model incorporating the clock network recapitulated experimental observations and enabled prediction of treatment timing. Our findings highlight the importance of timing in GBM therapy and propose combining circadian profiling with mathematical modeling to personalize GBM chronotherapy.

A prognostic model utilizing the RS value was successfully proposed. Meanwhile, we identified PDIA3, PGF, and GRP as novel treatment biomarkers for THCA.

Collectively, DCA inhibits noncancerous NCM460 colon cell proliferation via cell cycle arrest and apoptosis accompanied with a drop of Bmal1::Clock gene expression and altered Wnt signaling pathways. The Bmal1::Clock regulatory network is relatively normal in the DCA-treated noncancerous NCM460 colon cells but not in colon cancer tissues.

Pharmacological inhibition of REV-ERBα exhibits high potency in blocking the growth of NEPC tumors including patient-derived xenografts. Our findings reveal that therapy-induced LP development entails a coordinated induction of a network of LP drivers and that REV-ERBα is an unexpected master regulator of the network and a promising therapeutic target for treatment of advanced prostate cancer such as NEPC.

We highlight its clinical utility as a prognostic biomarker and therapeutic target, focusing on pharmacological modulators with demonstrated preclinical efficacy. We also critically discuss challenges in targeting NR1D1 and its potential in combination therapies, offering new insights for cancer treatment.

This research found that CCND1/Cyclin D1 was upregulated in Xp11.2 tRCC through three mechanisms, high-expression CCND1/Cyclin D1 inducing PDL1 degradation. Overall, the study provided a theoretical basis for sequentially using CDK4 inhibitors and anti-PDL1 for Xp11.2 tRCC treatment.

Background: Carrimycin is a mixture of spiramycin derivatives with antibacterial functions... h-SPM reduced the protein level of NR1D1, disrupted metabolic regulation, accumulating ceramide, and the subsequent increased ROS generation promoted apoptosis and pro-inflammatory-like response of cells. Our findings unveiled the anticancer mechanism of a potent anticancer derivative of spiramycin and unveiled its mechanism of action.

Br suppresses CRC progression via regulating lipid metabolism through the NR1D1-APOH axis. These findings establish Br as a potential therapeutic for CRC prevention and treatment.

We identified novel MAML2 fusion partners, most of which likely represent passenger alterations, possibly arising from genomic instability or impaired p53 function. However, ATXN3::MAML2 fusions, previously reported in a pre-cancerous pancreatic disease case, may represent a pathogenic alteration warranting further investigation.

Dysregulation of NR1D1 has been linked to cancer progression and poor prognosis in lung cancer. This study offers valuable insights into the impact of CS on NR1D1 gene regulation and its role in lung cancer development, which is mediated through disrupted redox balance and inflammation, while highlighting the potential therapeutic role of TQ in mitigating this process.

NR1D1 may play a crucial oncogenic role in the occurrence and development of CRC.