WITHDRAWN: Survivin knock down by short hairpin RNA inhibits proliferation and induces apoptosis in EJ bladder cancer cells

2010 ◽  
Author(s):  
Xin Gou ◽  
Hua-An Yang ◽  
Wei-Yang He ◽  
Ming-Chao Xiao ◽  
Ming Wang
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Short Hairpin Rna ◽  
Hairpin Rna ◽  
Knock Down ◽  
Bladder Cancer Cells ◽  
Short Hairpin

Inhibition of Telomerase Activity in Cancer Cells using Short Hairpin RNA Expression Vectors

2007 ◽  
Vol 25 (8) ◽  
pp. 691-698 ◽  
Author(s):  
Shi-Ming Chen ◽  
Ze-Zhang Tao ◽  
Qing-Quan Hua ◽  
Bo-Kui Xiao ◽  
Yu Xu ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Telomerase Activity ◽  
Short Hairpin Rna ◽  
Expression Vectors ◽  
Rna Expression ◽  
Hairpin Rna ◽  
Short Hairpin

Knock down of gfp and no tail expression in zebrafish embryo by in vivo-transcribed short hairpin RNA with T7 plasmid system

2007 ◽  
Vol 14 (6) ◽  
pp. 767-776 ◽  
Author(s):  
Na Wang ◽  
Yong-Hua Sun ◽  
Jing Liu ◽  
Gang Wu ◽  
Jian-Guo Su ◽  
...  
Keyword(s):  
Zebrafish Embryo ◽  
Short Hairpin Rna ◽  
Hairpin Rna ◽  
Knock Down ◽  
No Tail ◽  
Short Hairpin

Downregulation of MTDH using short hairpin RNA inhibited EMT in breast cancer cells

2013 ◽  
Vol 12 (7) ◽  
pp. 326-331
Author(s):  
Heng Cao ◽  
Zhaozhe Liu ◽  
Dongchu Ma ◽  
Zhenyu Ding ◽  
Cheng Du ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Short Hairpin Rna ◽  
Hairpin Rna ◽  
Short Hairpin

scholarly journals Coactivation of Janus Tyrosine Kinase (Jak)1 Positively Modulates Prolactin-Jak2 Signaling in Breast Cancer: Recruitment of ERK and Signal Transducer and Activator of Transcription (Stat)3 and Enhancement of Akt and Stat5a/b Pathways

2007 ◽  
Vol 21 (9) ◽  
pp. 2218-2232 ◽  
Author(s):  
Lynn M. Neilson ◽  
Jianquong Zhu ◽  
Jianwu Xie ◽  
M. Grazia Malabarba ◽  
Kazuhito Sakamoto ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tyrosine Kinase ◽  
Cancer Cells ◽  
Tyrosine Phosphorylation ◽  
Short Hairpin Rna ◽  
Signal Transducer ◽  
Hairpin Rna ◽  
Adenoviral Delivery ◽  
Short Hairpin ◽  
Dependent Mechanism

Abstract Prolactin (PRL) receptors (PRLRs) have been considered selective activators of Janus tyrosine kinase (Jak)2 but not Jak1, Jak3, or Tyk2. We now report marked PRL-induced tyrosine phosphorylation of Jak1, in addition to Jak2, in a series of human breast cancer cell lines, including T47D, MCF7, and SKBR3. In contrast, PRL did not activate Jak1 in immortalized, noncancerous breast epithelial lines HC11, MCF10A, ME16C, and HBL-100, or in CWR22Rv1 prostate cancer cells or MDA-MB-231 breast cancer cells. However, introduction of exogenous PRLR into MCF10A, ME16C, or MDA-MB-231 cells reconstituted both PRL-Jak1 and PRL-Jak2 signals. In vitro kinase assays verified that PRL stimulated enzymatic activity of Jak1 in T47D cells, and PRL activated Jak1 and Jak2 with indistinguishable time and dose kinetics. Relative Jak2 deficiency did not cause PRLR activation of Jak1, because overexpression of Jak2 did not interfere with PRL activation of Jak1. Instead, PRL activated Jak1 through a Jak2-dependent mechanism, based on disruption of PRL activation of Jak1 after Jak2 suppression by 1) lentiviral delivery of Jak2 short hairpin RNA, 2) adenoviral delivery of dominant-negative Jak2, and 3) AG490 pharmacological inhibition. Finally, suppression of Jak1 by lentiviral delivery of Jak1 short hairpin RNA blocked PRL activation of ERK and signal transducer and activator of transcription (Stat)3 and suppressed PRL activation of Jak2, Stat5a, Stat5b, and Akt, as well as tyrosine phosphorylation of PRLR. The data suggest that PRL activation of Jak1 represents a novel, Jak2-dependent mechanism that may serve as a regulatory switch leading to PRL activation of ERK and Stat3 pathways, while also serving to enhance PRL-induced Stat5a/b and Akt signaling.

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