首页> 中文期刊> 《中国临床医学》 >信号转导转录激活因子3抑制剂WP1066对肝细胞肝癌生物学特性影响的研究

信号转导转录激活因子3抑制剂WP1066对肝细胞肝癌生物学特性影响的研究

         

摘要

To explore the effects of an inhibitor of signal transducer and activator of transcription 3 (STAT3), WP1066, on the proliferation and invasion of hepatocellular carcinoma (HCC) cells in vitro and in vivo. Methods: The expression level and phosphorylation level of STAT3 in HCC cell lines with different malignant potential were detected by Western blotting and Transwell method. The antitumor activities of WP1066 and related mechanisms were studied in HCC cell line MH-CC-97H and also in a subcutaneous HCC model in nude mice. Results; STAT3 phosphorylation level was significantly higher in HCC cell lines with higher malignant potential. WP1066 significantly inhibited cell proliferation and invasion in MHCC-97H. WP1066 also significantly inhibited the growth of tumor in nude mice HCC model. Conclusions: WP 1066 can suppress the proliferation and invasion of HCC through inhibition of the phosphorylation level of STAT3.%目的:探讨信号转导转录激活因子3(signal transducer and activator of transcription 3,STAT3)的抑制剂WP1066在体外对人肝细胞肝癌(hepatocellular carcinoma,HCC)增殖、侵袭能力的影响以及在体内应用时对HCC的抑制效果.方法:采用蛋白印迹、Transwell等方法检测在不同恶性潜能的人HCC细胞株中STAT3总蛋白及磷酸化水平的差异,观察应用WP1066后人HCC细胞株MHCC-97H的增殖以及侵袭能力的改变.皮下接种MHCC-97H细胞株建立裸鼠的HCC模型后,观察WP1066对肿瘤生长的影响.结果:STAT3磷酸化水平在恶性潜能高的人HCC细胞株中显著高于恶性潜能低的HCC细胞株;WP1066能显著抑制MHCC-97H的增殖和侵袭.在裸鼠HCC模型中,WP1066能有效地抑制HCC生长.结论:WP1066能抑制STAT3磷酸化水平而有效抑制HCC增殖和侵袭.

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