Wu Q, Chen Z, Su W
State Laboratory for Tumor Cell Engineering, Xiamen University, Fujian 361005, China.
Chin Med J (Engl). 2000 Nov;113(11):972-6.
To determine the mechanism of all-trans retinoic acid (ATRA) on growth inhibition in human gastric cancer cells.
Gastric cancer cell lines: MGC80-3, BGC-823, SGC-7901 and MKN-45. CAT assay, Northern blot, Western blot, gene transfection and MTT assay.
ATRA can inhibit the activator protein-1 (AP-1) activity in ATRA-sensitive cell lines, but not in ATRA-resistant cell line, and the anti-AP-1 activity of ATRA is mediated by its receptor, retinoic acid receptor alpha (RAR alpha). ATRA can also inhibit the expression of cJun and cFos. One of the mechanisms for ATRA to inhibit the growth of gastric cancer cells may be through its inhibitory effect on the AP-1 activity and its influence on up-regulation of RAR alpha expression. The inhibition of cJun and cFos expressions by ATRA may also contribute to the anti-AP-1 activity.
ATRA inhibits the growth of gastric cancer cells through the regulation of AP-1 activity. This action is mediated by RAR alpha.
确定全反式维甲酸（ATRA）对人胃癌细胞生长抑制的机制。
胃癌细胞系：MGC80 - 3、BGC - 823、SGC - 7901和MKN - 45。采用CAT检测、Northern印迹、Western印迹、基因转染和MTT检测。
ATRA能抑制对ATRA敏感的细胞系中的激活蛋白-1（AP - 1）活性，但对ATRA耐药的细胞系无此作用，且ATRA的抗AP - 1活性由其受体维甲酸受体α（RARα）介导。ATRA还能抑制cJun和cFos的表达。ATRA抑制胃癌细胞生长的机制之一可能是通过其对AP - 1活性的抑制作用及其对RARα表达上调的影响。ATRA对cJun和cFos表达的抑制也可能有助于其抗AP - 1活性。
ATRA通过调节AP - 1活性抑制胃癌细胞生长。这一作用由RARα介导。
