Choroidal melanoma (CM) remains the most prevalent form of intraocular malignancy, and the prognosis of affected patients is poor. While the E3 ubiquitin ligase TRAF‐interacting protein (TRIP) is known to play key regulatory roles in multiple diseases, its relevance in CM remains uncertain. In the present study, we found that TRIP overexpression is sufficient to inhibit the proliferation, invasion, and epithelial–mesenchymal transition (EMT) of CM cells in vitro, whereas the opposite phenotypes are observed following TRIP knockdown. We further determined that TRIP is able to promote the K48‐polyubiquitination of EMT‐associated transcription factor Twist‐related protein 1, thereby suppressing EMT progression. Together, our results suggest that TRIP plays an important role in regulating the progression of CM and that it may therefore be an important therapeutic target for the treatment of this disease.

中文翻译：

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TRIP通过促进Twist1的蛋白酶体降解抑制脉络膜黑色素瘤的细胞增殖和侵袭

脉络膜黑色素瘤 (CM) 仍然是最常见的眼内恶性肿瘤，受影响患者的预后很差。虽然已知 E3 泛素连接酶 TRAF 相互作用蛋白 (TRIP) 在多种疾病中发挥关键调节作用，但其在 CM 中的相关性仍不确定。在本研究中，我们发现 TRIP 过表达足以抑制体外 CM 细胞的增殖、侵袭和上皮间质转化 (EMT)，而在 TRIP 敲低后观察到相反的表型。我们进一步确定 TRIP 能够促进 EMT 相关转录因子 Twist 相关蛋白 1 的 K48 多泛素化，从而抑制 EMT 进展。一起，