FRBI suppresses carcinogenesis of uterine cancers by regulating expressions of FHIT, PTEN and ARID1A

Abstract

ObjectiveIn order to seek out the novel diagnostic and prognostic biomarker of uterine cancer, the present study aimed to determine whether FSH receptor binding inhibitor (FRBI) impact the uterine tissue levels of FHIT, PTEN, ARID1A, estrogen receptor- beta (ERβ) and FSH receptor (FSHR) that are associated with tumorigenesis of uterine cancer. Methods150 prepuberty mice were randomized into four FRBI treatment groups and a control group (CG). Mice in FRBI-1, FRBI-2, FRBI-3, and FRBI-4 groups were intramuscularly injected with 10, 20, 30 and 40 mg/kg FRBI, respectively, for five consecutive days. Serum contents and expression levels in uterine tissues were determined using Elisa kit, qPCR and Western blotting, respectively. ResultsFHIT mRNA levels of FRBI-3 and FRBI-4 groups were greater than that in CG on days 20 and 30 (P < 0.05 or P < 0.01). On day 30, expression levels of FHIT proteins in four FRBI groups were increased by 28.03 %, 69.82 %, 118.33 % and 99.46 %, respectively as compared to CG. Serum contents of FHIT, PTEN and ARID1A had positive correlations with uterine expressions of FHIT, PTEN and ARID1A proteins, respectively. ConclusionsFRBI treatment could promote the production of FHIT and ARID1A, and also accelerate expression levels of FHIT proteins and mRNA in mice uterine tissues. These results provided potential biomarker for diagnosing uterine cancer.