NUP62 (Nucleoporin 62)

High ARMC12, MYC, NUP62, NUP93, or NUP98 levels served as markers of unfavorable patient outcomes in clinical cohorts. These findings collectively demonstrate that dual targeting of AMRC12 and Malassezia globosa disrupts MYC liquid condensates-driven NPC biogenesis during NB progression.

This work establishes NUP62 as a prognostic marker, revealing its dual function in promoting ERα-positive tumorigenesis and conferring endocrine resistance. These findings suggest that therapeutic targeting of NUP62 could be a viable strategy to enhance tamoxifen response and combat resistance in ERα-positive breast cancer.

These data substantiate the utility of UTMC for non-invasive delivery of oligonucleotide payloads to extravascular target sites and suggests the therapeutic potential of miR-27a* for the treatment of head and neck squamous cell carcinoma.

NUP62 plays a critical role in multiple cancers and shows potential as a biomarker for cancer diagnosis, prognosis, and therapeutic response prediction. Its role in tumour immunity and signalling pathways highlights its potential as a target for immunotherapy and precision medicine.

NUP155 interacted with NDC1 to complete the assembly of the nuclear pore complex, which promoted the development of NSCLC. Our study demonstrated that NUP155 was expected to be a potential target for the treatment of NSCLC.

Taking this into consideration, herein, we conducted a retrospective study in order to develop and validate a gene expression score for predicting clinical benefit to the anti-PD-1 antibody nivolumab in the context of patients diagnosed with advanced clear cell RCC enrolled in the CheckMate-009, CheckMate-010, and CheckMate-025 clinical trials...Lastly, we explored the correlation of our 3GES with different clinical, molecular, and immune tumor characteristics. If the results of this study are definitively validated in other retrospective and large-scale, prospective studies, the 3GES will represent a valuable tool for guiding the design of ICB-based clinical trials in the aRCC scenario in the near future.

Additionally, MLV capsid associated with the nuclear pore proteins NUP358 and NUP62 during infection. These findings suggest that simple retroviruses, like the complex retrovirus HIV, gain nuclear entry by traversing the nuclear pore complex in non-mitotic cells.

In addition, NUP62CL protein expression was positively associated with the abundance of CD3+CD4+ T cells (P<0.01), CD3+CD8+ T cells (P<0.01), CD56+ NK cells (P<0.05), CD68+CD86+ macrophages (P<0.01) and CD68+CD163+ macrophages (P<0.01), as well as the immune checkpoints, including PD-1 (P<0.001), PD-L1 (P<0.001), and CTLA-4 (P<0.001) protein expression. In conclusion, NUP62CL could be an effective prognostic and immunological biomarker for OSCC patients.

Our study identified several novel GRRDEGs and provided insight into the underlying mechanisms of gefitinib resistance in LUAD. Our results have implications for developing more effective treatment strategies and prognostic models for LUAD patients.

We identified CDC42 as a pivotal gene in the pathophysiology of HPV-related cancers. The upregulation of CDC42 could be a signal for afatinib treatment and the mechanism in which may be an increased affinity of EGFR to afatinib, inferred from a high stability in the quaternary complex of CDC42-GTPase-effector interface-EGFR-afatinib.

Expression of individual Nup62 domain constructs in human cells confirmed that the Nup62 C-terminal domain is essential for localization of the protein to the nuclear envelope. Our results raise the possibility that interactions between FUS and the C-terminal domain of Nup62 can influence the function of Nup62 under physiological and/or pathological conditions.

In conclusion, our data indicates that simultaneous overexpression of Nup62 and Nup88 in head and neck cancer stabilizes Nup88. Stabilized Nup88 interacts and activates p65 pathway, which perhaps is the underlying mechanism in Nup88 overexpressing tumors.