Stat3-siRNA inhibits the growth of gastric cancer in vitro and in vivo.
Gastric cancer remains one of the most prevalent and lethal malignancies in the world. Despite new advances in treatment and diagnosis, patients with advanced gastric cancer are still difficult to cure resulting in a high mortality rate and poor prognosis. Signal transducer and activator of transcription 3 (Stat3) is observed aberrant in multiple tumours, including gastric cancer. Stat3 overexpression was confirmed performing a vital role in tumorigenesis. In the present study, we constructed a pSi-Stat3 plasmid to silence Stat3 and investigated the effect of pSi-Stat3 on cell proliferation, apoptosis and cell cycle progression in gastric cancer cell line SGC-7901 and mice xenograft model. Downstream proteins of Stat3, including Cyclin-D1, Survivin and Bcl-2, were detected as well for the underlying mechanism exploration. It showed that pSi-Stat3 can effectively silence the expression of Stat3 and inhibits the growth of gastric tumour both in vitro and in vivo significantly via cell apoptosis and cell cycle shift induction. The findings suggest that Stat3 signal pathway might be a promising therapeutic target for tumour treatment, including gastric cancer.
Department of Plastic Surgery, the China- Japan Union Hospital, Jilin University, Changchun, China.
Ying
Y
Sun
Department of Plastic Surgery, the China- Japan Union Hospital, Jilin University, Changchun, China.
Bao-feng
BF
Guo
Department of Pathophysiology, College of Basic Medicine Sciences, Jilin University, Changchun, China.
Li-bo
LB
Xu
Department of Pathophysiology, College of Basic Medicine Sciences, Jilin University, Changchun, China.
Jia-teng
JT
Zhong
Department of Pathophysiology, College of Basic Medicine Sciences, Jilin University, Changchun, China.
Zhe-wen
ZW
Liu
Department of Pathophysiology, College of Basic Medicine Sciences, Jilin University, Changchun, China.
Hang
H
Liang
Department of Pathophysiology, College of Basic Medicine Sciences, Jilin University, Changchun, China.
Nai-yan
NY
Wen
Department of Pathophysiology, College of Basic Medicine Sciences, Jilin University, Changchun, China.
Wen-jing
WJ
Yun
Department of Pathophysiology, College of Basic Medicine Sciences, Jilin University, Changchun, China.
Ling
L
Zhang
Department of Pathophysiology, College of Basic Medicine Sciences, Jilin University, Changchun, China.
Xue-jian
XJ
Zhao
D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D002453:Cell Cycle; D045744:Cell Line, Tumor; D019938:Cyclin D1 / Q000378:metabolism; D005260:Female; D019254:Genes, bcl-2; D064593:Heterografts; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D012333:RNA, Messenger / Q000037:antagonists & inhibitors; D034741:RNA, Small Interfering / Q000494:pharmacology*; D050796:STAT3 Transcription Factor / Q000037:antagonists & inhibitors* / Q000235:genetics; D013274:Stomach Neoplasms / Q000188:drug therapy* / Q000378:metabolism; D000077022:Survivin
D000970:Antineoplastic Agents; C107489:BIRC5 protein, human; D051034:Inhibitor of Apoptosis Proteins; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D000077022:Survivin; D019938:Cyclin D1
Stat3; anti-tumour; apoptosis; gastric cancer; siRNA