An acetylated derivative of vitexin halts MDA-MB-231 cellular progression and improves its immunogenic profile through tuning miR- 20a-MICA/B axis. Issue 18 (17th September 2021)

• Record Type: Journal Article
• Authors: Awad, Aya R.; Youness, Rana A.; Ibrahim, M.; Motaal, Amira Abdel; El-Askary, Hesham I.; Assal, Reem.A.; Gad, Mohamed Z.
• Is Part Of: Natural product research. Volume 35:Issue 18(2021)
• Page Start: 3126
• Page End: 3130
• Publication Date: 2021-09-17
• Subjects: Vitexin -- 3'-O-acteylvitexin -- miR-20a -- MICA -- breast cancer -- MICB; Natural products -- Periodicals; Natural products -- Research -- Periodicals; Biological Factors -- Periodicals; Biological Products -- Periodicals; 547
• DOI: 10.1080/14786419.2019.1686372
• Languages: English
• ISSNs: 1478-6419

Abstract

Abstract: The activating immune ligands, MICA/B, act as a "kill me" signal through the NKG2D receptor expressed on natural killer (NK) cells. Recently, the oncogenic miR-20a was found to mediate immune escape through repressing MICA/B levels in breast cancer (BC) cells. However, targeting miR-20a-MICA/B using natural compounds has rarely been investigated. Our group has successfully isolated 3'-O-acetylvitexin that showed cytotoxic effects against colon cancer cells but has never been evaluated in BC. Our aim is to investigate the effects of 3'-O-acetylvitexin on BC cell lines and to further elucidate its molecular mechanism of action.The results showed that 3'-O-acetylvitex depicted a more pronounced dose-dependent repression of TNBC cellular viability, colonogenicity and migration capacity than Vitexin. 3'-O-acetylvitexin treatment resulted in a marked dose-dependent repression of miR-20a with a concomitant dose-dependent increase in MICA/B expression. In conclusion, 3'-O-acetylvitexin might act as a promising therapeutic agent for TNBC patients. Graphical Abstract: