Abstract
A scorpion peptide reported to exhibit both analgesic and antitumor activity in animal models may present as an alternative therapeutic agent for breast cancer. We aimed to investigate the effect of Buthus martensii Karsch antitumor-analgesic peptide (BmK AGAP) on breast cancer cell stemness and epithelial-mesenchymal transition (EMT). We treated MCF-7 and MDA-MB-231 cells with different concentrations of rBmK AGAP and observed that rBmK AGAP inhibited cancer cell stemness, epithelial-mesenchymal transition (EMT), migration, and invasion. Analysis by qPCR, ELISA, western blot, immunofluorescence staining, sphere formation, colony assay, transwell migration, and invasion assays demonstrated rBmK AGAP treatment decreased the expressions of Oct4, Sox2, N-cadherin, Snail, and increased the expression of E-cadherin. rBmK AGAP inhibited breast cancer cell stemness, EMT, migration, and invasion by down-regulating PTX3 through NF-κB and Wnt/β-catenin signaling Pathway in vitro and in vivo. Xenograft tumor model confirmed inhibition of tumor growth, stem-like features, and EMT by rBmK AGAP. Thus, rBmK AGAP is a potential therapeutic agent against breast cancer and related pain.
Highlights
Breast cancer is one of the leading cause of cancer-related morbidity and mortality among women worldwide with an estimated 25% of all newly diagnosed cancers being breast cancer annually [1]
The results showed a similar significantly increased pentraxin 3 (PTX3) expression in breast cancer tissues as the tumor advanced in stages compared with the normal breast tissues (Figures 1D,E)
We investigated the role of rBmK AGAP on stem-like features, epithelial-mesenchymal transition and tumor growth in vivo
Summary
Breast cancer is one of the leading cause of cancer-related morbidity and mortality among women worldwide with an estimated 25% of all newly diagnosed cancers being breast cancer annually [1]. Invasion and metastasis are major causes of breast cancer-associated morbidity and mortality [2]. Necrotic cell death and hypoxia associated with tumor progression trigger the release of inflammatory mediators which play critical role in tumorigenesis and cancer-related pain [4]. One such mediator is pentraxin 3 (PTX3), a member of the pentraxin superfamily. Expression of PTX3 is rapidly induced in a variety of cell types by several stimuli including cytokines and NF-κB activation [6]
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