Tu SH |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=5.684 ------>paper_class3=2 ------>paper_class2=1 ------>vol= ------>confirm_bywho=None ------>insert_bywho=cmbsycl ------>Jurnal_Rank=12.1 ------>authors4_c= ------>comm_author=1 ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=0 ------>page2= ------>medlineContent= ------>unit=E0104 ------>insert_date=20091106 ------>iam=7 ------>update_date=None ------>author=??? ------>change_event=2 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Breast Cancer Res Treat ------>paper_name=Increased expression of enolase alpha in human breast cancer confers tamoxifen resistance in human breast cancer cells ------>confirm_date=None ------>tch_id=083006 ------>pmid=19655245 ------>page1= ------>fullAbstract=Enolase-alpha (ENO-1) is a key glycolytic enzyme that has been used as a diagnostic marker to identify human lung cancers. To investigate the role of ENO-1 in breast cancer diagnosis and therapy, the mRNA levels of ENO-1 in 244 tumor and normal paired tissue samples and 20 laser capture-microdissected cell clusters were examined by quantitative real-time PCR analysis. Increased ENO-1 mRNA expression was preferentially detected in estrogen receptor-positive (ER+) tumors (tumor/normal ratio >90-fold) when compared to ER-negative (tumor/normal ratio >20-fold) tumor tissues. The data presented here demonstrate that those patients whose tumors highly expressed ENO-1 had a poor prognosis with greater tumor size (>2 cm, *P = .017), poor nodal status (N > 3, *P = .018), and a shorter disease-free interval (<==1 year, *P < .009). We also found that higher-expressing ENO-1 tumors confer longer distance relapse (tumor/normal ratio = 82.8-92.4-fold) when compared to locoregional relapse (tumor/normal ratio = 43.4-fold) in postsurgical 4-hydroxy-tamoxifen (4-OHT)-treated ER+ patients (*P = .014). These data imply that changes in tumor ENO-1 levels are related to clinical 4-OHT therapeutic outcome. In vitro studies demonstrated that decreasing ENO-1 expression using small interfering RNA (siRNA) significantly augmented 4-OHT (100 nM)-induced cytotoxicity in tamoxifen-resistant (Tam-R) breast cancer cells. These results suggest that downregulation of ENO-1 could be utilized as a novel pharmacological approach for overcoming 4-OHT resistance in breast cancer therapy. ------>tmu_sno=None ------>sno=22871 ------>authors2=Chang CC ------>authors3=Chen CS ------>authors4=Tam KW ------>authors5=Wang YJ ------>authors6=Lee CH, Lin HW, Cheng TC, Huang CS, Chu JS, Shih NY, Chen LC, Leu SJ*, Ho YS*, Wu CH* ------>authors6_c= ------>authors=Tu SH ------>delete_flag=0 ------>SCI_JNo=74480 ------>authors2_c= ------>publish_area=0 ------>updateTitle=Increased expression of enolase alpha in human breast cancer confers tamoxifen resistance in human breast cancer cells. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2009 ------>submit_flag=None ------>publish_month=10 |