TPX2 (TPX2 Microtubule Nucleation Factor)

We show that TPX2 and KIFC1 cooperate to ensure robust acentrosomal microtubule nucleation and organization. Our data show that this mechanism plays a major role in the clustering of supernumerary centrosomes in cancer cells.

Our findings uncover a mechanistic basis for EGFR inhibitor resistance of CDK4 and CDK6 amplified EGFR-mutant LUAD. They also provide a rationale for the biomarker-driven clinical development of combination EGFR and CDK4/6-targeted therapies for the treatment of a subset of EGFR-mutant LUAD patients.

The MD over 200 ns indicated that marine compounds, such as Shellmycin C (CID:156581889) and Rhodoptilometrin (CID:625242), displayed significantly greater stability compared to the control drug Alisertib (CID:24771867). Consequently, these findings underscore the potential for developing innovative therapeutic strategies that target the AURKA-TPX2 complex in LUAD, warranting further validation through in vitro and in vivo studies. The online version contains supplementary material available at 10.1007/s40203-025-00436-z.

Drug sensitivity analysis indicated resistance to several chemotherapeutics, but increased sensitivity to mitotic inhibitors and targeted agents. TPX2 is a key driver of proliferation and immune evasion in HCC, potentially serving as a diagnostic and prognostic biomarker to guide treatment strategies involving mitotic- or immune-based therapies.

In conclusion, the results indicate that TPX2 gene expression in the DMBA-induced breast cancer (BC) model is altered by biosynthesized silver nitrate NPs. The combined findings highlight IA-AgNPs' promise as a cutting-edge, targeted nanotherapeutic strategy with improved efficacy in treating cancer parameters compared to traditional therapies.

Additionally, this study explores the role of the TPX2 gene in HCC using bioinformatics and cellular experiments, assessing its feasibility as a potential therapeutic target. Through these investigations, we aim to provide new theoretical insights and application prospects for the precision diagnosis and treatment of HCC.

This study underscores the critical role of TPX2 in type 2 pRCC progression and highlights its potential as a prognostic biomarker and therapeutic target. The TPX2/LINC00894/miR-660-5p regulatory axis provides novel insights into the molecular mechanisms driving pRCC and offers a promising avenue for improving patient prognosis.

Interestingly, this infiltration of immune cells was found to be positively correlated with the expression levels of CDK molecules. The up-regulated expression of the TPX2 and CCNA2 genes is believed to be associated with abnormal regulation of the cell cycle, which in turn affects the infiltration patterns of immune cells within the affected tissues.

Combined knockdown of AURKA and TPX2 was effective in suppressing the malignant phenotype in CRC. Co-inhibition of gene expression is a potential developmental direction for CRC treatment.

This study highlights the essential role of NKX6.3 in regulating mitotic integrity and genomic stability in gastric carcinogenesis. The findings suggest that targeting NKX6.3 may offer a novel therapeutic strategy for improving treatment outcomes in gastric cancer by restoring mitotic fidelity and genomic stability.

These effects were potentially mediated by the activation of CD8+ T cell immune responses and the inhibition of cell cycle progression and adhesion mechanisms. Taken together, our findings indicate that TPX2 may serve as a critical biomarker for the diagnosis and clinical management of patients with PC.

This was mirrored by a reduction in the IC50 values for cisplatin and apatinib to 0.8257 µM and 10.79 µM, respectively. The E2F8-TPX2 axis promotes glycolysis and angiogenesis in LC cells, which in turn accelerates cancer progression and reduces chemosensitivity. The online version contains supplementary material available at 10.1007/s10616-024-00655-w.