SIGMAR1 (Sigma Non-Opioid Intracellular Receptor 1)

Analyses showed that API and HES were effective in preventing oxidative stress induced by 5FU in lung tissue, attenuating inflammation and apoptosis by suppressing MAPK/NFκB and Caspase-3/Bax/Bcl-2 pathways, suppressing autophagy by decreasing LC3B expression, and regulating Sigmar1 expression. These results suggest that the two flavonoids, when administered separately or in combination, may be useful in reducing side effects that often occur during the use of chemotherapeutics.

Functionally, FGFR inhibitors ameliorated PD1/PD-L1-mediated T cell suppression in co-culture assays. Together, these findings highlight a novel mechanism by which FGFR inhibitors suppress IFN-γ-induced PD-L1 via autophagy and suggest a potential strategy to improve ICI therapy in FGFR3-altered NMIBC.

We propose that SIGMAR1 serves as a potential functional marker of CSCs and plays a crucial role in regulating self-renewal capacity. Targeting SIGMAR1 may provide a novel therapeutic strategy for preventing metastasis and recurrence-major clinical challenges in lung cancer treatment. Future studies should investigate the underlying mechanisms by which SIGMAR1 modulates CSC properties.

Silencing SIGMAR1 increased HN13 cell sensitivity to cisplatin, indicating its role in drug resistance...These findings highlight SIGMAR1's critical role in OC pathogenesis and its potential as a therapeutic target to overcome chemoresistance. The results also pave the way for future research into RNA-based therapies and precision oncology interventions.

The construction of a BC-related GPCR-TME classifier enabled the effective prediction of the OS of BC patients and the identification of SIGMAR1, a key factor regulating ER stress in BC. The knockout of SIGMAR1 can destroy its protective effect on ER stress, enhance apoptosis of BC cells, and facilitate further investigation of novel treatment strategies for cancer therapy.

Based on these findings, we suggest that SIGMAR1 may influence mitochondrial membrane potential and energy production by modulating Ca2+ uptake, which is critically important to cellular survival. In addition, SIGMAR1 knockdown may offer a potential strategy to be further explored as treatment for OC.

Furthermore, SIGMAR1 inhibition led to a decrease in PD-L1 expression and sensitized oral cancer cells to cisplatin treatment by enhancing apoptosis. These results suggest that SIGMAR1 knockdown may present a promising strategy worthy of further exploration in the management of oral cancer.

Elevation of SIGMAR1 partially blunted the affection of butorphanol on the biological events of CRC cells. To sum up, butorphanol may extenuate the aggressive cellular behaviors to produce tumor-suppressing activity on CRC via binding with SIGMAR1.

Here, we review its role in breast cancer and the current therapies that have been considered based on its known functions. As SigmaR1 is not classified as an oncoprotein, we propose a model in which it serves as an oligomerization adaptor in key cellular pathways, which may help illuminate its association with variable diseases and pave the way for clinical utility in personalized medicine.