Team 12, Study of the melanocytic differentiation applied to vitiligo and melanoma: from the patient to the molecular mechanisms, Centre Méditerranéen de Médecine Moléculaire (C3M), Institut national de la santé et de la recherche médicale (INSERM) U1065, Université Nice Côte d'Azur, Nice, France; Department of Dermatology, Centre hospitalier universitaire (CHU) de Nice, Université Nice Côte d'Azur, Nice, France.
Team 12, Study of the melanocytic differentiation applied to vitiligo and melanoma: from the patient to the molecular mechanisms, Centre Méditerranéen de Médecine Moléculaire (C3M), Institut national de la santé et de la recherche médicale (INSERM) U1065, Université Nice Côte d'Azur, Nice, France.
J Invest Dermatol. 2022 Feb;142(2):425-434. doi: 10.1016/j.jid.2021.05.035. Epub 2021 Jul 24.
The potential role of CLEC12B, a gene predominantly expressed by skin melanocytes discovered through transcriptomic analysis, in melanoma is unknown. In this study, we show that CLEC12B expression is lower in melanoma and melanoma metastases than in melanocytes and benign melanocytic lesions and that its decrease correlates with poor prognosis. We further show that CLEC12B recruits SHP2 phosphatase through its immunoreceptor tyrosine-based inhibition motif domain, inactivates signal transducer and activator of transcription 1/3/5, increases p53/p21/p27 expression/activity, and modulates melanoma cell proliferation. The growth of human melanoma cells overexpressing CLEC12B in nude mice after subcutaneous injection is significantly decreased compared with that in the vehicle control group and is associated with decreased signal transducer and activator of transcription 3 phosphorylation and increased p53 levels in the tumors. Reducing the level of CLEC12B had the opposite effect. We show that CLEC12B represses the activation of the signal transducer and activator of transcription pathway and negatively regulates the cell cycle, providing a proliferative asset to melanoma cells.
通过转录组分析发现,CLEC12B 主要在皮肤黑素细胞中表达,但其在黑色素瘤中的潜在作用尚不清楚。在这项研究中,我们表明,CLEC12B 的表达在黑色素瘤和黑色素瘤转移灶中低于黑素细胞和良性黑素细胞病变,其减少与预后不良相关。我们进一步表明,CLEC12B 通过其免疫受体酪氨酸抑制基序域募集 SHP2 磷酸酶,使转录激活因子 1/3/5 失活,增加 p53/p21/p27 的表达/活性,并调节黑色素瘤细胞的增殖。与载体对照组相比,过表达 CLEC12B 的人黑色素瘤细胞在裸鼠皮下注射后的生长明显减少,并且与肿瘤中信号转导和转录激活因子 3 磷酸化减少以及 p53 水平增加相关。降低 CLEC12B 的水平则产生相反的效果。我们表明,CLEC12B 抑制信号转导和转录激活因子通路的激活,并负调控细胞周期,为黑色素瘤细胞提供增殖优势。