All-trans retinoic acid decreases susceptibility of a gastric cancer cell line to lymphokine-activated killer cytotoxicity.

All-trans retinoic acid decreases susceptibility of a gastric cancer cell line to lymphokine-activated killer cytotoxicity.
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全反式视黄酸降低胃癌细胞系对淋巴因子激活的杀伤细胞毒性的敏感性。

DOI:
--
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发表时间:
1997
影响因子:
8.8
通讯作者:
TM Chu
TM Chu
中科院分区:
医学1区
文献类型:
--
作者:
TY Chao;SY Jiang;RY Shyu;MY Yeh;TM Chu

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全反式维甲酸(RA)先前被证明可以调节来源于SC-M1细胞系的胃癌细胞的生长。本研究旨在探讨维甲酸对SC-M1细胞对淋巴因子激活的杀伤细胞(LAK)敏感性的影响。在0.001-10微米的浓度范围内,RA以剂量依赖的方式诱导SC-M1细胞对LAK活性产生抵抗。动力学研究表明,SC-M1细胞与RA共培养2天后抵抗力显著增加,培养6天后达到最大。在另外两种癌细胞株:早幼粒细胞白血病HL-60和肝癌Hep 3B中也得到了类似的结果。结合实验表明,RA不改变靶细胞SC-M1与效应性LAK细胞的结合效率。流式细胞仪分析显示,RA对细胞表面分子的表达无明显影响,包括HLAI类和II类抗原、细胞间黏附分子-1和-2、淋巴细胞功能抗原-3。细胞周期分析显示,RA作用于SC-M1细胞后,细胞周期G0/G1期增加,S期减少,Northern印迹分析显示细胞周期蛋白A和B1mRNA表达下降。此外,维甲酸可促进SC-M1细胞维甲酸受体α(RARα)的表达,而对RARβ或RARGamma的表达无影响。综上所述,上述结果表明,维甲酸可通过细胞周期调节机制,通过细胞抑制作用显著增强胃癌细胞SC-M1抵抗LAK细胞毒的能力。流行的想法,如减少效应器与靶细胞的结合,减少MHC I类抗原的表达或改变RARbeta的表达,都没有涉及到。
All-trans retinoic acid (RA) was previously shown to regulate the growth of gastric cancer cells derived from the cell line SC-M1. This study was designed to investigate the effect of RA on the sensitivity of SC-M1 cells to lymphokine-activated killer (LAK) activity. RA at the concentration range of 0.001-10 microM was shown to induce SC-M1 cells to exhibit resistance to LAK activity in a dose-dependent manner. A kinetics study indicated that a significantly increased resistance was detected after 2 days of co-culturing SC-M1 cells with RA and reached a maximum after 6 days of culture. Similar results were obtained from two other cancer cell lines: promyelocytic leukaemia HL-60 and hepatic cancer Hep 3B. A binding assay demonstrated that the binding efficacy between target SC-M1 cells and effector LAK cells was not altered by RA. Flow cytometric analyses revealed that RA exhibited no effect on the expression of cell surface molecules, including HLA class I and class II antigens, intercellular adhesion molecule-1 and -2, and lymphocyte function antigen-3. Cell cycle analysis revealed that culture of SC-M1 cells with RA resulted in an increase in G0/G1 phase and a decrease in S phase, accompanied by a decrease in cyclin A and cyclin B1 mRNA as determined by Northern blot analysis. Additionally, RA was shown to enhance the expression of retinoic acid receptor alpha (RAR alpha) in SC-M1 cells, and to have no effect on the expression of RARbeta or RARgamma. Taken together, these results indicate that RA can significantly increase gastric cancer cells SC-M1 to resist LAK cytotoxicity by means of a cytostatic effect through a mechanism relating to cell cycle regulation. The prevailing ideas, such as a decrease in effector to target cell binding, a reduced MHC class I antigen expression or an altered RARbeta expression, are not involved.
人乳腺癌细胞系 MCF-7 的他莫昔芬敏感和耐药亚系对视黄酸的反应。
DOI: --
发表时间: 1992
期刊: Cancer research
影响因子: 11.2
作者:
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通过干扰素-γ 间接抑制脾细胞培养物中鼠淋巴因子激活的杀伤细胞活性的产生。
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发表时间: 1990
期刊: Immunology
影响因子: 6.4
作者:
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DOI: --
发表时间: 1995-09
期刊: The American journal of pathology
影响因子: --
作者:
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DOI: 10.4049/jimmunol.145.10.3194
发表时间: 1990-11
影响因子: 4.4
作者:
Michael J. Robertson;Michael A. Caligiuri;Thomas J. Manley;H. Levine;Jerome Ritz
通讯作者: Michael J. Robertson;Michael A. Caligiuri;Thomas J. Manley;H. Levine;Jerome Ritz
视黄酸 (RA) 对人头颈鳞状细胞癌细胞系中鳞状细胞分化、细胞 RA 结合蛋白和核 RA 受体的调节。
DOI: --
发表时间: 1994
期刊: Cancer research
影响因子: 11.2
作者:
Zou,CP;Clifford,JL;Xu,XC;Sacks,PG;Chambon,P;Hong,WK;Lotan,R
通讯作者: Lotan,R