GOLM1 (Golgi Membrane Protein 1)

Notably, the present review summarizes and discusses the clinical value of these proteins in PCa prediction, diagnosis, prognosis and drug resistance monitoring. These emerging peripheral blood protein biomarkers are promising for improving PCa stratification and management.

Our results delineate multiple acquired resistance mechanisms to trastuzumab and T-DXd in HER2+ GC in vivo. This information may guide trials combining trastuzumab or T-DXd with new agents to enhance the efficacy and durability of HER2 blockade.

Our findings suggest that, under the control of GOLM1, HCC cell-derived exosomal miR-4449 and miR-3651 increase angiogenesis and vascular permeability by targeting KEAP1 and ZO-1, highlighting the potential of exosomal miRNAs as promising therapeutic targets for HCC.

Specifically, CRISPR interference of KPNA2 or TK1 inhibited cellular proliferation and invasion while also phenocopying a pro-apoptotic effect with cisplatin...Their membrane expression (notable in the case of PD-L1) and functional roles in immune modulation, make them reasonable targets of CAR T-cell immunotherapy. We posit that a combined strategy targeting KPNA2, GOLM1 and TK1 with or without PD-1/PD-L1 axis inhibitors could provide a better strategy to treat patients with ICI resistant LUAD and generate prolonged and stable immune remodeling.

TBS has potential implications for the prediction, risk guidance, and treatment of HF patients. S100B is a pivotal biomarker and therapeutic target for HF.

Our findings reveal a novel mechanism involving the GOLM1-ACLY axis within macrophages that regulates tumor progression, which suggest a potential strategy for tumor intervention.

Moreover, neutralizing GOLM1 by an antibody suppressed mouse inflammation and atherogenesis. GOLM1 is an atherogenic mediator and a promising therapeutic target for the intervention of atherosclerotic diseases.

This comprehensive approach provides novel insights into lung adenocarcinoma biology, emphasizing the role of genetic and immune factors in tumor progression. The findings support the development of personalized therapeutic strategies targeting both tumor cells and the immune microenvironment.

Transcriptomic analyses showed that both CC-885 treatment and GOLM1 knockdown modulate critical pathways involved in apoptosis. These findings position CC-885 as a promising therapeutic candidate for HCC, acting primarily through CRBN-dependent degradation of GOLM1, and support its further development for clinical application.

Further, to validate select key roles, GOLM1 was silenced in MMNK-1 cholangiocytes and the effects on cell functions were studied. The silencing resulted in impaired mitochondrial function, reduced mitochondrial and P-body markers, increased apoptosis, and reduced cell adhesion, suggesting crucial roles of GOLM1 in maintaining normal cholangiocyte metabolism and function.

Our findings demonstrate that GOLM1 enhances ubiquitin proteasome activity by binding to PSMD1, thereby facilitating AR-driven transcriptional activity and PCa progression. These results indicate that GOLM1 and its associated proteins may become potential therapeutic targets for PCa characterized by dysregulated AR-driven transcriptional activation.

Finally, GOLM1 knockdown was found to act in synergy with Lenvatinib in subcutaneous and orthotopic mouse model. Overall, these findings identify a mechanism of resistance to Lenvatinib treatment for HCC, highlight an effective predictive biomarker of Lenvatinib response in HCC and show that targeting GOLM1 may improve the clinical benefit of Lenvatinib.