Antitumor activity of niclosamide-mediated oxidative stress against acute lymphoblastic leukemia

Author:

Yang Jing12,Liu Yong12,Du Zefan12,Zhou Qin12,Yang Luo34,Ye Qianyun34,Pan Jingxuan34,Zou Waiyi56,Chen Chun12ORCID,Jin Bei34ORCID

Affiliation:

1. Division of Hematology/Oncology, Department of Pediatrics , 628 Zhenyuan Road, Xinhu Street, Guangming District, Shenzhen ,  , Shenzhen , China

2. The Seventh Affiliated Hospital, Sun Yat-sen University , 628 Zhenyuan Road, Xinhu Street, Guangming District, Shenzhen ,  , Shenzhen , China

3. State Key Laboratory of Ophthalmology, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science , 54 South Xianlie Road, Guangzhou 510060 ,  , Guangzhou , China

4. Zhongshan Ophthalmic Center, Sun Yat-sen University , 54 South Xianlie Road, Guangzhou 510060 ,  , Guangzhou , China

5. Department of Hematology, The First Affiliated Hospital , 58 Zhongshan Road II, Guangzhou 510080 ,  , Guangzhou , China

6. Sun Yat-sen University , 58 Zhongshan Road II, Guangzhou 510080 ,  , Guangzhou , China

Abstract

Abstract Acute lymphoblastic leukemia (ALL) is a heterogeneous clonal disease originated from B- or T-cell lymphoid precursor cells. ALL is often refractory or relapses after treatment. Novel treatments are anxiously needed in order to achieve a better response and prolonged overall survival in ALL patients. In the present study, we aimed at examining the antitumor effect of niclosamide on ALL. We investigated the effects of niclosamide on the proliferation and apoptosis in vitro, the growth of ALL cells in xenografted NOD-Prkdcem26Cd52 il2rgem26Cd22 /Nju (NCG) mice. The results showed that niclosamide treatment potently inhibited the growth of ALL cells and induced apoptosis via elevating the levels of reactive oxygen species and activating TP53. These findings suggest that niclosamide may be a promisingly potential agent for ALL therapy.

Funder

Sanming Project of Medicine in Shenzhen

Shenzhen Healthcare Research Project

Shenzhen Science and Technology Innovation Commission

Publisher

Oxford University Press (OUP)

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