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Targeting the Senescence-Overriding Cooperative Activity of Structurally Unrelated H3K9 Demethylases in Melanoma.

Abstract：

:Oncogene-induced senescence, e.g., in melanocytic nevi, terminates the expansion of pre-malignant cells via transcriptional silencing of proliferation-related genes due to decoration of their promoters with repressive trimethylated histone H3 lysine 9 (H3K9) marks. We show here that structurally distinct H3K9-active demethylases-the lysine-specific demethylase-1 (LSD1) and several Jumonji C domain-containing moieties (such as JMJD2C)-disable senescence and permit Ras/Braf-evoked transformation. In mouse and zebrafish models, enforced LSD1 or JMJD2C expression promoted Braf-V600E-driven melanomagenesis. A large subset of established melanoma cell lines and primary human melanoma samples presented with a collective upregulation of related and unrelated H3K9 demethylase activities, whose targeted inhibition restored senescence, even in Braf inhibitor-resistant melanomas, evoked secondary immune effects and controlled tumor growth in vivo.

journal_name

Cancer Cell

journal_title

Cancer cell

authors

Yu Y,Schleich K,Yue B,Ji S,Lohneis P,Kemper K,Silvis MR,Qutob N,van Rooijen E,Werner-Klein M,Li L,Dhawan D,Meierjohann S,Reimann M,Elkahloun A,Treitschke S,Dörken B,Speck C,Mallette FA,Zon LI,Holmen SL,Peeper DS

doi

10.1016/j.ccell.2018.01.002

subject

Has Abstract

pub_date

2018-02-12 00:00:00

pages

322-336.e8

issue

2

eissn

1535-6108

issn

1878-3686

pii

S1535-6108(18)30002-3

journal_volume

33

pub_type

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