Exploratory transcriptomic profiling of melittin's efficacy in the treatment of murine cervical cancer cells.
6 affiliations
- 1Guangdong Medical University, Dongguan, China.
- 2Dongguan Maternal and Children Health Hospital, Dongguan, China.
- 3Apitherapy Research Institute of Fujian Agriculture and Forestry University, Fuzhou, China.
- 4College of Bee Science, Fujian Agriculture and Forestry University, Fuzhou, China.
- 5National & Local United Engineering Laboratory of Natural Biotoxin, Fuzhou, China.
- 6Dongguan Technology Transfer Center of National & Local United Engineering Laboratory of Natural Biotoxin, Dongguan, China.
Abstract
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. This study systematically evaluated the anti-cancer properties and potential molecular mechanisms of melittin on murine U14 cervical cancer cells. 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). 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.
Related
- Circulating and tumor microenvironment immunomarkers associate with immunotherapy efficacy in advanced bladder urothelial carcinoma: an exploratory multicenter study integrating genomic and immunophenotypic profiling
- PATIENT PROFILING AND OUTCOME OF ANTIHYPERTENSIVE TREATMENT. An Exploratory Analysis of the VALUE Trial.
- Pre-transplant whole blood transcriptomic profiling identifies mRNAs linked to cirrhosis-associated immune dysfunction as candidate predictors of clinical outcomes after liver transplantation: an exploratory study
- Exploratory Transcriptomic Profiling of Vein Tissue from Diabetic Patients Undergoing Arteriovenous Fistula Creation for Hemodialysis
- Exploratory mRNA and microRNA profiling identifies transcriptomic alterations in the PIK3CA-related overgrowth spectrum
BibTeX
@article{jiang2026exploratory,
title = {{Exploratory transcriptomic profiling of melittin's efficacy in the treatment of murine cervical cancer cells.}},
author = {Jianrong Jiang and Yuwei Zhang and Mengyi Wang and Ronghua Zhang and Yueliang Li and Jianfeng Qiu and Dafu Chen and Tizhen Yan and Rui Guo and Yanhui Liu},
journal = {Frontiers in cell and developmental biology},
year = {2026},
month = oct,
doi = {10.3389/fcell.2026.1975665},
url = {https://europepmc.org/article/MED/42953088},
note = {CC BY},
}
RIS
TY - JOUR
TI - Exploratory transcriptomic profiling of melittin's efficacy in the treatment of murine cervical cancer cells.
AU - Jianrong Jiang
AU - Yuwei Zhang
AU - Mengyi Wang
AU - Ronghua Zhang
AU - Yueliang Li
AU - Jianfeng Qiu
AU - Dafu Chen
AU - Tizhen Yan
AU - Rui Guo
AU - Yanhui Liu
PY - 2026
DA - 2026/10/14
JO - Frontiers in cell and developmental biology
DO - 10.3389/fcell.2026.1975665
UR - https://europepmc.org/article/MED/42953088
AB - 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. This study systematically evaluated the anti-cancer properties and potential molecular mechanisms of melittin on murine U14 cervical cancer cells. 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). 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.
SN - 2296-634X
ER -