Abstract
BackgroundEndometriosis is a chronic hormonal inflammatory disease characterized by the presence of endometrial tissue outside the uterus. Endometriosis often causes infertility, which brings physical and mental pain to patients and their families.MethodsWe examined the functions of heat shock factor 1 (HSF1) in endometriosis development through cell count assay, cell-scratch assay and clone formation experiments. We used quantitative real-time PCR (qRT-PCR) and Western blot (WB) to detect HSF1 expression. Glucose and lactate levels were determined using a glucose (GO) assay kit and a lactate assay kit. Furthermore, we used a HSF1 inhibitor-KRIBB11 to establish a mouse model of endometriosis.ResultsOur data demonstrated that HSF1 promoted endometriosis development. Interestingly, HSF1 enhanced glycolysis via up-regulating PFKFB3 expression in endometriosis cells, which was a key glycolysis enzyme. Consistently, the HSF1 inhibitor KRIBB11 could abrogate endometriosis progression in vivo and in vitro.ConclusionsFindings indicate that HSF1 plays an important role in endometriosis development, which might become a new target for the treatment of endometriosis.Electronic supplementary materialSupplementary data are available.
Highlights
Endometriosis is a chronic hormonal inflammatory disease characterized by the presence of endometrial tissue outside the uterus
Our data demonstrated that heat shock factor 1 (HSF1) promoted endometriosis development via enhancing PFKFB3 expression
We found that HSF1 overexpression significantly promoted cell proliferation in endometriosis cells (Fig. 1A)
Summary
Endometriosis is a chronic hormonal inflammatory disease characterized by the presence of endometrial tissue outside the uterus. Endometriosis often causes infertility, which brings physical and mental pain to patients and their families. Endometriosis is a disease with features of chronic inflammation, which is defined as the functional endometrial stroma and glands outside the uterine cavity [1]. There are approximately 6–10% of women of childbearing age suffering from endometriosis in the world, and the infertility rate among them is as high as 50%, seriously affecting the women health [2]. There are many stressors that can cause protein damage and induce an evolutionally conserved cytoprotective mechanism, the heat shock response (HSR), to maintain protein stability [7]. The heat shock factor 1 (HSF1) plays a central role in refolding or degrading intracellular proteins [8].
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