School of Clinical Medicine, Weifang Medical University, Weifang, China.
Department of Dermatology, ZiBo Central Hospital, No. 54 Gongqingtuan West Road, Zibo, 255000, Shandong, China.
Sci Rep. 2024 Nov 12;14(1):27736. doi: 10.1038/s41598-024-76794-z.
Recent studies have uncovered that TIPE2 is involved in the development of cancer. However, less research has been conducted on the role of TIPE2 in melanoma. Our study aims to elucidate the mechanism of action of TIPE2 in the development of melanoma. We examined TIPE2 expression in paracarcinoma tissue and melanoma tissues and found that TIPE2 expression was downregulated in melanoma tissue compared with paracarcinoma tissue. Overexpression of TIPE2 significantly inhibited the proliferation of melanoma cells in vitro and even inhibited tumor formation in vivo. The CCK8 assay results indicated that TIPE2 overexpression suppressed the proliferation of melanoma cells. The colony-forming ability and wound healing ability of TIPE2-overexpressing melanoma cells were significantly reduced compared with those of control cells. Moreover, immunohistochemistry experiments using a nude mouse tumor model showed consistent results. TIPE2 inhibited the phosphorylation of MEK and ERK. In summary, TIPE2 suppresses the proliferation and migration of melanoma cells by affecting proliferation-related factors and possibly by regulating the MEK/ERK pathway. TIPE2 could be used to inhibit melanoma growth and is a potential drug target for future drug development.
最近的研究揭示了 TIPE2 参与癌症的发展。然而，关于 TIPE2 在黑色素瘤中的作用的研究较少。我们的研究旨在阐明 TIPE2 在黑色素瘤发展中的作用机制。我们检查了癌旁组织和黑色素瘤组织中的 TIPE2 表达，发现与癌旁组织相比，黑色素瘤组织中 TIPE2 的表达下调。TIPE2 的过表达显著抑制了黑色素瘤细胞在体外的增殖，甚至抑制了体内肿瘤的形成。CCK8 检测结果表明，TIPE2 的过表达抑制了黑色素瘤细胞的增殖。与对照细胞相比，过表达 TIPE2 的黑色素瘤细胞的集落形成能力和伤口愈合能力显著降低。此外，使用裸鼠肿瘤模型的免疫组织化学实验也得到了一致的结果。TIPE2 抑制了 MEK 和 ERK 的磷酸化。综上所述，TIPE2 通过影响增殖相关因子并可能通过调节 MEK/ERK 通路来抑制黑色素瘤细胞的增殖和迁移。TIPE2 可用于抑制黑色素瘤的生长，是未来药物开发的潜在药物靶点。
