p65的RNA屏蔽是增强TET2突变克隆性造血中的致癌性炎症所必需的。
RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in TET2-Mutated Clonal Hematopoiesis.
作者信息
Ben-Crentsil Nana Adjoa, Mohammed Ismail Wazim, Balasis Maria E, Newman Hannah, Quintana Ariel, Binder Moritz, Kruer Traci, Neupane Surendra, Ferrall-Fairbanks Meghan C, Fernandez Jenna, Lasho Terra L, Finke Christy M, Ibrahim Mohammed L, McGraw Kathy L, Wysota Michael, Aldrich Amy L, Ryder Christopher B, Letson Christopher T, Traina Joshua, McLemore Amy F, Droin Nathalie, Shastri Aditi, Yun Seongseok, Solary Eric, Sallman David A, Beg Amer A, Ma Li, Gaspar-Maia Alexandre, Patnaik Mrinal M, Padron Eric
机构信息
Department of Malignant Hematology, H. Lee Moffitt Cancer Center, Tampa, Florida.
Epigenomics Program, Center for Individualized Medicine, Mayo Clinic, Rochester, Minnesota.
出版信息
Cancer Discov. 2024 Dec 2;14(12):2509-2531. doi: 10.1158/2159-8290.CD-24-0093.
This work identifies MALAT1 as a requisite downstream effector of oncogenic feedforward inflammatory circuits necessary for the development of TET2-mutated CH and fulminant myeloid malignancy. We elucidate a novel mechanism by which MALAT1 "shields" p65 from dephosphorylation to potentiate this circuit and nominate MALAT1 inhibition as a future therapeutic strategy.
这项研究确定了MALAT1是TET2突变的慢性粒单核细胞白血病（CH）和暴发性髓系恶性肿瘤发生所必需的致癌前馈炎症回路的下游效应因子。我们阐明了一种新机制，即MALAT1通过“保护”p65不被去磷酸化来增强这一回路，并提出抑制MALAT1作为未来的治疗策略。
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