ArticleOncology reports2022
Niclosamide suppresses T‑cell acute lymphoblastic leukemia growth through activation of apoptosis and autophagy.
Article in Oncology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Niclosamide-Modulated Apoptosis and Autophagy in Breast Cancer Cells via Phosphorylated JNK as a Common Regulator.International journal of medical sciences · 2025Article
- Lysosome targeted therapies in hematological malignancies.Frontiers in oncology · 2025Review
- Exploration of drug repurposing for Mpox outbreaks targeting gene signatures and host-pathogen interactions.Scientific reports · 2024Article
- Exploring the impact of mitochondrial-targeting anthelmintic agents with GLUT1 inhibitor BAY-876 on breast cancer cell metabolism.BMC cancer · 2024Article
- Drug Repurposing: Research Progress of Niclosamide and Its Derivatives on Antibacterial Activity.Infection and drug resistance · 2024Review
- Regulating TKT activity inhibits proliferation of human acute lymphoblastic leukemia cells.American journal of cancer research · 2024Article
- High G9a Expression in DLBCL and Its Inhibition by Niclosamide to Induce Autophagy as a Therapeutic Approach.Cancers · 2023Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T‑cell acute lymphoblastic leukemia (T‑ALL) is a common pediatric malignancy, characterized by the abnormal presence of immature T‑cell progenitors. Conventional treatments for T‑ALL fail to prevent or cure the disease, with a high‑risk of recurrence after the first remission. Thus, medical options are in demand to develop novel therapies for patients suffering with T‑ALL. Niclosamide, a traditional oral anti‑helminthic drug, has been reported to be a potential anticancer agent that regulates intracellular signaling pathways. Few studies have yet investigated the effects of niclosamide on the development of T‑ALL. Here, the present study aimed to investigate the anti‑leukemia effects of niclosamide on T‑ALL. We first hypothesized that the suppressive effects of niclosamide on the tumor growth of T‑ALL are exerted by regulating autophagy and apoptosis. Following niclosamide treatment, T‑ALL cell viability was evaluated using MTT assay, and apoptosis with Annexin V/propidium iodide staining. In T‑ALL cells treated with niclosamide, changes in apoptosis‑ and autophagy‑related proteins were analyzed by western blotting. In addition, in an
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