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SF/HGF-c-Met自分泌和旁分泌促进肝细胞癌转移。

SF/HGF-c-Met autocrine and paracrine promote metastasis of hepatocellular carcinoma.

作者信息

Xie Q, Liu K D, Hu M Y, Zhou K

机构信息

Experimental Research Center of Zhongshan Hospital, Fudan University, Shanghai, 200032, China.

出版信息

World J Gastroenterol. 2001 Dec;7(6):816-20. doi: 10.3748/wjg.v7.i6.816.

DOI:10.3748/wjg.v7.i6.816
PMID:11854908
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4695601/
Abstract

AIM

To explore the role of SF/HGF-Met autocrine and paracrine in metastasis of hepatocellular carcinoma (HCC).

METHODS

SF/HGF and c-met transcription and protein expression in HCC were examined by RT-PCR and Western Blot in 4 HCC cell lines, including HepG2, Hep3B, SMMC7721 and MHCC-1, the last cell line had a higher potential of metastasis. sf/hgf cDNA was transfected by the method of Lipofectin into SMMC7721. SF/HGF and c-met antibody were used to stimulate and block SF/HGF-c-met signal transduction. Cell morphology, mobility, and proliferation were respectively compared by microscopic observation, wound healing assay and cell growth curve.

RESULTS

HCC malignancy appeared to be relative to its met-SF/HGF expression. In MHCC-1, c-met expression was much stronger than that in other cell lines with lower potential of metastasis and only SF/HGF autocrine existed in MHCC-1. After sf/hgf cDNA transfection or conditioned medium of MHCC-1 stimulation, SMMC7721 changed into elongated morphology, and the abilities of proliferation (P < 0.05) and mobility increased. Such bio-activity could be blocked by c-met antibody (P < 0.05).

CONCLUSION

The system of SF/HGF-c-met autocrine and paracrine played an important role in development and metastasis potential of HCC. Inhibition of SF/HGF-c-met signal transduction system may reduce the growth and metastasis of HCC.

摘要

目的

探讨SF/HGF-Met自分泌和旁分泌在肝细胞癌(HCC)转移中的作用。

方法

采用RT-PCR和Western Blot检测4种肝癌细胞系(包括HepG2、Hep3B、SMMC7721和MHCC-1,最后一种细胞系具有较高的转移潜能)中SF/HGF和c-met的转录及蛋白表达。采用脂质体转染法将sf/hgf cDNA转染至SMMC7721。使用SF/HGF和c-met抗体刺激和阻断SF/HGF-c-met信号转导。通过显微镜观察、伤口愈合试验和细胞生长曲线分别比较细胞形态、迁移能力和增殖能力。

结果

肝癌的恶性程度似乎与其met-SF/HGF表达相关。在MHCC-1中,c-met表达比其他转移潜能较低的细胞系强得多,且MHCC-1中仅存在SF/HGF自分泌。sf/hgf cDNA转染或MHCC-第1条件培养基刺激后,SMMC7721细胞形态变为细长型,增殖能力(P<0.05)和迁移能力增强。这种生物活性可被c-met抗体阻断(P<0.05)。

结论

SF/HGF-c-met自分泌和旁分泌系统在肝癌的发生发展和转移潜能中起重要作用。抑制SF/HGF-c-met信号转导系统可能会降低肝癌的生长和转移。

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Hepatocyte growth factor/scatter factor-induced activation of MEK and PI3K signal pathways contributes to expression of proangiogenic cytokines interleukin-8 and vascular endothelial growth factor in head and neck squamous cell carcinoma.肝细胞生长因子/分散因子诱导的MEK和PI3K信号通路激活有助于头颈部鳞状细胞癌中促血管生成细胞因子白细胞介素-8和血管内皮生长因子的表达。
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