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黑色素瘤对长非编码RNA的成

Eleonora Leucci^1,2, Roberto Vendramin^1,2, Marco Spinazzi²

¹Laboratory For Molecular Cancer Biology, Center for Human Genetics, KULeuven, Herestraat 49, 3000 Leuven, Belgium.

|March 25, 2016

概括

长非编码RNASAMSON是一种与MITF共同增强的黑色素瘤基因. 向SAMSON会破坏线粒体功能,并增强黑色素瘤治疗的反应.

科学领域:

癌症学
分子生物学
遗传学

背景情况:

在~10%的黑色素瘤中发现了染色体3p13-3p14的焦点放大,与预后不佳相关.
黑色素瘤特异性瘤基因MITF位于这个片的中心,但其他共同放大基因的作用仍然不清楚.

研究的目的:

在黑色素瘤发育和治疗反应中,研究位于3p13- 3p14的长非编码RNA (lncRNA) 基因SAMSON的作用.

主要方法:

在黑色素瘤中分析SAMSON与MITF的联合放大.
在黑色素瘤细胞和患者样本中评估SAMSON表达.
研究SAMSON调节 (过度表达和降低) 对黑色素瘤细胞活力和克隆性的功能影响.
在实验室和体内评估SAMSON向黑色素瘤对MAPK抑制剂的敏感性.
阐明SAMSON作用的分子机制,包括它与p32和线粒体功能的相互作用.

主要成果:

在3p13- 3p14放大中,SAMSON与MITF一致获得,并且是SOX10标,在90%以上的黑色素瘤中表达.
在不同黑色素瘤亚型中,SAMSON的过度表达增强了黑色素瘤细胞的克隆性,而它的抑制严重损害了细胞活力.
向SAMSON使黑色素瘤细胞对MAPK向疗法在体外和患者衍生异体移植敏感.
SAMMSON与p32相互作用,促进其线粒体局部化和亲瘤活性,从而破坏线粒体平衡.

结论:

在黑色素瘤中,SAMSON作为一种血统上性瘤基因.
沉默SAMSON以癌症特定的方式破坏了重要的线粒体功能.
针对SAMSON的研究有望开发有效的,受组织限制的抗黑色素瘤疗法.

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