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  3. FSH receptor binding inhibitor restrains follicular development and possibly attenuates carcinogenesis of ovarian cancer through down-regulating expression levels of FSHR and ERβ in normal ovarian tissues

FSH receptor binding inhibitor restrains follicular development and possibly attenuates carcinogenesis of ovarian cancer through down-regulating expression levels of FSHR and ERβ in normal ovarian tissues

  • Gene. 2018 Aug 20;668:174-181. doi: 10.1016/j.gene.2018.05.068.
Gong Zhuandi 1,  Che Tuanjie 2,  Lai Luju 3,  Ayimuguli Abdiryim 3,  Deng Yingying 4,  Liang Haoqin 3,  Wei Suocheng 5,  Ding Li 6
Affiliations

Affiliations

  • 1 Hospital of Medicine College, Northwest Minzu University, China.
  • 2 Key Laboratory of Functional Genomic and Molecular Diagnosis of Gansu Province, China.
  • 3 Life Science and Engineering College, Northwest Minzu University, China.
  • 4 Research Center of Animal Cell Engineering and Technology of Gansu Province, Northwest Minzu University, China.
  • 5 Life Science and Engineering College, Northwest Minzu University, China; Research Center of Animal Cell Engineering and Technology of Gansu Province, Northwest Minzu University, China. Electronic address: weisc668@163.com.
  • 6 Technology Center of Hunan Entry-exit Inspection and Quarantine Bureau, China. Electronic address: dingli0824@126.com.
PMID: 29783074 DOI: 10.1016/j.gene.2018.05.068
Abstract

Objectives: The current study aimed to investigate FSH Receptor binding inhibitor (FRBI) effects in the expressions of FSH Receptor (FSHR) and estrogen receptor-beta (ERβ) in the mice ovaries at the gene and protein levels, also to find the potential efficacy of FRBI on suppressing ovarian Cancer through down-regulating over-expression of FSHR and ERβ in the normal ovarian tissues.

Methods: 180 female mice were randomized into six groups (n = 30). Mice of FRBI-1, FRBI-2 and FRBI-3, FRBI-4 were intramuscularly injected with FRBI of 10, 20, 30 and 40 mg/kg, respectively, for five consecutive days. The qPCR and Western blotting were used to determine expression levels of FSHR and ERβ mRNAs and proteins in mouse ovaries.

Results: The ovarian cortex thickness (OCT) of the FRBI-4 group were less than that FSH group on day 30 (P < 0.05). The numbers of secondary follicles (SF) and the maximum transverse diameters (MTD) of secondary follicles of FRBI-3 and FRBI-4 groups were decreased as compared to FSH group (P < 0.05 or P < 0.01) by 24.11% and 27.47% on day 20 based on the control group (CG) levels. On day 15, the reductions of FSHR mRNA levels in FRBI-2, FRBI-3 and FRBI-4 were 27.78%, 29.37% and 43.65% (P < 0.05 or P < 0.01), respectively in comparison with CG. ERβ and FSHR protein levels of FRBI-treated mice were gradually decreased as compared to and CG and FSH group. ERβ protein level of FRBI-4 was less than that of CG on day 20 (P < 0.05). On days 15 and 20, estradiol (E2) concentrations of FRBI-2, FRBI-3 and FRBI-4 groups were lower than those of the CG and FSH group (P < 0.05 or P < 0.01).

Conclusions: FRBI could reduce OCT and follicle numbers. A high dose of FRBI (30 mg/kg to 40 mg/kg) could suppress ovarian and follicular development, and attenuate expression levels of ERβ and FSHR mRNAs and proteins in the ovaries, additionally inhibit E2 production. Therefore, FRBI will possibly be utilized to restrain the carcinogenesis of ovarian Cancer by down-regulating overexpression of FSHR and ERβ in the ovaries.

Keywords

Estrogen receptor; FSH receptor binding inhibitor; Follicle stimulating hormone; Mice; Ovarian cancer; Overexpression.

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