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Fos表达可诱导致瘤性神经视网膜细胞生长停滞。

Fos expression induces growth arrest in tumorigenic neuroretina cells.

作者信息

Garrido C, Plaza S, Gospodarowicz D, Saule S

机构信息

Cancer Research Institute, University of California, Medical Center, San Francisco 94143-0128.

出版信息

Oncogene. 1993 Oct;8(10):2713-9.

PMID:8397368
Abstract

E26-infected chicken neuroretina (CNR) cells expressing P135gag-myb-ets are non-transformed and growth can be stimulated by basic fibroblast growth factor (bFGF). In contrast, MHE226-infected CNR cells, which express p61/63myc in addition to the P135gag-myb-ets of E26, are transformed, tumorigenic cells and are growth inhibited by bFGF. We looked for differences in both cells types which could help to understand the molecular basis of the bFGF response. We found marked differences in c-fos expression. In MHE226-CNR cells c-fos mRNA was induced by 12-O-tetradecanoyl phorbol 13-acetate (TPA) and bFGF, both inhibitors of MHE226-infected cell growth. In contrast, serum, a strong growth inducer, did not stimulate c-fos expression. In E26-infected cells all of these factors induced cell growth and c-fos expression. MHE226-CNR cells superinfected with v-fosFBJ-expressing retrovirus were inhibited in their growth and unresponsive to bFGF. Introduction of v-fosFBJ in E26 CNR cells transformed them but they remained sensitive to bFGF. These results suggest that fos is involved in the induced growth arrest of MHE226-CNR cells.

摘要

表达P135gag-myb-ets的E26感染的鸡神经视网膜(CNR)细胞未发生转化,碱性成纤维细胞生长因子(bFGF)可刺激其生长。相比之下,MHE226感染的CNR细胞除了表达E26的P135gag-myb-ets外,还表达p61/63myc,这些细胞是已转化的致瘤细胞,bFGF可抑制其生长。我们寻找这两种细胞类型之间的差异,以帮助理解bFGF反应的分子基础。我们发现c-fos表达存在显著差异。在MHE226-CNR细胞中,12-O-十四酰佛波醇-13-乙酸酯(TPA)和bFGF均可诱导c-fos mRNA表达,而这两种物质都是MHE226感染细胞生长的抑制剂。相比之下,作为强生长诱导剂的血清并未刺激c-fos表达。在E26感染的细胞中,所有这些因子均可诱导细胞生长和c-fos表达。用表达v-fosFBJ的逆转录病毒超感染的MHE226-CNR细胞生长受到抑制,且对bFGF无反应。将v-fosFBJ导入E26 CNR细胞可使其发生转化,但它们对bFGF仍敏感。这些结果表明,fos参与了MHE226-CNR细胞的诱导性生长停滞。

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