Pro-Apoptotic and Cytotoxic Effects of Melittin on HL-60 Acute Promyelocytic Leukemia Cells: Implications for Retinoid-Independent Therapy

These findings confirm and extend established evidence by demonstrating that melittin's mitochondrial apoptotic mechanism is consistently active in promyelocytic HL-60 model (PML/RARα-negative). This retinoid-independent mechanism suggests potential therapeutic utility for ATRA-resistant cases or as a complementary strategy in APL treatment. However, selectivity validation in non-cancerous hematopoietic cells represents an important future research priority.

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Publication Details

Journal
Molecules
Published
2025-10-15
DOI
https://doi.org/10.3390/molecules30204093
Citations
1
Primary Topic
Healthcare and Venom Research
Type
article
Field-Weighted Citation Impact
1.39
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article

Pro-Apoptotic and Cytotoxic Effects of Melittin on HL-60 Acute Promyelocytic Leukemia Cells: Implications for Retinoid-Independent Therapy

Maksymilian Stela, Michał Bijak, Marcin Podogrocki, Tomasz Popławski et al.
1 citations
Molecules
Healthcare and Venom Research
1.39
article

Pro-Apoptotic and Cytotoxic Effects of Melittin on HL-60 Acute Promyelocytic Leukemia Cells: Implications for Retinoid-Independent Therapy

Maksymilian Stela, Michał Bijak, Marcin Podogrocki, Tomasz Popławski, Michał Ceremuga, Natalia Cichoń, Leslaw Gorniak
article en
1 citations

Abstract

These findings confirm and extend established evidence by demonstrating that melittin's mitochondrial apoptotic mechanism is consistently active in promyelocytic HL-60 model (PML/RARα-negative). This retinoid-independent mechanism suggests potential therapeutic utility for ATRA-resistant cases or as a complementary strategy in APL treatment. However, selectivity validation in non-cancerous hematopoietic cells represents an important future research priority.

MoleculesVol. 30(20)
University of Łódź (PL), Wojskowy Instytut Techniki Pancernej i Samochodowej (PL), Medical University of Lodz (PL)
Openalex Percentile: Top 15%
Healthcare and Venom Research
1.39
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