ENHANCEMENT OF GAP JUNCTIONAL COMMUNICATION BY RETINOIDS CORRELATES WITH THEIR ABILITY TO INHIBIT NEOPLASTIC TRANSFORMATION
ENHANCEMENT OF GAP JUNCTIONAL COMMUNICATION BY RETINOIDS CORRELATES WITH THEIR ABILITY TO INHIBIT NEOPLASTIC TRANSFORMATION
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DOI：
10.1093/carcin/10.9.1743
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发表时间：
1989-09-01
期刊：
影响因子：
4.7
通讯作者：
BERTRAM, JS
中科院分区：
文献类型：
--
作者：
HOSSAIN, MZ;WILKENS, LR;BERTRAM, JS
Retinoids that cause inhibition of methylcholanthrene-induced neoplastic transformation of C3H/10T1/2 cells enhance gap-junctional communication in carcinogen-initiated cells. Dose-response studies using retinoids of diverse structures and potency demonstrated a good correlation between these two events. Junctional permeability was enhanced by retinol and tetrahydrotetramethylnaphthalenyl propenylbenzoic acid (TTNPB) at concentrations from 10-10 to 10-6 M, and by retinoic acid between 10-8 and 10-6 M, the same concentrations that inhibited neoplastic transformation. Retinoic acid inhibited permeability at 10-1 M, at which concentration transformation was enhanced. Retinoids caused similar alterations in communication in parental 10T1/2 cells. Communication between initiated and 10T1/2 cells was not influenced by TTNPB. The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibited junctional communication in initiated cells, in 10T1/2 cells and between these two cell lines. After repeated exposure of 10T1/2 cells to TPA only retinoid-enhanced communication was blocked; in contrast, basal comunication became refractory. It is proposed that much of the chemopreventive action of retinoids can be explained by the enhanced junctional communication of growth regulatory signals.
