期刊
NEOPLASMA
卷 58, 期 6, 页码 538-547出版社
AEPRESS SRO
DOI: 10.4149/neo_2011_06_538
关键词
STAT3; RNA interference; breast cancer; metastasis
类别
资金
- Hi-tech Research and Development Program (863 Program) of China [2007AA021008, 2009ZX09102-241]
- National Key Basic Research Program (973 Program) of China [2010CB529900]
Signal transducer and activator of transcription 3 (STAT3) plays an important role in the tumor formation and metastasis. In this study, short hairpin RNA targeting STAT3 was cloned into pGenesil-2 plasmid vector and the effects of STAT3 silencing in 4T1 breast cancer cells were analyzed both in vitro and in vivo. Forty-eight hours after transfecting with pSi-STAT3, the expression level of STAT3, the upstream regulator and downstream targets were measured using Western blot. Moreover, the effects of pSi-STAT3 on migration and invasion in 4T1 cells were tested using wound-healing and tube formation assay. Furthermore, 4T1 subcutaneous mice model was used to evaluate the effects of pSi-STAT3 on tumor growth and metastasis. Proliferation, apoptosis, angiogenesis in tumor tissues and lung metastases were measured by PCNA, TUNEL, and CD31 immunostaining, respectively. Our results indicated that siRNA targeting STAT3 could significantly silence STAT3 expression in 4T1 breast cancer cells and result in inhibition of 4T1 breast cells migration and HUVECs tube formation. In vivo, pSi-STAT3 delayed tumor growth (p<0.01) and reduced tumor weight (p<0.01) by 67.19% and lung metastases (p<0.01) by 86.81% compared with the 5% GS control group, accompanied with apoptosis induction (p<0.01) and angiogenesis inhibition (p<0.01). In summary, our data showed that knockdown of STAT3 by plasmid-based siRNA might be a potential therapy against breast cancer.
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