CSE1L regulates gastric cancer progression via molecular crosstalk with TRIP13.

Gastric cancer (GC) is one of the most common malignant tumours worldwide, with adenocarcinoma comprising more than 95 % of cases. A significant challenge is that most GC patients exhibit no symptoms during early disease stages, underscoring the critical need for reliable biomarkers to enable early diagnosis and the exploration of innovative therapeutic approaches. CSE1L, a member of the cellular apoptosis susceptibility protein family, interacts with microtubules and mitotic spindles. Growing evidence suggests that CSE1L is overexpressed in various cancers and plays a crucial role in tumour proliferation. This study reveals that CSE1L is significantly upregulated in GC tissue samples and plays a key role in tumorigenesis and metastasis. Experimental results demonstrated that the genetic knockdown of CSE1L exerts potent anti-tumour effects, significantly suppressing the proliferative capacity and metastatic potential of GC cells in vitro and in vivo. Mechanistically, an interaction between CSE1L and TRIP13 was identified, with their expression levels displaying a strong positive correlation in GC tissues. Additionally, CSE1L was found to repress TRIP13 ubiquitination degradation, stabilizing its expression and promoting GC progression. Interestingly, TRIP13 reciprocally regulates the stability of the CSE1L protein, indicating a bidirectional regulatory loop. The CSE1L-TRIP13 axis provides a robust theoretical foundation to develop targeted therapeutic strategies, offering novel insights into the clinical treatment of GC patients.