Cisplatin resistance is frequently occurred in ovarian cancer therapy, understanding its regulatory mechanisms is critical for developing novel treatment methods and drugs. Here, we found ovarian cancer patients with low FAM83B levels had shorter survival time, tissues with cisplatin resistance also had low FAM83B levels, suggesting FAM83B might inhibit cisplatin resistance. FAM83B overexpression inhibits cisplatin resistance showed in increased ovarian cancer cell proliferation and growth rate, and reduced apoptosis rate, while FAM83B knockdown promotes cisplatin resistance. Mechanism analysis showed FAM83B interacted with APC to inhibit Wnt pathway activity, causing ovarian cancer cisplatin resistance. We also found FAM83B levels were negative with Wnt pathway activity in clinic samples, confirming FAM83B inhibited Wnt pathway activity. In summary, we found FAM83B inhibits ovarian cancer cisplatin resistance through inhibiting Wnt pathway, providing a new target for ovarian cancer therapy.

顺铂耐药在卵巢癌治疗中经常发生，了解其调控机制对于开发新的治疗方法和药物至关重要。在这里，我们发现低 FAM83B 水平的卵巢癌患者生存时间较短，顺铂耐药的组织也具有低 FAM83B 水平，表明 FAM83B 可能抑制顺铂耐药。FAM83B过表达抑制顺铂耐药表现为卵巢癌细胞增殖和生长速率增加，细胞凋亡率降低，而FAM83B敲低促进顺铂耐药。机制分析显示FAM83B与APC相互作用抑制Wnt通路活性，引起卵巢癌顺铂耐药。我们还发现 FAM83B 水平与临床样本中的 Wnt 通路活性呈负相关，证实 FAM83B 抑制了 Wnt 通路活性。