Knockdown of HSF1 inhibits invasion, metastasis, and proliferation of endometrial carcinoma cells while promoting apoptosis
Background
Heat shock factor 1 (
HSF1
), the principal transcriptional regulator of cellular stress responses, has been exhibited to play a role in the progression of various human cancer types. However, the function of
HSF1
in endometrial cancer (EC) has not yet been evaluated.
Objective
This study examined the expression and role of
HSF1
in EC.
Methods
Immunohistochemistry was performed to explore HSF1 level in 135 endometrial tissue specimens. The relationship between HSF1 level and EC patients’ clinicopathological characteristics was analyzed. Quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and Western blotting were employed to explore HSF1 expression level in tissues
in vitro
. Small interfering RNA (siRNA) was employed to suppress
HSF1
expression level. The invasion and migration capacities were evaluated using transwell and wound healing assays. Cell cycle arrest and apoptosis were assessed by flow cytometric analysis.
Results
EC tissues exhibited higher HSF1 expression level compared with normal endometrial and atypical endometrial hyperplasia tissues. High HSF1 expression level was associated with histological grade, muscular invasion, lymph node metastasis, and estrogen receptor (ER) expression level in EC tissues and cells. Kaplan–Meier analysis indicated that EC patients with elevated
HSF1
expression level had poorer overall survival. Knockdown of
HSF1
in EC cells resulted in cell cycle arrest, increased apoptosis, and inhibited EC cell proliferation, invasion, and migration.
Conclusion
The results demonstrated that
HSF1
could function as an oncogene in EC.
HSF1
could play a notable role in EC progression.
HSF1
may be a potential molecular target for both the treatment and prognosis of patients with EC.
