Last update 01 Nov 2024

ILF3 x survivin

Last update 01 Nov 2024

Basic Info

Related Targets

ILF3survivin

Drugs associated with ILF3 x survivin

AQIM-I

Target

ILF3 x survivin

Mechanism

ILF3 modulators [+1]

Active Org.

Shanghai Jiao Tong University

Originator Org.

Shanghai Jiao Tong University

Active Indication

Solid tumor

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ILF3 x survivin

100 Translational Medicine associated with ILF3 x survivin

0 Patents (Medical) associated with ILF3 x survivin

Literatures (Medical) associated with ILF3 x survivin

28 Dec 2023·Journal of Medicinal ChemistryQ1 · MEDICINE

Pioneering 4,11-Dioxo-4,11-dihydro-1H-anthra[2,3-d]imidazol-3-ium Compounds as Promising Survivin Inhibitors by Targeting ILF3/NF110 for Cancer Therapy

Q1 · MEDICINE

Article

Author: Zhang, Zhenfeng ; Gao, Feng ; Luo, Yanli ; Xia, Xuelin ; Yan, Deyue ; Yuan, Jing ; Dong, Yachun ; Zhang, Wanbin ; Wang, Penghui ; Liu, Zhanxiong

Survivin is a novel attractive target for cancer therapy; however, it is considered undruggable because it lacks enzymatic activities. Herein, we describe our efforts toward the discovery of a novel series of 4,11-dioxo-4,11-dihydro-1H-anthra[2,3-d]imidazol-3-ium derivatives as survivin inhibitors by targeting ILF3/NF110. Intensive structural modifications led us to identify a lead compound AQIM-I, which remarkably inhibited nonsmall cell lung cancer cells A549 with an IC₅₀ value of 9 nM and solid tumor cell proliferation with more than 700-fold selectivity against human normal cells. Further biological studies revealed that compound AQIM-I significantly inhibited survivin expression and colony formation and induced ROS production, apoptosis, cell cycle arrest, DNA damage, and autophagy. Furthermore, the promoter-luciferase reporter assay showed that AQIM-I attenuated the survivin promoter activity enhanced by the overexpression of ILF3/NF110 in a concentration-dependent manner, and specific binding (K_D = 163 nM) of AQIM-I to ILF3/NF110 was detected by surface plasmon resonance.

01 Jul 2016·VirologyQ3 · MEDICINE

Novel interactions between the HTLV antisense proteins HBZ and APH-2 and the NFAR protein family: Implications for the HTLV lifecycles

Q3 · MEDICINE

Article

Author: Hall, William W ; Sheehy, Noreen ; Ratner, Lee ; Murphy, Jane

The human T-cell leukaemia virus type 1 and type 2 (HTLV-1/HTLV-2) antisense proteins HBZ and APH-2 play key roles in the HTLV lifecycles and persistence in the host. Nuclear Factors Associated with double-stranded RNA (NFAR) proteins NF90/110 function in the lifecycles of several viruses and participate in host innate immunity against infection and oncogenesis. Using GST pulldown and co-immunoprecipitation assays we demonstrate specific novel interactions between HBZ/APH-2 and NF90/110 and characterised the protein domains involved. Moreover we show that NF90/110 significantly enhance Tax mediated LTR activation, an effect that was abolished by HBZ but enhanced by APH-2. Additionally we found that HBZ and APH-2 modulate the promoter activity of survivin and are capable of antagonising NF110-mediated survivin activation. Thus interactions between HTLV antisense proteins and the NFAR protein family have an overall positive impact on HTLV infection. Hence NFARs may represent potential therapeutic targets in HTLV infected cells.

01 Sep 2012·Biochemical and Biophysical Research CommunicationsQ3 · BIOLOGY

Sepantronium Bromide (YM155) induces disruption of the ILF3/p54nrb complex, which is required for survivin expression

Q3 · BIOLOGY

Article

Author: Tomohiro Yamauchi ; Shuichi Tawara ; Masahiro Takeuchi ; Masato Kobori ; Naoki Kaneko ; Naoto Nakamura ; Shigeki Kawabata ; Isao Kinoyama ; Takahito Nakahara ; Masashi Hiramoto ; Hiroshi Koutoku ; Masatoshi Yuri ; Masao Sasamata ; Kentaro Yamanaka ; Hiroyuki Yokota ; Akira Matsuhisa ; Kiyoshi Furuichi ; Aya Kita ; Masanori Naitou ; Masao Katou

YM155, a small-molecule survivin suppressant, specifically binds to the transcription factor ILF3, which regulates the expression of survivin[1]. In this experiment we have demonstrated that p54(nrb) binds to the survivin promoter and regulates survivin expression. p54(nrb) forms a complex with ILF3, which directly binds to YM155. YM155 induces disruption of the ILF3/p54(nrb) complex, which results in a different subcellular localization between ILF3 and p54(nrb). Thus, identification of molecular targets of YM155 in suppression of the survivin pathway, might lead to development of its use as a novel potential target in cancers.

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