We found that chidamide, an HDAC inhibitor, exerts an antitumor effect on T-ALL cell lines and primary cells including an anti-NOTCH1 activity. In particular, chidamide inhibits the NOTCH1-MYC signaling axis by down-regulating the level of the intracellular form of NOTCH1 (NICD1) as well ...
ARTICLE OPENACUTE LYMPHOBLASTIC LEUKEMIATargeting the NOTCH1-MYC-CD44 axis in leukemia-initiatingcells in T-ALLSujan Piya1,5 ✉ , Yaling Yang 2,5 , Seemana Bhattacharya 1 , Priyanka Sharma 1 , Huaxian Ma 1 , Hong Mu 1 , Hua He 2 , Vivian Ruvolo 1 ,Natalia Baran1 , R. Eric Davis...
A NOTCH1-driven MYC enhancer promotes T cell development, transformation and acute lymphoblastic leukemia. Nat Med 2014;20:1130-7.Herranz, D., Ambesi-Impiombato, A., Palomero, T., Schnell, S. A., Belver, L., Wendorff, A. A., Xu, L., Castillo-Martin, M., Llobet-Nava麓s, D....
研究。而C.MYC是NOTCH信号通路下游一重要分子,又作为原癌基因在 许多肿瘤中都存在过表达,降低或阻断其过表达能够抑制肿瘤细胞的生长 并促进其凋亡,但其触发T-ALL发生发展的机制尚未明确,但是可能作为 连接PTEN/AKT与NOTCHl的桥梁而对白血病提供靶向治疗。本研究旨在 ...
结果:Notch1,Notch2及c-Myc在肾癌组织中表达水平明显高于相应的癌旁组织(P0.001),相关性分析表明在肿瘤组织中c-Myc与Notch2的mR-NA水平呈正相关(r=0.629,P0.001),而与Notch1的mRNA水平无相关(P=0.389).结论:Notch信号通路及c-Myc的异常高表达可能与肾透明细胞癌的发生发展有关,而且c-Myc可能作为Notch信号...
硼替佐米对T-ALL细胞株CCRF-CEM的作用及对Notch1通路的影响 目的:1、探讨硼替佐米单药及与MTX联合用药对T-ALL细胞增殖的影响;2、研究硼替佐米作用于T-ALL细胞株后Notch1信号通路的基因表达情况,以探讨硼替佐米对T-ALL细胞株的作... 黄灿 - 山西医科大学 被引量: 1发表: 2012年 S1P-S1PR3激活RAS信号...
SNORA72 Activates the Notch1/c-Myc Pathway to Promote Stemness Transformation of Ovarian Cancer Cells Frontiers in Cell and Developmental Biology (2020) -3Comments pubmed: 33224949 doi: 10.3389/fcell.2020.583087 issn: 2296-634x Liwen Zhang,Rong Ma,Mengcong Gao,Yanyun Zhao,Xuemei Lv,Wenjing Zhu...
RT-PCR and agarose gel electropho- resis also verified the increased expression of c-Myc and Notch1 in OS cells (Fig. 6b). Next, we assessed the effects of SNORD89 interference on the expression of c-Myc and Notch1 in ovarian can- cer cells. The Notch1 and c-Myc expression ...
Human acute T-cell lymphoblastic leukemias and lymphomas (T-ALL) are commonly associated with gain-of-function mutations in Notch1 that contribute to T-ALL induction and maintenance. Starting from an expression-profiling screen, we identified c-myc as a direct target of Notch1 in Notch-d...
Thus, Myc can substitute for Notch1 in leukemogenesis, whereas Akt cannot. These findings in primary tumors extend recent work using human T-ALL cell lines and xenografts and suggest that the Notch/Myc signaling axis is of predominant importance in understanding both the selective pressure for ...