烟酰胺介导的氧化应激对急性淋巴细胞白血病的抗肿瘤活性。

IF 3.3 3区医学 Q2 ONCOLOGY

Carcinogenesis Pub Date : 2024-05-31 DOI:10.1093/carcin/bgae035

Jing Yang, Yong Liu, Zefan Du, Qin Zhou, Luo Yang, Qianyun Ye, Jingxuan Pan, Waiyi Zou, Chun Chen, Bei Jin

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引用次数: 0

摘要

急性淋巴细胞白血病（ALL）是一种起源于B细胞或T细胞淋巴前体细胞的异质性克隆疾病。急性淋巴细胞白血病往往难治或治疗后复发。为了使 ALL 患者获得更好的反应和更长的总生存期，我们急需新的治疗方法。本研究旨在探讨尼可刹米对 ALL 的抗肿瘤作用。我们研究了烟酰胺对体外ALL细胞增殖和凋亡的影响，以及对异种移植NCG小鼠ALL细胞生长的影响。结果表明，尼可刹米能有效抑制ALL细胞的生长，并通过提高活性氧（ROS）水平和激活TP53诱导细胞凋亡。这些研究结果表明，尼可刹米可能是一种很有潜力的治疗 ALL 的药物。

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Anti-tumor activity of niclosamide-mediated oxidative stress against acute lymphoblastic leukemia.

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 anti-tumor 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 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 (ROS) and activating TP53. These findings suggest that niclosamide may be a promisingly potential agent for ALL therapy.

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来源期刊

Carcinogenesis 医学-肿瘤学

CiteScore

9.20

自引率

2.10%

发文量

审稿时长

1 months

期刊介绍： Carcinogenesis: Integrative Cancer Research is a multi-disciplinary journal that brings together all the varied aspects of research that will ultimately lead to the prevention of cancer in man. The journal publishes papers that warrant prompt publication in the areas of Biology, Genetics and Epigenetics (including the processes of promotion, progression, signal transduction, apoptosis, genomic instability, growth factors, cell and molecular biology, mutation, DNA repair, genetics, etc.), Cancer Biomarkers and Molecular Epidemiology (including genetic predisposition to cancer, and epidemiology), Inflammation, Microenvironment and Prevention (including molecular dosimetry, chemoprevention, nutrition and cancer, etc.), and Carcinogenesis (including oncogenes and tumor suppressor genes in carcinogenesis, therapy resistance of solid tumors, cancer mouse models, apoptosis and senescence, novel therapeutic targets and cancer drugs).