GTSE1 (G2 And S-Phase Expressed 1)

9 core genes (CCNB1, CCNB2, MAD2L1, BUB1, TTK, CDC20, AURKA, RRM2, GTSE1) were obtained through the KEGG pathway enrichment, which mainly enriched in 4 pathways, namely, Cell cycle, Oocyte meiosis, p53 signaling pathway, and Progesterone-mediated oocyte maturation, respectively. Nine critical dependable DEGs were identified in limited-stage NSCLC using integrated bioinformatical approaches, and these core genes show great potential as prospective biomarkers and therapeutic targets in the progression of limited-stage NSCLC. non-small cell lung cancer, biomarkers, therapeutic targets, p53 signaling pathway, bioinformatics analysis.

Correlation analysis unveiled that GTSE1 + OB cells and monocytes were the negatively correlated populations at the single-cell level, a finding validated in 4 independent osteosarcoma datasets comprising 226 samples. Our findings suggest that GTSE1 overexpression serves as a potential biomarker for metastasis in osteosarcoma and provides a promising strategy to prevent metastasis by targeting GTSE1 + OB cells.

Our findings suggest that the MEX3 family is associated with the prognosis of hepatocellular carcinoma patients and contributes to disease progression by modulating the cell cycle and protein post-transcriptional modifications. Furthermore, this family is related to the tumor microenvironment, particularly in hypoxia and immune responses, which holds significant value for predicting liver cancer outcomes.

These results indicate that METTL16-mediated m6A modification of GTSE1 accelerates LUAD progression by regulating p53 pathway and cell cycle. The aforementioned findings suggest METTL16 and GTSE1 may serve as potential targets for LUAD management.

We evaluated its potential as a diagnostic, prognostic, predictive, and pharmacodynamic biomarker in HCC, emphasizing its relevance in precision medicine. Finally, we summarized emerging survivin-targeted therapeutics and ongoing clinical trials, underscoring the need for novel strategies to effectively target survivin in HCC.

Functionally, the phosphorylation of GTSE1 promotes cellular proliferation and is associated with poor prognosis within a pan-cancer cohort. Our findings provide insights into cyclin D1's role in cell cycle control and oncogenesis beyond RB phosphorylation.

Interactions between MCM2 and the candidate proteins CD2BP2, VRK1, and GTSE1 were confirmed by bimolecular fluorescence complementation. This research establishes a basis for further study of the component proteins of the conserved DNA replication initiation complex and the transient regulatory network involving its proximal proteins.

The 16 key genes identified in this study significantly correlate with PCa stem cell characteristics and showed prognosis-oriented effects in PCa patients. Further, the NUF2 gene may be used as a drug target for treating PCa.

Increased expression of GTSE1 in patients with LUAD showed significant diagnostic and prognostic significance. It was also associated with increased immune infiltration and an unfavorable response to targeted medication.

Furthermore, Y18 exhibited a suitable half-life and oral bioavailability (16.27%), with limited inhibitory activity on CYP isoforms. Taken together, these results suggested that Y18 could be a potential chemotherapeutic drug for cancer treatment, particularly in cases of GTSE1 overexpressed cancers.

We demonstrated that NUSAP1 and GTSE1 overexpression was closely related to the poor prognostic clinicopathological features of ccRCC and predicted an unfavorable prognosis. Therefore, NUSAP1 and GTSE1 might act together as potential futuristic prognostic indicators and therapeutic targets for ccRCC patients. However, further analysis in molecular studies on larger scale are mandatory to highlight the interactive crosstalk regulatory mechanisms between both markers and their combined effect on ccRCC.