HSF1 promotes endometriosis development and glycolysis by up-regulating PFKFB3 expression
- Reprod Biol Endocrinol. 2021 Jun 9;19(1):86. doi: 10.1186/s12958-021-00770-9.
- 1. Department of Reproductive Medicine, Affiliated Hospital of Weifang Medical University, Weifang, Shandong Province, People's Republic of China.
- 2. Department of Reproductive Medicine, Affiliated Hospital of Weifang Medical University, Weifang, Shandong Province, People's Republic of China. [email protected].
- 3. Department of Reproductive Medicine, Affiliated Hospital of Weifang Medical University, Weifang, Shandong Province, People's Republic of China. [email protected].
Background: 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.
Methods: We 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.
Results: Our 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.
Conclusions: Findings indicate that HSF1 plays an important role in endometriosis development, which might become a new target for the treatment of endometriosis.
Electronic supplementary material: Supplementary data are available.