目的觀察肝細(xì)胞生長(zhǎng)因子/離散因子(HGF/SF)在姜黃素誘導(dǎo)的大腸癌細(xì)胞凋亡中的作用。
方法采用MTT法分析姜黃素對(duì)大腸癌細(xì)胞的抑制作用; 流式細(xì)胞術(shù)評(píng)價(jià)HGF抗凋亡作用。
結(jié)果不同濃度姜黃素作用Caco-2細(xì)胞后發(fā)現(xiàn),只在64 μg/ml濃度發(fā)揮作用,即抑制細(xì)胞增殖; 而同時(shí)加入不同濃度的HGF后可以拮抗姜黃素引起的Caco-2細(xì)胞生長(zhǎng)的抑制作用,但HGF發(fā)揮作用無(wú)濃度依賴關(guān)系。流式細(xì)胞術(shù)檢測(cè)結(jié)果發(fā)現(xiàn),姜黃素只在64 μg/ml濃度下誘導(dǎo)Caco-2細(xì)胞凋亡,在加入不同濃度HGF后,凋亡明顯減少,但并無(wú)劑量依賴關(guān)系。MAPK途徑在HGF拮抗姜黃素誘導(dǎo)的Caco-2細(xì)胞凋亡中的作用發(fā)現(xiàn),阻斷p42/p44 MAPK和p38 MAPK后,并不影響HGF對(duì)Caco-2細(xì)胞凋亡的保護(hù)作用。
結(jié)論HGF拮抗姜黃素誘導(dǎo)的Caco-2細(xì)胞凋亡,MAPK信號(hào)傳導(dǎo)途徑可能不參與此過(guò)程。
引用本文: 李宏武,單吉賢. HGF/SF對(duì)姜黃素誘導(dǎo)大腸癌細(xì)胞凋亡的作用. 中國(guó)普外基礎(chǔ)與臨床雜志, 2006, 13(1): 74-76. doi: 復(fù)制
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- 1. Montesano R, Matsumoto K, Nakamura T, et al. Identification of a fibroblastderived epithelial morphogen as hepatocyte growth factor [J]. Cell, 1991; 67(5)∶901.
- 2. Nakamura T, Nishizawa T, Hagiya M, et al. Molecular cloning and expression of human hepatocyte growth factor [J]. Nature, 1989; 342(6248)∶440.
- 3. Rubin JS, Bottaro DP, Aaronson SA. Hepatocyte growth factor/scatter factor and its receptor, the cmet protooncogene product [J]. Biochim Biophys Acta, 1993; 1155(3)∶357.
- 4. Stoker M, Gherardi E, Perryman M, et al. Scatter factor is a fibroblastderived modulator of epithelial cell mobility [J]. Nature, 1987; 327(6119)∶239.
- 5. Jeffers M, Rong S, Vande Woude GF. Enhanced tumorigenicity and invasionmetastasis by hepatocyte growth factor/scatter factormet signalling in human cells concomitant with induction of the urokinase proteolysis network [J]. Mol Cell Biol, 1996; 16(3)∶1115.
- 6. Weidner KM, Di Cesare S, Sachs M, et al. Interaction between Gab1 and the cMet receptor tyrosine kinase is responsible for epithelial morphogenesis [J]. Nature, 1996; 384(6605)∶173.
- 7. Kosai K, Matsumoto K, Nagata S, et al. Abrogation of Fasinduced fulminant hepatic failure in mice by hepatocyte growth factor [J]. Biochem Biophys Res Commun, 1998; 244(3)∶683.
- 8. Huang TS, Lee SC, Lin JK. Suppression of cJun/AP1 activation by an inhibitor of tumor promotion in mouse fibroblast cells [J]. Proc Natl Acad Sci USA, 1991; 88(12)∶5292.
- 9. Samaha HS, Kelloff GJ, Steele V, et al. Modulation of apoptosis by sulindac, curcumin, phenylethyl3methylcaffeate, and 6phenylhexyl isothiocyanate: apoptotic index as a biomarker in colon cancer chemoprevention and promotion [J]. Cancer Res, 1997; 57(7)∶1301.
- 10. Huang MT, Lou YR, Xie JG, et al. Effect of dietary curcumin and dibenzoylmethane on formation of 7,12dimethylbenz [a] anthraceneinduced mammary tumors and lymphomas/leukemias in Sencar mice [J]. Carcinogenesis, 1998; 19(9)∶1697.
- 11. Chen H, Zhang ZS, Zhang YL, et al. Curcumin inhibits cell proliferation by interfering with the cell cycle and inducing apoptosis in colon carcinoma cells [J]. Anticancer Res, 1999; 19(5A)∶3675.
- 12. Moragoda L, Jaszewski R, Majumdar AP. Curcumin induced modulation of cell cycle and apoptosis in gastric and colon cancer cells [J]. Anticancer Res, 2001; 21(2A)∶873.
- 13. Ishiki Y, Ohnishi H, Muto Y, et al. Direct evidence that hepatocyte growth factor is a hepatotrophic factor for liver regeneration and has a potent antihepatitis effect in vivo [J]. Hepatology, 1992; 16(5)∶1227.
- 14. Xiao GH, Jeffers M, Bellacosa A, et al. Antiapoptotic signaling by hepatocyte growth factor/Met via the phosphatidylinositol 3kinase/Akt and mitogenactivated protein kinase pathways [J]. Proc Natl Acad Sci USA, 2001; 98(1)∶247.