Anthelmintic drug niclosamide enhances the sensitivity of chronic myeloid leukemia cells to dasatinib through inhibiting Erk/Mnk1/eIF4E pathway

Liu, Zhong; Li, Yong; Lv, Cao; Wang, Li; Song, Ho-Young

doi:10.1016/j.bbrc.2016.08.047

Cited by 23 publications

(22 citation statements)

References 29 publications

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“…Furthermore, niclosamide was also revealed to exert a synergistic effect with numerous cancer drugs in human cancer cells. Compared with cancer drug treatment alone, the combination treatment of niclosamide with bicalutamide, cisplatin, paclitaxel, carboplatin, erlotinib, dasatinib, or sorafenib exhibited an improved antineoplastic efficacy in prostate (32), lung (52), cervical (14), ovarian (30), colon (53), chronic myeloid leukemia (22) and renal cancer (34), respectively. To date, the frontline chemotherapeutic agents for advanced esophageal cancer cells are 5-FU, cisplatin, and paclitaxel.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism of niclosamide action is through the inhibition of glucose uptake, oxidative phosphorylation, and anaerobic metabolism in the target worms (7). Except for antiprotozoal function, the antineoplastic effects of niclosamide has been revealed in many human cancer cells, including adrenocortical carcinoma (8), breast (9)(10)(11), colorectal (12,13) and cervical cancer (14), glioblastoma (15), hepatocellular carcinoma (16,17), head and neck (18,19) and lung cancer (20,21), leukemia (22,23), nasopharyngeal cancer (24), osteosarcoma (25), oral squamous cell carcinoma (26,27), ovarian (28)(29)(30), prostate (31)(32)(33), renal (34) and thyroid cancer (35). Niclosamide treatment was reported to induce apoptosis of cancer cells in vitro (7,10,23) and suppress tumor size in animal studies (11,29).…”

Section: Introductionmentioning

confidence: 99%

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Niclosamide inhibits the cell proliferation and enhances the responsiveness of esophageal cancer cells to chemotherapeutic agents

Lee¹,

Chen

Hsu

et al. 2019

Oncol Rep

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Niclosamide is an FDA-approved anthelmintic drug, and may elicit antineoplastic effects through direct STAT3 inhibition, which has been revealed in numerous human cancer cells. Chemotherapy is the standard treatment for advanced esophageal cancers, but also causes severe systemic side effects. The present study represents the first study evaluating the anticancer efficacy of niclosamide in esophageal cancers. Through western blot assay, it was demonstrated that niclosamide suppressed the STAT3 signaling pathway in esophageal adenocarcinoma cells (BE3) and esophageal squamous cell carcinoma cells (CE48T and CE81T). In addition, niclosamide inhibited cell proliferation as determined by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay and soft agar colony forming assay, and induced cell apoptosis as determined by Annexin V and PI staining. The induction of p21 and G1 arrest of the cell cycle also was revealed in niclosamide-treated CE81T cells by qPCR and flow cytometric assays, respectively. Furthermore, in the combination analysis of niclosamide and chemotherapeutic agents by MTS assay, low IC 50 values were detected in cells co-treated with niclosamide, with the exception of cisplatin-treated CE81T cells. To confirm the results using an apoptosis assay, the apoptotic enhancement of niclosamide was only demonstrated in CE48T cells co-treated with 5-FU, cisplatin, or paclitaxel, and in BE3 cells co-treated with paclitaxel, but not in CE81T cells. These findings indicate a future clinical application of niclosamide in esophageal cancers.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Niclosamide inhibits the cell proliferation and enhances the responsiveness of esophageal cancer cells to chemotherapeutic agents

Lee¹,

Chen

Hsu

et al. 2019

Oncol Rep

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“…For instance, the combination of niclosamide with cisplatin led to the inhibition of cisplatin‐resistant triple‐negative breast cancer and exhibited synergistic effects in cisplatin‐resistant lung cancer cells . Enhanced sensitivity of chronic myeloid leukemia cells to dasatinib and that of cervical cancer cells to paclitaxel was also achieved when these drugs were used in combination with niclosamide. Synergistic effects with erlotinib in colon cancer, head and neck cancer, and in erlotinib‐resistant non‐small lung cancer cells have also been described.…”

Section: Pharmacological Activities Of Niclosamidementioning

confidence: 99%

Niclosamide, a Drug with Many (Re)purposes

2018

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Niclosamide is an anthelmintic drug that has been used for over 50 years mainly to treat tapeworm infections. However, with the increase in drug repurposing initiatives, niclosamide has emerged as a true hit in many screens against various diseases. Indeed, from being an anthelmintic drug, it has now shown potential in treating Parkinson's disease, diabetes, viral and microbial infections, as well as various cancers. Such diverse pharmacological activities are a result of niclosamide's ability to uncouple mitochondrial phosphorylation and modulate a selection of signaling pathways, such as Wnt/β-catenin, mTOR and JAK/STAT3, which are implicated in many diseases. In this highlight, we discuss the plethora of diseases that niclosamide has shown promise in treating.

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“…The use of imatinib with MNK inhibitors prevents eIF4E phosphorylation in vivo with an antiproliferative effect that could help to combat late-stage disease and to understand other pathways and cellular processes that are dysregulated by Bcr-Abl [119]. In addition, pharmacologic targeting of MNK and mTORC1 kinases, employing rapamycin together with novel MNK inhibitors (MNK1/2 53-54 or MNKI-4 and MNKI- 57) or niclosamide (an anthelminthic drug), abolished cell growth by triggering cell apoptotic death and abrogated eIF4E phosphorylation, which may offer a new therapeutic opportunity [76,96,110,121].…”

Section: Mnk In Hematological Cancersmentioning

confidence: 99%

Deeping in the Role of the MAP-Kinases Interacting Kinases (MNKs) in Cancer

Pinto-Díez

Ferreras-Martín

Carrión-Marchante

et al. 2020

IJMS

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The mitogen-activated protein kinase (MAPK)-interacting kinases (MNKs) are involved in oncogenic transformation and can promote metastasis and tumor progression. In human cells, there are four MNKs isoforms (MNK1a/b and MNK2a/b), derived from two genes by alternative splicing. These kinases play an important role controlling the expression of specific proteins involved in cell cycle, cell survival and cell motility via eukaryotic initiation factor 4E (eIF4E) regulation, but also through other substrates such as heterogeneous nuclear ribonucleoprotein A1, polypyrimidine tract-binding protein-associated splicing factor and Sprouty 2. In this review, we provide an overview of the role of MNK in human cancers, describing the studies conducted to date to elucidate the mechanism involved in the action of MNKs, as well as the development of MNK inhibitors in different hematological cancers and solid tumors.

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Anthelmintic drug niclosamide enhances the sensitivity of chronic myeloid leukemia cells to dasatinib through inhibiting Erk/Mnk1/eIF4E pathway

Cited by 23 publications

References 29 publications

Niclosamide inhibits the cell proliferation and enhances the responsiveness of esophageal cancer cells to chemotherapeutic agents

Niclosamide inhibits the cell proliferation and enhances the responsiveness of esophageal cancer cells to chemotherapeutic agents

Niclosamide, a Drug with Many (Re)purposes

Deeping in the Role of the MAP-Kinases Interacting Kinases (MNKs) in Cancer

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