Rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid.
Rodent fibroblast model for studies of response of malignant cells to exogenous 5-aminolevulinic acid.
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DOI：
10.1038/sj.bjc.6690409
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发表时间：
1999-05
影响因子：
8.8
通讯作者：
Kennedy, JC
中科院分区：
文献类型：
--
作者：
Li, G;Szewczuk, MR;Raptis, L;Johnson, JG;Weagle, GE;Pottier, RH;Kennedy, JC
关键词：
当暴露于外源5-氨基乙酰丙酸（ALA）时，所有有核哺乳动物细胞都会合成原卟啉IX （PpIX）。标准条件下对外源ALA的反应（ALA表型）是每种细胞类型的特征。PpIX在恶性和癌前细胞中的积累明显多于其来源的正常细胞。我们建立了啮齿动物成纤维细胞模型来研究造成这种现象的机制。外源性ALA诱导纤维肉瘤细胞和转染癌基因c-myc、IGF-1受体、IGF-1及其受体、v-fos、v-raf、v-Ki-ras、v-abl或具有G418抗性选择的多瘤病毒中间T抗原的永活成纤维细胞中大量PpIX的积累。在原代成纤维细胞培养物、永生化成纤维细胞系和仅转染g418抗性基因的永生化成纤维细胞中积累的PpIX浓度要低得多。因此，转化细胞中ALA诱导的PpIX积累增加的机制（恶性ALA表型）似乎与恶性转化的机制密切相关。确定这种联系的性质可能会导致癌症治疗的新方法。©1999癌症研究运动
All nucleated mammalian cells synthesize protoporphyrin IX (PpIX) when exposed to exogenous 5-aminolevulinic acid (ALA). The response to exogenous ALA under standard conditions (the ALA phenotype) is characteristic for each cell type. Significantly more PpIX accumulates in malignant and premalignant cells than in the normal cells from which they were derived. A rodent fibroblast model was developed to study the mechanisms responsible for this phenomenon. Exogenous ALA induced the accumulation of substantial concentrations of PpIX in fibrosarcoma cells, and in immortalized fibroblasts transfected with the oncogene c-myc, IGF-1 receptor, IGF-1 and its receptor, v-fos, v-raf, v-Ki-ras, v-abl, or polyomavirus middle T antigen with G418 resistance selection. Much lower concentrations of PpIX accumulated in primary fibroblast cultures, in immortalized fibroblast cell lines, and in immortalized fibroblasts transfected with the G418-resistance gene only. The mechanisms responsible for the increased accumulation of ALA-induced PpIX by transformed cells (the malignant ALA phenotype) therefore appear to be closely linked to the mechanisms responsible for malignant transformation. Identification of the nature of that linkage may lead to new approaches to cancer therapy. © 1999 Cancer Research Campaign
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DOI：
10.1016/1011-1344(90)85083-9
发表时间：
1990-06-01
影响因子：
5.4
作者：
KENNEDY, JC;POTTIER, RH;PROSS, DC
通讯作者：
PROSS, DC
影响因子：
5.3
作者：
RAPTIS, L;LAMFROM, H;BENJAMIN, TL
通讯作者：
BENJAMIN, TL
影响因子：
64.8
作者：
LAND, H;PARADA, LF;WEINBERG, RA
通讯作者：
WEINBERG, RA
DOI：
10.1111/j.1749-6632.1992.tb21058.x
发表时间：
1992-10-28
期刊：
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES-SERIES
影响因子：
--
作者：
BASERGA, R;REISS, K;SURMACZ, E
通讯作者：
SURMACZ, E
影响因子：
3.3
作者：
Campbell, DL;Fisher, ME;Kennedy, JC
通讯作者：
Kennedy, JC