乳腺癌已成为女性癌症患者发病率和死亡率最高的恶性疾病。转移性乳腺癌的预后非常糟糕，治疗效果仍有待改进。乳腺癌的分子机制尚未完全阐明。本研究采用生物信息学分析，找到了影响乳腺癌发生和发展的差异表达基因。此外，采用刮痕实验、转移室实验、免疫荧光和免疫印迹等方法确定了DEPDC1B对乳腺癌细胞的生物行为的影响。通过质谱分析、共免疫沉淀和泛素酶活性分析研究了其分子机制。我们发现DEPDC1B在乳腺癌细胞和组织中表达高，并与患者的总体生存率低相关。我们发现DEPDC1B干扰显著抑制了体外肿瘤侵袭和迁移以及体内肿瘤转移。机制上，我们首次发现DEPDC1B作为乳腺癌细胞的癌基因通过激活wnt/β-catenin信号通路。此外，我们还证实了DEPDC1B、USP5和β-catenin之间的相互作用。然后，我们发现DEPDC1B通过USP5介导β-catenin的去泛素化，从而促进细胞侵袭和迁移。我们的研究揭示了DEPDC1B的致癌机制的新见解，表明DEPDC1B可以作为乳腺癌的潜在治疗靶点。

Breast cancer has become the malignant disease with the highest morbidity and mortality among female cancer patients. The prognosis of metastatic breast cancer is very poor, and the therapeutic effects still need to be improved. The molecular mechanism of breast cancer has not been fully clarified.Bioinformatics analysis was used to find the differentially expressed gene that affects the occurrence and development of breast cancer. Furthermore, scratch assays, transwell assays, immunofluorescence and western blotting were used to determine the biological behaviour of breast cancer cells affected by DEPDC1B. The molecular mechanism was investigated by mass spectrometry analysis, coimmunoprecipitation and ubiquitin assays.Here, we found that DEPDC1B was highly expressed in breast cancer cells and tissues and was associated with lower overall survival (OS) in patients. We found that DEPDC1B interference significantly inhibited tumour invasion and migration in vitro and tumour metastasis in vivo. Mechanistically, DEPDC1B was first shown to activate the wnt/β-catenin signalling pathway as an oncogene in breast cancer cells. In addition, we also confirmed the interaction between DEPDC1B, USP5 and β-catenin. Then, we found that DEPDC1B mediates the deubiquitination of β-catenin via USP5, which promotes cell invasion and migration.Our findings provide new insights into the carcinogenic mechanism of DEPDC1B, suggesting that DEPDC1B can be considered a potential therapeutic target for breast cancer.