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Front Oncol. 2018 Dec 7;8:598. doi: 10.3389/fonc.2018.00598. eCollection 2018.

Curaxin CBL0137 Exerts Anticancer Activity via Diverse Mechanisms.

Jin MZ1, Xia BR2, Xu Y1, Jin WL3,4,5.

Author information

1
Shanghai Jiao Tong University School of Medicine, Shanghai, China.
2
Department of Gynecology, The Affiliated Tumor Hospital, Harbin Medical University, Harbin, China.
3
Key Laboratory for Thin Film and Microfabrication Technology of Ministry of Education, Department of Instrument Science and Engineering, Shanghai Engineering Center for Intelligent Diagnosis and Treatment Instrument, School of Electronic Information and Electronic Engineering, Institute of Nano Biomedicine and Engineering, Shanghai Jiao Tong University, Shanghai, China.
4
National Center for Translational Medicine, Collaborative Innovational Center for System Biology, Shanghai Jiao Tong University, Shanghai, China.
5
Shaanxi Key Laboratory of Brain Disorders and Institute of Basic and Translational Medicine, Xi'an Medical University, Xi'an, China.

Abstract

Chemotherapy with or without radiation remains the first choice for most cancers. However, intolerant side effects and conventional drug resistance restrict actual clinical efficacy. Curaxin CBL0137 is designed to regulate p53 and nuclear factor-κB simultaneously and to prevent the resistance caused by a single target. Functionally, CBL0137 exhibits an antitumor activity in multiple cancers, including glioblastoma, renal cell carcinoma, melanoma, neuroblastoma, and small cell lung cancer (SCLC). Mechanistically, CBL0137 is originally identified to act by facilitates chromatin transcription (FACT) complex. Further investigations reveal that several pathways, such as NOTCH1 and heat shock factor 1 (HSF1), are involved in the process. CBL0137 has been reported to target cancer stem cells (CSCs) and enhance chemotherapy/monotherapy efficacy. The translational advance of CBL0137 into clinical practice is expected to provide a promising future for cancer treatment.

KEYWORDS:

CBL0137; cancer stem cells; chemotherapy; facilitates chromatin transcription; p53

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