Helminth Infection and Control / Parasitic Diseases Research and Treatment · Journal article
Cells · September 7, 2026
Raises a question worth testing. It does not answer one.
This in vitro mechanistic study demonstrates that ivermectin impairs stress granule disassembly in neuroblastoma cells by suppressing de novo hsp70 synthesis at the translational level, independent of changes in hsp70 transcription or Hsf1. The finding is cell-line dependent and does not establish clinical relevance or efficacy in cancer therapy.
In vitro mechanistic study in cultured mammalian cell lines. Human neuroblastoma and cervical carcinoma cell lines. Intervention: Ivermectin treatment during stress recovery.
Ivermectin interferes with stress granule disassembly in neuroblastoma cells Ivermectin reduces de novo hsp70 protein synthesis in neuroblastoma during stress recovery, as measured by bioorthogonal non-canonical amino acid tagging ivermectin reduces hsp70 abundance in neuroblastoma but not cervical carcinoma cells
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This mechanistic observation may inform preclinical development of ivermectin-based anti-cancer strategies, but the translational pathway from cell line stress granule phenotype to clinical efficacy remains unestablished.
Mechanistic in vitro study in cell lines identifying a pathway by which ivermectin may affect stress granule clearance; does not test clinical efficacy or measure patient-relevant outcomes.
As stated by the source record.
This mechanistic observation may inform preclinical development of ivermectin-based anti-cancer strategies, but the translational pathway from cell line stress granule phenotype to clinical efficacy remains unestablished.
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What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Cytoplasmic stress granules (SGs) form in response to diverse insults; they are dismantled when the stress subsides. SG clearance is facilitated by molecular chaperones, nuclear transport factors, and other components. The anti-parasitic drug ivermectin inhibits nuclear trafficking and has potential anti-cancer activities. However, the molecular pathways that promote ivermectin’s therapeutic actions are poorly understood. Our study defined the effects of ivermectin on stress recovery in human neuroblastoma and cervical carcinoma cells. We demonstrate that ivermectin interferes with SG disassembly in neuroblastoma cells. The delay of SG dissolution is accompanied by significant changes in the proteostasis network. Notably, ivermectin diminishes de novo protein synthesis in unstressed and stressed cells. During recovery, ivermectin reduces the abundance of hsp70 in neuroblastoma, but not in cervical carcinoma cells. Surprisingly, ivermectin has no effect on Hsf1 abundance and localization. Moreover, ivermectin does not diminish the levels of transcripts encoding hsp70. Bioorthogonal Non-Canonical Amino Acid Tagging revealed that ivermectin markedly reduces the stress-induced de novo synthesis of hsp70 in neuroblastoma cells. Taken together, ivermectin can derail stress responses by a unique mechanism that alters the translation of hsp70 mRNA and is determined by the cellular context. This information is directly relevant to ivermectin-based anti-cancer therapies.
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