Abstract
Background and Aim: Animal venoms comprise a mix of bioactive molecules with high affinity for multiple targets in cells and tissues. Scorpion and spider venoms and purified peptides exhibit significant effects on cancer cells, encompassing four potential mechanisms: 1) induction of cell cycle arrest, growth inhibition, and apoptosis; 2) inhibition of angiogenesis; 3) inhibition of invasion and metastasis; and 4) blocking of specific transmembrane channels. Tumor biology is complex and entails many intertwined processes, as reflected in the putative hallmarks of cancer. This complexity, however, gives rise to numerous (potential) pharmacological intervention sites. Molecules that target multiple proteins or pathways, such as components of animal venoms, may therefore be effective anti-cancer agents. The objective of this review was to address the anti-cancer properties and in vitro mechanisms of scorpion and spider venoms and toxins, and highlight current obstacles in translating the preclinical research to a clinical setting. Relevance for patients: Cancer is a considerable global contributor to disease-related death. Despite some advances being made, therapy remains palliative rather than curative for the majority of cancer indications. Consequently, more effective therapies need to be devised for poorly responding cancer types to optimize clinical cancer management. Scorpion and spider venoms may occupy a role in the development of improved anti-cancer modalities.
Highlights
Animal venoms comprise a mix of bioactive molecules with high affinity for multiple targets in cells and tissues
Animal venoms are a mix of bioactive molecules that have a high affinity for multiple targets in prey or enemy organisms [1]
Buthus mar- Whole venom tensii Karsch (BmK) venom upregulates P27 and inactivates the PI3K/AKT signaling pathway through PTEN
Summary
Animal venoms are a mix of bioactive molecules that have a high affinity for multiple targets in prey or enemy organisms [1]. The development of cancer involves four categorical hallmarks (Figure 1): 1) dysregulated cell proliferation (due to the self-sufficiency of growth signals or insensitivity to growth inhibitory signals); 2) evasion of programmed cell death; 3) sustained angiogenesis; and 4) tissue invasion and metastasis [5, 6] These characteristics are a consequence of DNA mutations which can be inherited or acquired (caused by e.g., virus and substance exposure, chronic inflammation, and oxidative stress) [7]. Of 98 new anticancer drugs approved by the US Food and Drug Administration (FDA) between 1981 and 2010, 78 were natural products or were derived from natural products, and only 20 were synthetic [9] Despite their potential for use in the treatment of cancer, animal-derived molecules (mainly arthropods) are rarely used as drug prototypes or in clinical trials and practice. The difficulties with translating the use of these molecules to the clinical setting are discussed
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
