{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,25]],"date-time":"2026-06-25T15:50:41Z","timestamp":1782402641649,"version":"3.54.5"},"reference-count":39,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2011,9,1]],"date-time":"2011-09-01T00:00:00Z","timestamp":1314835200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cell Biochemistry &amp;amp; Function"],"published-print":{"date-parts":[[2011,12]]},"abstract":"<jats:p>Curcumin from the rhizome of the <jats:italic>Curcuma longa<\/jats:italic> plant has been noted for its chemo\u2010preventative and chemo\u2010therapy activities, and it inhibits the growth of many types of human cancer cell lines. In this study, the mechanisms of cell death involved in curcumin\u2010induced growth inhibition, including cell cycle arrest and induction of apoptosis in human tongue cancer SCC\u20104 cells, were investigated. Herein, we observed that curcumin inhibited cell growth of SCC\u20104 cells and induced cell death in a dose\u2010dependent manner. Treatment of SCC\u20104 cells with curcumin caused a moderate and promoted the G<jats:sub>2<\/jats:sub>\/M phase arrest, which was accompanied with decreases in cyclin B\/CDK1 and CDC25C protein levels. Moreover, curcumin significantly induced apoptosis of SCC\u20104 cells with a decrease of the Bcl\u20102 level, reduction of mitochondrial membrane potential (<jats:italic>\u0394\u03a8<jats:sub>m<\/jats:sub><\/jats:italic>), and promoted the active forms of caspase\u20103. Curcumin also promoted the releases of AIF and Endo G from the mitochondria in SCC\u20104 cells by using confocal laser microscope. Therefore, we suggest that curcumin induced apoptosis through a mitochondria\u2010dependent pathway in SCC\u20104 cells. In addition, we also found that curcumin\u2010induced apoptosis of SCC\u20104 cells was partly through endoplasmic reticulum stress. In conclusion, curcumin increased G<jats:sub>2<\/jats:sub>\/M phase arrest and induced apoptosis through ER stress and mitochondria\u2010dependent pathways in SCC\u20104 cells. Copyright \u00a9 2011 John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/cbf.1800","type":"journal-article","created":{"date-parts":[[2011,9,1]],"date-time":"2011-09-01T16:08:59Z","timestamp":1314893339000},"page":"641-650","source":"Crossref","is-referenced-by-count":31,"title":["Induction of apoptotic death by curcumin in human tongue squamous cell carcinoma SCC\u20104 cells is mediated through endoplasmic reticulum stress and mitochondria\u2010dependent pathways"],"prefix":"10.1002","volume":"29","author":[{"given":"Siu\u2010Wan","family":"Ip","sequence":"first","affiliation":[{"name":"Department of Nutrition China Medical University  Taichung Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shan\u2010Ying","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Nutrition China Medical University  Taichung 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Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zen\u2010Pin","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Holistic Wellness Mingdao University  Changhua Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shang\u2010Ming","family":"Chiou","sequence":"additional","affiliation":[{"name":"Department of Functional Neurosurgery and Gamma Knife Center China Medical University Hospital  Taichung Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hsiung\u2010Kwang","family":"Chung","sequence":"additional","affiliation":[{"name":"Departments of Otorhinolaryngology\u2010Head and Neck Surgery China Medical University Hospital  Taichung Taiwan"},{"name":"Graduate Institute of Clinical Medical Science China Medical University  Taichung Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heng\u2010Chien","family":"Ho","sequence":"additional","affiliation":[{"name":"Department of 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