title: Estrogen-independent effects of ER-α36 in ER-negative breast cancer.
abstract: Estrogen receptor-alpha 36 (ER-α36) is a variant of ER-α that has been found to be expressed in conventional ER (ER-α66)-negative breast cancer cell lines and human breast cancer samples. In this study, we found that, using immunohistochemical study, ER-α36 expression was significantly higher in ER-negative tumors than in ER-positive tumors although the expression was not associated with other clinicopathological characteristics. We then constructed an ER-α36-specific microRNA hairpin vector and established stable ER-α36 knockdown cells, and found that the knockdown cells were more sensitive to paclitaxel; the c-Jun N-terminal kinase pathway appeared to be involved in the mechanism. Downregulation of ER-α36 also resulted in decreased migration and invasion. These changes were estrogen independent. Our findings indicated that target ER-α36 may be a strategy for treating ER-negative breast cancers.
authors.affiliation: Department of Surgical Oncology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province 310003, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Zhang
authors.forename: Guangliang
authors.initials: G
authors.lastname: Li
authors.forename: Zhongqi
authors.initials: Z
authors.lastname: Li
authors.forename: Xiongfei
authors.initials: X
authors.lastname: Yu
authors.forename: Yi
authors.initials: Y
authors.lastname: Zheng
authors.forename: Ketao
authors.initials: K
authors.lastname: Jin
authors.forename: Haohao
authors.initials: H
authors.lastname: Wang
authors.forename: Yun
authors.initials: Y
authors.lastname: Gong
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Sun
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Teng
authors.forename: Jiang
authors.initials: J
authors.lastname: Cao
authors.forename: Lisong
authors.initials: L
authors.lastname: Teng
mesh_terms: D000328:Adult; D001943:Breast Neoplasms / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects; D015536:Down-Regulation / Q000187:drug effects; D047628:Estrogen Receptor alpha / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D004967:Estrogens / Q000378:metabolism; D005260:Female; D059565:G2 Phase Cell Cycle Checkpoints / Q000187:drug effects; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D055785:Gene Knockdown Techniques; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D059566:M Phase Cell Cycle Checkpoints / Q000187:drug effects; D035683:MicroRNAs / Q000235:genetics; D008875:Middle Aged; D058990:Molecular Targeted Therapy; D009361:Neoplasm Invasiveness; D017239:Paclitaxel / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects; D014162:Transfection
chemical_list: D047628:Estrogen Receptor alpha; D004967:Estrogens; D035683:MicroRNAs; D048031:JNK Mitogen-Activated Protein Kinases; D017239:Paclitaxel