Abstract：
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.
摘要：
恶性黑色素瘤是一种高度侵袭性的皮肤肿瘤，在全球范围内发病率不断上升。非SMC凝集素II复合物亚基G2（NCAPG2）在几种肿瘤的发病机理中发挥重要的生物学功能。在这项研究中,在体外和体内实验中揭示了NCAPG2敲低在恶性黑色素瘤中的功能作用。体外研究表明，NCAPG2耗竭可以抑制恶性黑色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了NCAPG2敲低减弱了恶性黑色素瘤的肿瘤生长。有趣的是,NCAPG2通过激活信号转导和转录激活因子3（STAT3）驱动恶性黑色素瘤的肿瘤发展。总之,本研究阐述了NCAPG2对恶性黑色素瘤的促肿瘤作用,NCAPG2可能是恶性黑色素瘤治疗的潜在治疗靶点。
