Exploratory transcriptomic profiling of melittin's efficacy in the treatment of murine cervical cancer cells
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Published on: August 23, 2019
Jianrong Jiang1,2,3, Yuwei Zhang3,4,5,6, Mengyi Wang4,5,6
1Guangdong Medical University, Dongguan, China.
Introduction:
Melittin, a highly active antimicrobial peptide derived from honeybee venom, holds immense pharmacological potential against solid tumors, yet its specific anti-tumor efficacy and transcriptomic dynamics in cervical carcinoma remain inadequately characterized.
Methods:
This study systematically evaluated the anti-cancer properties and potential molecular mechanisms of melittin on murine U14 cervical cancer cells.
Results:
Phenotypic assessments demonstrated that melittin potently inhibited U14 cell viability and dose-dependently suppressed cellular migration, culminating in near-complete migratory arrest at high concentrations. Additionally, flow cytometry revealed a dramatic, dose-dependent surge in the Annexin V+/PI+ cell population. Given the well-established membranolytic properties of melittin, this lethal effect structurally corroborated by scanning electron microscopy (SEM) showing severe plasma membrane perforation and morphological collapse, may reflect a possible mixture of true late apoptosis and secondary necrosis, though the exact mode of cell death remains undefined. Following the rigorous identification of differentially expressed genes (DEGs) in U14 cells, subsequent enrichment analyses indicated that the physical membrane disruption inflicted by melittin translated into a severe metabolic crisis, marked by a global suppression of ribosomal biogenesis and mitochondrial oxidative phosphorylation. Furthermore, melittin significantly downregulated Etv2, a key transcription factor in vascular development, suggesting not only a potential suppression of angiogenesis-related networks but also the potential involvement of an AP-1 transcriptional stress complex (evidenced by the profound upregulation of Jun, Fos, and Fosb).
Discussion:
Collectively, these findings outline the pharmacological networks underlying melittin's cytotoxicity, providing an exploratory molecular framework for its future development as a natural therapeutic agent against cervical cancer.
