Journal:
:hepatitis monthly
0
guo-hua qiu institute of biomedical engineering and health sciences, changzhou university, changzhou, pr china; department of physiology, faculty of medicine, national university of singapore, singapore, republic of singapore; institute of biomedical engineering and health sciences, changzhou university, changzhou, jiangsu 213164, pr china. tel/fax: +86-59786330103, e-mail:; shing chuan hooi, department of physiology, faculty of medicine, national university of singapore, singapore, republic of singapore. tel: +65-65163222, fax: +65-67788161
xiaojin xie department of physiology, faculty of medicine, national university of singapore, singapore, republic of singapore
linhong deng institute of biomedical engineering and health sciences, changzhou university, changzhou, pr china
shing chuan hooi department of physiology, faculty of medicine, national university of singapore, singapore, republic of singapore; institute of biomedical engineering and health sciences, changzhou university, changzhou, jiangsu 213164, pr china. tel/fax: +86-59786330103, e-mail:; shing chuan hooi, department of physiology, faculty of medicine, national university of singapore, singapore, republic of singapore. tel: +65-65163222, fax: +65-67788161
conclusions dlec1 suppresses tumor cell growth the presence of ap-2α2 and stimulates cell proliferation in the down-regulation of ap-2α2 in dlec1 over-expression stable clones of htc116. results the dlec1 over-expression was found to reduce the number of colonies in colony formation and to induce g1 arrest in seven clones, and apoptosis in one clone in the cell cycle analysis. furthermore, rega...
