JPT1 (Jupiter Microtubule Associated Homolog 1)

CD4⁺ T-cell subsets serve as central determinant of the immune landscape and clinical outcome in PC. The CD4⁺ T cell-anchored six-gene signature enables risk stratification, links immune contexture to stromal ecology, and motivates biomarker-guided trials and rational combinations that alleviate immunosuppression while targeting metabolic-stress pathways.

This study elucidates genes in NSCLC that are highly associated with both disease progression and type II pneumocyte features as potential biomarkers of NSCLC, and predicts their potential regulatory functions as well as their impact on the immune infiltration profile of NSCLC, providing guidance for the unraveling of the immune mechanisms of NSCLC.

In addition, the prognostic signature retained independent predictive value for HCC RFS, and it was validated successfully by another publicly available dataset and RT-qPCR experiments using patient tissues. In conclusion, the present study constructed a prognostic model for predicting RFS in patients with HCC via integrated analysis of scRNA-seq and bulk RNA-seq data that could serve as a valuable reference tool for clinicians.

JPT1 plays a pivotal role in HCC progression, with its overexpression strongly linked to tumor advancement and poor prognosis. JPT1 likely contributes to the malignant evolution of HCC by modulating tumor metabolism, cell cycle regulation, and the immune microenvironment. This study provides a comprehensive insight into the role of JPT1 in HCC and establishes a theoretical foundation for its potential as a molecular biomarker and therapeutic target.

These findings suggest that E2F target genes, including JPT1 and TBRG4, may act as prognostic biomarkers and contribute to immune evasion in BC. E2F target genes can also offer good potential for classifying and treating patients.

Accordingly, components of the translation machinery aggregate with a distinct speckled pattern, lose their essential interactions and ultimately impair mRNA translation efficiency when the HN1 is depleted. These results suggest that HN1 is an essential component of the nucleolus, required for ribosome biogenesis as well as global mRNA translation.

Further, the PLK1 and Aurora A kinase's phosphorylations also decreased, confirming the hypothesis that the cells struggle in mitotic progression, display nuclear and cytokinetic abnormalities with supernumerary but immature mononucleated centrosomes. In summary, we described the role of HN1 in centrosome nucleation/maturation in PLK1-Eg5 axis and concomitant mitotic spindle formation in human cells.

This dual modulation of HN1 affected lipid formation, hindering it upon HN1 silencing and promoting it upon HN1 overexpression. Moreover, HN1 triggers the Akt pathway, fostering tumorigenesis via SREBP1-mediated lipogenesis and silencing HN1 effectively curbed HCC tumor growth in mouse xenograft models by deactivating SREBP-1, emphasizing the potential of HN1 as a therapeutic target, impacting both external and internal factors, it holds promise as an effective therapeutic strategy for HCC.

Validation of the efficacy and safety of HN1 inhibition, along with the development of diagnostic methods to determine HN1 expression levels in patients, is essential for the translation of HN1-targeted therapies into clinical practice. Overall, HN1 emerges as a valuable prognostic marker and therapeutic target in cancer, and further investigations hold the potential to improve patient outcomes by impeding metastasis and enhancing treatment strategies.

Additionally, we demonstrate that peptoid-induced changes in Aβ oligomerization correlate with attenuation of oligomer-induced nuclear factor-κB activation in SH-SY5Y human neuroblastoma cells. These findings support the therapeutic potential of peptoids to target early stages of Aβ aggregation and impact the associated Aβ-induced cellular response.

Moreover, HN1 expression is also correlated with the microtubule stability in SH-SY5Y cells, which was investigated with nocodazole and taxol treatments...Moreover, cell cycle dynamics also changed upon HN1 overexpression with alternating effects on SH-SY5Y and RA-differentiated (N-type) cells. Therefore, HN1 is a potential cell cycle regulatory element in the development of neuroblastoma or dedifferentiation of neurons, which requires further studies to decipher its mechanistic role.

Our research demonstrated the crucial role of HN1 in H. pylori-induced acquisition of a malignant phenotype in GES-1 cells. Knockdown of HN1 blocked the pathogenic mechanism of H. pylori-induced GC and downregulated the expression of GSK3Β, β-catenin and Vimentin via Integrin β1.