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Abstract
Experiments were conducted to determine if the follicle-stimulating hormone (FSH) receptor binding inhibitor (FRBI) impacts the expression levels of AT-rich interactive domain-containing protein 1A (ARID1A) and phosphatase and tensin homolog (PTEN) in ovaries and blood, as well as expressions of follicle-stimulating hormone cognate receptor (FSHR) gene and proteins. Mice in FRBI-10, FRBI-20, FRBI-30, and FRBI-40 groups were intramuscularly injected with 10, 20, 30, and 40 mg FRBI/kg, respectively, for five consecutive days. Western blotting and qRT-PCR were utilized to determine expression levels of ARID1A and PTEN proteins and mRNAs. Serum ARID1A and PTEN concentrations of the FRBI-40 group were higher than the control group (CG) and FSH group (P<0.05). FSHR mRNA levels of FRBI-20, FRBI-30, and FRBI-40 groups were lower than that of CG and FSH groups on day 15 (P<0.05 or P<0.01). Expression levels of FSHR proteins of FRBI-30 and FRBI-40 groups were lower than those of CG and FSH groups (P<0.05). Levels of ARID1A and PTEN proteins of the FRBI-30 group were greater than CG on days 20 and 30 (P<0.05). FRBI doses had significant positive correlations to levels of ARID1A and PTEN proteins. Additionally, ARID1A and PTEN had negative correlations to FSHR mRNAs and proteins. A high dose of FRBI could promote the expression levels of ARID1A and PTEN proteins in ovarian tissues. FRBI increased serum concentrations of ARID1A and PTEN. However, FRBI depressed expression levels of FSHR mRNAs and proteins in mouse ovaries.
Highlights
Diagnosis of ovarian cancers is a critical factor in improving the survival rate of patients
The present study aimed to evaluate the effects of FRBI on the levels of AT-rich interactive domain-containing protein 1A (ARID1A) and phosphatase and tensin homolog (PTEN) genes in ovarian tissues and blood, to determine the regulating effects of FRBI on expressions of follicle-stimulating hormone cognate receptor (FSHR) genes and proteins as well as phosphorylation of FSHR in the ovarian tissues
ARID1A and PTEN proteins (Figure 1A), indicating that they were expressed in mice ovaries at the different levels
Summary
Diagnosis of ovarian cancers is a critical factor in improving the survival rate of patients. The pathogenesis of ovarian cancer is closely related to ARID1A (AT-rich interactive domain-containing protein 1A), which is present in up to 57% of patients [2] and acts as a tumor suppressor in various cancers [3]. Loss of ARID1A expression has been associated with a shorter progression-free survival [5]. Dysfunction of ARID1A can lead to abnormal chromatin remodeling, resulting in the carcinogenesis of ovarian and gynecologic cancers. Earlier studies reported that ARID1A mRNA expression was lower in endometriosis tissues than that in normal endometrial tissues. Low expression levels of ARID1A gene may contribute to the tumor’s tendency to transform malignantly [6]. The comprehensive study of ARID1A gene can provide a basis for earlier diagnosis and effective molecular target therapy [7]
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