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In this study, we investigated how Raddeanin A potentiate NK activity using KHYG\u20101 cells. The results indicated that Raddeanin A increased the expression levels of cytolytic molecules such as perforin, granzymes A and granzymes B, granulysin and FasL in KHYG\u20101 cells. Raddeanin A treatment increased CREB phosphorylation, p65 phosphorylation, NFAT1 and acetyl\u2010histone H3 expression. Raddeanin A elevated caspase 3 and PARP cleavage, increased t\u2010Bid expression, promoting apoptosis in K562 cells. Furthermore, it reduced the expression of HMGB2, SET and Ape1, impairing the DNA repair process and causing K562 cells to die caspase\u2010independently. Additionally, Raddeanin A increased ERK, p38 and JNK phosphorylation at the molecular level, which increased granzyme B production in KHYG\u20101 cells. Raddeanin A treatment increased Ras, Raf phosphorylation, MEK phosphorylation, NKG2D, NKp44 and NKp30 expression in KHYG\u20101 cells. Collectively, our data indicate that Raddeanin A enhances the cytotoxic activity of NK cells against different cancer cells.<\/jats:p>","DOI":"10.1111\/jcmm.70016","type":"journal-article","created":{"date-parts":[[2024,8,23]],"date-time":"2024-08-23T04:01:33Z","timestamp":1724385693000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Raddeanin A augments the cytotoxicity of natural killer cells against chronic myeloid leukaemia cells by modulating <scp>MAPK<\/scp> and Ras\/Raf signalling pathways"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9726-3234","authenticated-orcid":false,"given":"Ming\u2010Ju","family":"Hsieh","sequence":"first","affiliation":[{"name":"Oral Cancer Research Center Changhua Christian Hospital  Changhua Taiwan"},{"name":"Doctoral Program in Tissue Engineering and Regenerative Medicine, College of Medicine National Chung Hsing University  Taichung 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