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Tumor necrosis factor and interleukin-1 cause a rapid and transient stimulation of c-fos and c-myc mRNA levels in human fibroblasts.肿瘤坏死因子和白细胞介素-1可引起人成纤维细胞中c-fos和c-myc mRNA水平的快速短暂刺激。
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Tumor necrosis factor induces phosphorylation of a 28-kDa mRNA cap-binding protein in human cervical carcinoma cells.肿瘤坏死因子可诱导人宫颈癌细胞中一种28 kDa的mRNA帽结合蛋白发生磷酸化。
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肿瘤坏死因子-α可诱导肿瘤坏死因子敏感细胞系中蛋白激酶C的易位。

Tumour necrosis factor-alpha induces translocation of protein kinase C in tumour necrosis factor-sensitive cell lines.

作者信息

Matsubara N, Fuchimoto S, Orita K

机构信息

First Department of Surgery, Okayama University Medical School, Japan.

出版信息

Immunology. 1991 Aug;73(4):457-9.

PMID:1916896
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1384576/
Abstract

In this study we investigated whether the anti-proliferative effect of tumour necrosis factor-alpha (TNF-alpha) was associated with the activation of protein kinase C (PKC), using PANC-1 cells (TNF-alpha sensitive) and LoVo cells (TNF-alpha resistant). In combination with 12-0-tetradecanoylphorbol-13-acetate (TPA), a potent activator of PKC, TNF-alpha caused marked inhibition of the growth of LoVo cells. Inhibition of PANC-1 cell growth by TNF-alpha was blocked by pretreatment with TPA for 24 hr, along with down-regulation of PKC activity. Intracellular translocation of PKC from cytosol to membrane was induced by TNF-alpha treatment in PANC-1 cells but not in LoVo cells.

摘要

在本研究中，我们使用PANC-1细胞（对肿瘤坏死因子-α敏感）和LoVo细胞（对肿瘤坏死因子-α耐药），研究肿瘤坏死因子-α（TNF-α）的抗增殖作用是否与蛋白激酶C（PKC）的激活有关。与PKC的强效激活剂12-0-十四烷酰佛波醇-13-乙酸酯（TPA）联合使用时，TNF-α可显著抑制LoVo细胞的生长。用TPA预处理24小时可阻断TNF-α对PANC-1细胞生长的抑制作用，同时PKC活性下调。TNF-α处理可诱导PANC-1细胞中PKC从胞质溶胶向细胞膜的细胞内转位，但在LoVo细胞中则不会。