Wang, Sheng-ChiehSheng-ChiehWangYen, Ching-YuChing-YuYenShiau, Jun-PingJun-PingShiauChang, Meng-YangMeng-YangChangHou, Ming-FengMing-FengHouJIIANG-HUEI JENGTang, Jen-YangJen-YangTangChang, Hsueh-WeiHsueh-WeiChang2023-05-042023-05-042022-05-082076-3921https://scholars.lib.ntu.edu.tw/handle/123456789/630845SK2, a nitrated [6,6,6]tricycle derivative with an n-butyloxy group, showed selective antiproliferation effects on oral cancer but not on normal oral cells. This investigation assessed for the first time the synergistic antiproliferation potential of cisplatin/SK2 in oral cancer cells. Cell viability assay at 24 h showed that a low dose of combined cisplatin/SK2 (10 μM/10 μg/mL) provided more antiproliferation than cisplatin or SK2 alone. Cisplatin/SK2 triggered also more apoptosis inductions in terms of subG1 accumulation, annexin V, pancaspase, and caspase 3/8/9 measurements. Moreover, cisplatin/SK2 provided more oxidative stress and DNA damage in oral cancer cells than independent treatments. Oxidative stress inhibitors rescued the cisplatin/SK2-induced antiproliferation and oxidative stress generation. Moreover, cisplatin/SK2 induced more antiproliferation, apoptosis, oxidative stress, and DNA damage in oral cancer cells than in normal oral cells (S-G). In conclusion, low-dose cisplatin/SK2 combined treatment promoted selective and synergistic antiproliferation in oral cancer cells depending on oxidative-stress-associated responses.enantiproliferation; combined treatment; nitrated [6,6,6]tricycles; oral cancer[SDGs]SDG3journal article10.3390/antiox11050926356247902-s2.0-85132175346WOS:000802528200001https://api.elsevier.com/content/abstract/scopus_id/85132175346