| 侯新垓,刘 长,阮祥信.STAT3小分子化合物LLL-HS-1抑制人肺癌A549细胞增殖的研究[J].肿瘤学杂志,2016,22(7):565-568. |
| STAT3小分子化合物LLL-HS-1抑制人肺癌A549细胞增殖的研究 |
| Study on the Inhibition of Small Molecule Compound of STAT3 LLL-HS-1 on Proliferation of Human Lung Cancer Cells A549 |
| 投稿时间：2015-07-13 |
| DOI：10.11735/j.issn.1671-170X.2016.07.B008 |
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| 中文关键词: 信号转导与转录因子3 裸鼠 肺肿瘤 LLL-HS-1 |
| 英文关键词:signal transduction and transcription factor 3 nude mice lung neoplasms LLL-HS-1 |
| 基金项目:武汉市重点攻关计划（201161038347） |
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| 中文摘要: |
| 摘 要：［目的］探讨信号转导与转录因子3(STAT3)在肺癌细胞中的表达，并观察以其为靶点的化合物LLL-HS-1腹腔给药对肿瘤的抑制作用。［方法］ 皮下接种A549细胞成瘤1周后，15只小鼠随机3组，以低剂量（10mg/kg）和高剂量（20mg/kg）LLL-HS-1腹腔给药，对照组接受安慰剂。采用Western blot检测肺癌A549细胞蛋白中STAT3的表达及其磷酸化STAT3(p-STAT3)状态。最终以肿瘤体积大小为衡量药效学的指标。［结果］ 体外研究发现，化合物LLL-HS-1可以抑制STAT3 酪氨酸残基705 磷酸化，而且具有靶点特异性。持续3周给药，发现高和低剂量组对肿瘤的增长有明显的抑制效果，平均肿瘤体积分别为（336.8±60.5）mm3，（487.2±78.6）mm3，明显小于对照组（1989.5±214.3）mm3（F=33.8，P=0.0001；F=17.4，P=0.005）。对照组瘤重明显高于高和低剂量组，各组间比较，F=9.2，P=0.02。［结论］ 化合物LLL-HS-1对肺腺癌细胞有明显抑制作用，可能通过下调STAT3的磷酸化，诱导肿瘤细胞凋亡来实现。 |
| 英文摘要: |
| Abstract：［Objective］ To investigate the expression of the signal transduction and transcription factor 3 (STAT3) in lung cancer cells，and to study the inhibition of LLL-HS-1 intraperitoneal administertion targeting on STAT3 on proliferation of tumor. ［Methods］ After one week of subcutaneous inoculation of A549 cells in mice，15 mice were randomly divided into three groups：low-dose group (10mg/kg)，high-dose group (20mg/kg)，and control group (placebo). Protein expression of STAT3 and phosphorylated STAT3 (p-STAT3) state were detected by Western blot method. Tumor volume was analyzed as final pharmacodynamic indicator. ［Results］ The study in vitro indicated that LLL-HS-1 inhibited phosphorylation of STAT3 tyrosine residue 705 with a target-specificity. After three weeks administration，LLL-HS-1 significantly inhibited tumor growth. Average volumes in high- and low-dose groups were significantly less than those in the control group［(336.8 ± 84.5)mm3 and (487.2 ± 96.1)mm3 vs (1989.5 ± 234.3)mm3(F=33.8，P=0.0001；F=17.4，P=0.005)］. Tumor’s weight in control group was significantly higher than that in high- and low-dose group(F=9.2，P=0.02). ［Conclusion］ LLL-HS-1 might significantly inhibit lung adenocarcinoma cells，which is possibly through down-regulation of STAT3 phosphorylation，and inducement of apoptosis in cancer cells. |
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