We recently demonstrated that Cav1 (caveolin-1) is a negative regulator of Stat3 (signal transducer and activator of transcription-3) activity in mouse fibroblasts and human lung carcinoma SHP77 cells. We now examined whether the cellular context may affect their levels as well as the relationship between them, by assessing Cav1 and Stat3-ptyr705 amounts in different cell lines. In MDA-MB-231, A549, and HaCat cells, Cav1 levels were high and Stat3-ptyr705 levels were low, consistent with the notion of a negative effect of endogenous Cav1 on Stat3-ptyr705 levels in these lines. In addition, manipulation of Cav1 levels revealed a negative effect in MCF7 and mouse fibroblast cells, while Cav1 upregulation induced apoptosis in MCF7 cells. In contrast, however, line MRC9 had high Cav1 and high Stat3-ptyr705 levels, indicating that high Cav1 is insufficient to reduce Stat3-ptyr705 levels in this line. MCF7 and LuCi6 cells had very low Cav1 and Stat3-ptyr705 levels, indicating that the low Stat3-ptyr705 can be independent from Cav1 levels altogether. Our results reveal a further level of complexity in the relationship between Cav1 and Stat3-ptyr705 than previously thought. In addition, we demonstrate that in a feedback loop, Stat3 inhibition upregulates Cav1 in HeLa cells but not in other lines tested.

中文翻译：

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Caveolin-1对乳腺癌和肺癌细胞中Stat3-ptyr705水平的影响。

我们最近证明，Cav1（caveolin-1）是小鼠成纤维细胞和人肺癌SHP77细胞中Stat3（信号转导和转录激活因子）活性的负调节剂。现在，我们通过评估不同细胞系中的Cav1和Stat3-ptyr705量来检查细胞环境是否会影响它们的水平以及它们之间的关系。在MDA-MB-231，A549和HaCat细胞中，Cav1水平较高而Stat3-ptyr705水平较低，这与这些细胞系中内源性Cav1对Stat3-ptyr705水平产生负面影响的观念一致。此外，Cav1水平的操纵揭示了MCF7和小鼠成纤维细胞的负面影响，而Cav1的上调诱导了MCF7细胞的凋亡。相反，MRC9品系的Cav1和Stat3-ptyr705含量较高，表示高Cav1不足以降低该谱线中的Stat3-ptyr705水平。MCF7和LuCi6细胞的Cav1和Stat3-ptyr705水平非常低，表明Stat3-ptyr705的低水平可能完全独立于Cav1水平。我们的结果表明，Cav1和Stat3-ptyr705之间的关系比以前想象的要复杂得多。此外，我们证明了在反馈回路中，Stat3抑制可在HeLa细胞中上调Cav1，但在其他受测细胞系中则不会。