卵巢晚期癌（OC）预后差，转移率高，但其潜在的分子机制尚不清楚。RNA结合蛋白（RBPs）在肿瘤新生和肿瘤转移背景下发挥重要作用，参与后转录调控。本研究探究了一个典型的RBP，变压器2β同源物（TRA2B）在癌细胞中的分子功能。通过TRVO展示.TRA2B调控的位点和样本进行了分析。我们在上皮卵巢癌细胞中干扰TRA2B表达，并进行了多个实验以验证对于卵巢癌细胞增殖、凋亡和侵袭的影响。TRA2B调控的AS与细胞有丝分裂周期、凋亡和多个癌症通路密切相关。此外，数百个基因的表达受到TRA2B的调控，并且这些基因在细胞增殖、细胞粘附和血管生成等功能方面富集，与卵巢癌的恶性表型相关。通过整合AS事件和差异表达基因，我们发现AS事件和基因表达是独立调控的。然后，我们通过在OC细胞中敲低TRA2B的表达来探究并验证其致癌功能。高TRA2B表达与OC患者预后差相关，在卵巢组织中，TRA2B表达呈逐渐增加的趋势与恶性程度的增加相关。我们证明了TRA2B在卵巢新生和侵袭性OC行为中的重要作用，并确定了其潜在的分子机制，为OC的靶向治疗提供了便利。© 2023年包括周在内的作者。

Late-stage ovarian cancer (OC) has a poor prognosis and a high metastasis rate, but the underlying molecular mechanism is unclear. RNA binding proteins (RBPs) play important roles in posttranscriptional regulation in the contexts of neoplasia and tumor metastasis. In this study, we explored the molecular functions of a canonical RBP, Transformer 2β homolog (TRA2B), in cancer cells. TRA2B knockdown in HeLa cells and subsequent whole-transcriptome RNA sequencing (RNA-seq) analysis revealed the TRA2B-regulated alternative splicing (AS) profile. We disrupted TRA2B expression in epithelial OC cells and performed a series of experiments to confirm the resulting effects on OC cell proliferation, apoptosis and invasion. TRA2B-regulated AS was tightly associated with the mitotic cell cycle, apoptosis and several cancer pathways. Moreover, the expression of hundreds of genes was regulated by TRA2B, and these genes were enriched in the functions of cell proliferation, cell adhesion and angiogenesis, which are related to the malignant phenotype of OC. By integrating the alternatively spliced and differentially expressed genes, we found that AS events and gene expression were regulated independently. We then explored and validated the oncogenic functions of TRA2B by knocking down its expression in OC cells. The high TRA2B expression was associated with poor prognosis in patients with OC. In ovarian tissue, TRA2B expression showed a gradual increasing trend with increasing malignancy. We demonstrated the important roles of TRA2B in ovarian neoplasia and aggressive OC behaviors and identified the underlying molecular mechanisms, facilitating the targeted treatment of OC.© 2023 Zhou et al.