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Updated: Dec 14, 2025
Extraction of Venom and Venom Gland Microdissections from Spiders for Proteomic and Transcriptomic Analyses
Published on: November 3, 2014
Kinome scale profiling of venom effects on cancer cells reveals potential new venom activities
Danielle McCullough1, Cristina Atofanei1, Emily Knight2
1School of Human and Life Sciences, Canterbury Christ Church University, Canterbury, CT1 1QU, UK.
Abstract:
The search for novel and relevant cancer therapeutics is continuous and ongoing. Cancer adaptations, resulting in therapeutic treatment failures, fuel this continuous necessity for new drugs to novel targets. Recently, researchers have started to investigate the effect of venoms and venom components on different types of cancer, investigating their mechanisms of action. Receptor tyrosine kinases (RTKs) comprise a family of highly conserved and functionally important druggable targets for cancer therapy. This research exploits the novelty of complex venom mixtures to affect phosphorylation of the epidermal growth factor receptor (EGFR) and related RTK family members, dually identifying new activities and unexplored avenues for future cancer and venom research. Six whole venoms from diverse species taxa, were evaluated for their ability to illicit changes in the phosphorylated expression of a panel of 49 commonly expressed RTKs. The triple negative breast cancer cell line MDA-MB-468 was treated with optimised venom doses, pre-determined by SDS PAGE and Western blot analysis. The phosphorylated expression levels of 49 RTKs in response to the venoms were assessed with the use of Human Phospho-RTK Arrays and analysed using ImageLab 5.2.1 analysis software (BioRad). Inhibition of EGFR phosphorylation occurred with treatment of venom from Acanthoscurria geniculata (Theraphosidae), Heterometrus swammerdami (Scorpionidae), Crotalus durissus vegrandis (Crotalidae) and Naja naja (Elapidae). Western green mamba Dendroaspis viridis venom increased EGFR phosphorylation. Eph, HGFR and HER were the most affected receptor families by venoms. Whilst the importance of these changes in terms of effect on MDA-MB-468 cells' long-term viability and functionality are still unclear, the findings present exciting opportunities for further investigation as potential drug targets in cancer and as tools to understand better how these pathways interact.
Insights
Researchers explored how snake and spider venoms affect cancer cell signaling. Some venoms inhibited epidermal growth factor receptor (EGFR) phosphorylation, suggesting potential new cancer therapeutics.
Area of Science:
- Biochemistry
- Pharmacology
- Oncology
Background:
- The continuous need for novel cancer therapeutics is driven by cancer's adaptation and treatment failures.
- Receptor tyrosine kinases (RTKs) are crucial targets for cancer drug development.
- Natural compounds, like venoms, offer a novel source for identifying anti-cancer agents.
Purpose of the Study:
- To investigate the effects of diverse whole venoms on the phosphorylation of 49 receptor tyrosine kinases (RTKs) in cancer cells.
- To identify specific venom components or mixtures that modulate RTK activity, particularly the epidermal growth factor receptor (EGFR).
- To explore the potential of venoms as a source for new cancer drug discovery and as tools for understanding signaling pathways.
Main Methods:
- Six whole venoms from different species were screened for their impact on RTK phosphorylation.
- The triple-negative breast cancer cell line MDA-MB-468 was treated with optimized venom doses.
- Phosphorylated RTK levels were assessed using Human Phospho-RTK Arrays and analyzed via ImageLab software.
Main Results:
- Venoms from Acanthoscurria geniculata, Heterometrus swammerdami, Crotalus durissus vegrandis, and Naja naja inhibited EGFR phosphorylation.
- Dendroaspis viridis venom increased EGFR phosphorylation.
- Eph, HGFR, and HER receptor families were most significantly affected by the venoms.
Conclusions:
- Certain venoms modulate RTK phosphorylation, including key targets like EGFR, in triple-negative breast cancer cells.
- These findings highlight the potential of venoms as a source for novel anti-cancer drug leads.
- Further research is needed to clarify the long-term effects on cancer cell viability and to explore venom-derived compounds as therapeutic agents.
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