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EIF3B 通过拮抗 MDM2 介导的泛素化稳定 PTGS2 的表达,从而促进恶性黑色素瘤的发生和发展。

EIF3B stabilizes PTGS2 expression by counteracting MDM2-mediated ubiquitination to promote the development and progression of malignant melanoma.

机构信息

Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Oncology Department of Laiyang People's Hospital, Laiyang, China.

出版信息

Cancer Sci. 2022 Dec;113(12):4181-4192. doi: 10.1111/cas.15543. Epub 2022 Sep 29.

Abstract

Malignant melanoma (MM) is a neoplasm that develops from human melanocytes. It was reported that eukaryotic translation initiation factor 3 subunit B (EIF3B) is associated with multiple types of cancers, but its role in MM has not been reported. In the present study, we found that EIF3B was abundantly expressed in MM and was strongly related to lymphatic metastasis and pathological stage of MM patients. In addition, EIF3B depletion could block the progression of MM in vitro and in vivo. In contrast, EIF3B overexpression increased cell proliferation and migration in melanoma cells. More importantly, we identified that EIF3B's driver role in MM was mediated by PTGS2. In detail, we found that EIF3B stabilized PTGS2 expression by inhibiting PTGS2 ubiquitination, which is mediated by the E3 ligase MDM2. Moreover, like EIF3B, silencing PTGS2 could suppress MM development, and more interestingly, it could reverse the situation caused by overexpression of EIF3B in vitro and in vivo. Furthermore, the proliferation and migration inhibited by silencing of EIF3B were also partially recovered by overexpression of PTGS2. Overall, our findings revealed the potential of EIF3B as a therapeutic target for MM. Identification of EIF3B's function in MM may pave the way for future development of more specific and more effective targeted therapy strategies against MM.

摘要

恶性黑色素瘤(MM)是一种源自人类黑色素细胞的肿瘤。有报道称,真核翻译起始因子 3 亚基 B(EIF3B)与多种类型的癌症有关,但它在 MM 中的作用尚未被报道。在本研究中,我们发现 EIF3B 在 MM 中大量表达,并与 MM 患者的淋巴转移和病理分期密切相关。此外,EIF3B 耗竭可以阻断 MM 在体外和体内的进展。相反,EIF3B 的过表达增加了黑色素瘤细胞的增殖和迁移。更重要的是,我们确定了 EIF3B 在 MM 中的驱动作用是由 PTGS2 介导的。具体而言,我们发现 EIF3B 通过抑制 PTGS2 的泛素化来稳定 PTGS2 的表达,这是由 E3 连接酶 MDM2 介导的。此外,与 EIF3B 一样,沉默 PTGS2 可以抑制 MM 的发展,更有趣的是,它可以逆转体外和体内过表达 EIF3B 引起的情况。此外,沉默 EIF3B 引起的增殖和迁移也部分被过表达 PTGS2 所恢复。总的来说,我们的研究结果揭示了 EIF3B 作为 MM 治疗靶点的潜力。EIF3B 在 MM 中的功能的鉴定可能为未来开发更特异和更有效的针对 MM 的靶向治疗策略铺平道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d31/9746036/029dfa58e01f/CAS-113-4181-g004.jpg

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