Scorpion Venom Causes Upregulation of p53 and Downregulation of Bcl-x and BID Protein Expression by Modulating Signaling Proteins Erk and STAT3, and DNA Damage in Breast and Colorectal Cancer Cell Lines

Scorpion venoms efficiently block the normal neurotransmitter signaling pathway by prejudicing the ion channel operating mechanism in the body system. Besides its negative effect, venoms also possess some beneficial qualities for humans. They have also been shown to exhibit anticancer properties in...

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Veröffentlicht in:Integrative cancer therapies 2018-06, Vol.17
Hauptverfasser: Abdulrahman Khazim Al-Asmari PhD, Anvarbatcha Riyasdeen PhD, Mozaffarul Islam PhD
Format: Artikel
Sprache:eng
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Zusammenfassung:Scorpion venoms efficiently block the normal neurotransmitter signaling pathway by prejudicing the ion channel operating mechanism in the body system. Besides its negative effect, venoms also possess some beneficial qualities for humans. They have also been shown to exhibit anticancer properties in various cancer types. This unique property of the venom as an anticancer agent is mainly a result of its role in initiating apoptosis and inhibiting several signaling cascade mechanisms that promote cancer cell proliferation and growth. In this study, we examine the effect of venom on phenotypic changes as well as changes at the molecular levels in colorectal and breast cancer cell lines. A dramatic decrease in cell invasion was observed in both cancer cell lines on venom treatment. Additionally, there was decrease in IL-6, RhoC, Erk 1/2 , and STAT3 in venom-treated cell lines, providing strong evidence of its anticancer properties. Furthermore, decrease in the expression of antiapoptotic proteins and also upregulation of proapoptotic ones by these lines were observed on venom treatment. Moreover, a vivid picture of DNA damage was also detected on venom treatment. In conclusion, scorpion venom possesses significant potential as an anticancer agent against colorectal and breast cancer cell lines.
ISSN:1534-7354
1552-695X
DOI:10.1177/1534735417704949