Targeting heat shock transcription factor 1 for novel hyperthermia therapy (review)

Abstract

Hyperthermia (HT) has shown promising antitumor effects against various types of malignant tumors, and its pleiotropic effects support its combined use with radiotherapy and/or chemotherapy. However, HT is rendered less effective by the acquisition of thermoresistance in tumors, which arises through the elevation of heat shock proteins (HSPs) or other tumor responses. In mammals, the induction of HSPs is principally regulated at the transcriptional level by the activation of heat shock transcription factor 1 (HSF1). This transactivator has been shown to be abundantly expressed in a wide variety of tumors in humans. In addition, HSF1 participates in the initiation, proliferation and maintenance of tumors. Of note, HSF1 silencing has been shown to prevent the progression of tumors and to enhance their sensitivity to HT. Here, we review the physiological and pathological roles of HSF1 in cancer cells, and discuss its potential as a therapeutic target for HT therapy.