热休克因子1是一个强大多方位的致癌调节物

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Heat Shock Factor 1 Is a Powerful Multifaceted Modifier of Carcinogenesis
Heat shock factor 1 (HSF1) is the master regulator of the heat shock response in eukaryotes, a very highly conserved protective mechanism. 热休克因子1（HSF-1）在真核生物中是主要的热休克反应调节物，热休克反应是一个高度保守的保护机制。
HSF1 function increases survival under a great many pathophysiological conditions. 在许多病理生理条件下，HSF-1的功能增加了（个体）存活。
How it might be involved in malignancy remains largely unexplored. 在恶性肿瘤中它可能是如何起作用这个问题至今仍未有大量研究。
We report that eliminating HSF1 protects mice from tumors induced by mutations of the RAS oncogene or a hot spot mutation in the tumor suppressor p53. 我们报道去除HSF-1可以防止小鼠发生由癌基因RAS突变或者抑癌基因p53热点突变诱发的肿瘤。
In cell culture, HSF1 supports malignant transformation by orchestrating a network of core cellular functions including proliferation, survival, protein synthesis, and glucose metabolism. 在细胞培养中，HSF-1通过精细调节细胞核心功能包括增殖，存活，蛋白合成和葡萄糖代谢的网络促进恶性转化。
The striking effects of HSF1 on oncogenic transformation are not limited to mouse systems or tumor initiation; human cancer lines of diverse origins show much greater dependence on HSF1 function to maintain proliferation and survival than their nontransformed counterparts. 在致癌性转化中HSF-1最显著的作用是不仅局限于小鼠或者肿瘤的起始阶段；多种不同起源的人类肿瘤细胞系要比未转化的对应的细胞更加依赖HSF-1的功能以维持增殖和存活。
While it enhances organismal survival and longevity under most circumstances, HSF1 has the opposite effect in supporting the lethal phenomenon of cancer. 尽管在大多数情况下HSF-1可以增加生物体的存活和生存时间，它有支持癌的致命现象的反作用。

在早期发育阶段，母体来源的HSF-1所起的关键作用提示了HSF-1缺陷可能是造成受精后异常的一个原因，这种异常与哺乳动物的不育有关,人类也不例外