NUPR1 (Nuclear Protein 1 Transcriptional Regulator, Candidate Of Metastasis 1)

We identified the H4K8la-NUPR1 axis as a key regulatory pathway that mediates protective autophagy and developed targeted therapeutic strategies to disrupt this pathway. These findings provide novel insights into epigenetic regulation and targeted therapy for GBM.

These findings highlight sdAb#07.81 as a promising therapeutic agent and validate the platform's effectiveness for addressing intracellular disordered targets like NUPR1. This work underscores the potential of sdAbs as a cancer therapeutic and provides a foundation for advancing sdAb#07.81 into preclinical and clinical development to address the critical unmet needs of TNBC treatment.

These findings suggest that targeting NUPR1 signaling and associated metabolic rewiring could help overcome drug resistance. The resistance model presented may serve as a useful tool to explore combination strategies for improving therapeutic outcomes in PDAC.

Furthermore, the expression of NUPR1 (encoding nuclear protein 1, transcriptional regulator), LDLRAD4 (encoding low density lipoprotein receptor class A domain containing 4) and MDM2 (encoding mouse double min 2) were verified by RT‑qPCR. Overall, the present study contributes to the understanding of the carcinogenic role of WSB2 in different types of cancer.

Our work underscores the role of Gln transporters and the NUPR1-mediated stress response in PCa cell survival, oxidative stress, mitochondrial functions, and radioresistance. Our findings provide a potential therapeutic in vivo strategy to enhance the efficacy of RT and suggest a potential synergism between the depletion of Gln transporters or NUPR1 and OXPHOS inhibition.

Clinically, elevated NR3C1 positively correlates with NUPR1 expression in OT patients, and both are positively associated with poorer prognosis. Overall, our study identified the NR3C1/NUPR1 axis as a critical regulatory pathway in psychological stress-induced OT metastasis, suggesting a potential therapeutic target for intervention in OT metastasis.

PD promotes PCa cell ferroptosis to enhance the therapeutic effect of DTX in PCa via the METTL16/m6A/NUPR1 axis. Our findings offer a novel strategy for improving the therapeutic efficacy of DTX in PCa.

Additionally, tumor-derived lactate is shown to upregulate NUPR1 expression in macrophages via histone lactylation, perpetuating a feedback loop that intensifies immune suppression. Pharmacological targeting of NUPR1 reverses M2 polarization, curtails tumor growth, and augments the efficacy of PD-1 blockade in preclinical models, positioning NUPR1 as both a potential biomarker for immunotherapy responsiveness and a therapeutic target to boost immunotherapy efficacy in HCC.

Then, we performed RNA sequencing to compare gene expression between parental and RR cells, and cells pretreated with or without RSL3...Overall, our findings identify ferroptosis inactivation linked with resistance to radiotherapy. Besides, NUPR1 can promote radiation resistance by inhibiting ferroptosis, and targeting NUPR1 may be a potential strategy to relieve radioresistance associated with ferroptosis in CRC.

Intriguingly, MCF7-TamC3 cells also exhibit characteristics that resemble the luminal B-ERBB2+ breast tumor subtype, like the increased expression of ERBB2 and the increased sensitivity to monoclonal ERBB2-targeting antibody Trastuzumab in vitro...Results of the bioinformatics analysis showed that the NUPR1 mRNA expression level is also correlated with the clinical grading of the Tamoxifen-treated ER+ primary breast cancer...These findings indicate that dysregulation of NUPR1 promotes the development of estrogen independence in ER+ breast cancer cells in part through expression regulation of HDAC5, ERBB2, and BIRC5. Targeting NUPR1 or its downstream regulating molecules may offer a potential strategy for overcoming resistance to endocrine therapy in patients with ER+ breast cancer.

This study suggests that MYH11 activates the PI3 K/AKT pathway by up-regulating the expression of NUPR1, and promotes bladder cancer progression by inhibiting ferroptosis and promoting M2 polarization of macrophages.

These findings have implications for the therapeutic modulation of cellular iron homeostasis in regenerative medicine and in cancer prevention. Furthermore, our findings are consistent with a model whereby most human cancers initiate at a young age, thereby highlighting the importance of directing cancer prevention efforts towards young individuals.