Department of Burn and Plastic Surgery, Shandong Provincial Hospital, Shandong First Medical University, Jinan, Shandong 250021, China.
Biochem Cell Biol. 2022 Dec 1;100(6):473-484. doi: 10.1139/bcb-2022-0048. Epub 2022 Oct 20.
Malignant melanoma is a highly aggressive cutaneous neoplasm with increasing incidence worldwide. Non-SMC condensin II complex subunit G2 (NCAPG2) exerts import biological function in the pathogenesis of several tumors. In this study, the functional roles of NCAPG2 knockdown in malignant melanoma were revealed in in vitro and in vivo experiments. In vitro study demonstrated that NCAPG2 depletion could inhibit proliferation and migration and promote apoptosis of malignant melanoma cells. Our in vivo date further confirmed that NCAPG2 knockdown attenuated tumor growth of malignant melanoma. Interestingly, NCAPG2 drove tumor development of malignant melanoma through activating the signal transducer and activator of transcription 3 (STAT3). In conclusion, this study elaborated the tumor-promoting effects of NCAPG2 on malignant melanoma, and NCAPG2 may be a potential therapeutic target for malignant melanoma therapy.
恶性黑素瘤是一种具有全球发病率上升趋势的高度侵袭性皮肤肿瘤。非SMC 凝聚素 II 复合物亚基 G2（NCAPG2）在几种肿瘤的发病机制中发挥着重要的生物学功能。在这项研究中，通过体外和体内实验揭示了 NCAPG2 敲低在恶性黑素瘤中的功能作用。体外研究表明，NCAPG2 耗竭可抑制恶性黑素瘤细胞的增殖和迁移，并促进其凋亡。我们的体内数据进一步证实，NCAPG2 敲低可减弱恶性黑素瘤的肿瘤生长。有趣的是，NCAPG2 通过激活信号转导子和转录激活子 3（STAT3）驱动恶性黑素瘤的肿瘤发展。总之，本研究阐述了 NCAPG2 对恶性黑素瘤的促瘤作用，NCAPG2 可能是恶性黑素瘤治疗的潜在治疗靶点。
