Müllerian inhibiting substance/anti-Müllerian
hormone (MIS/AMH) is a regulator of the female reproductive system, an
indicator of ovarian reserve and a
growth inhibitor of Müllerian duct-derived
tumors in vivo and in vitro. The objective of the present study was to analyze MIS/AMH type II
receptor (MIS/AMHRII)
protein and
mRNA expression in healthy human endometria compared with patients with
endometrial hyperplasia and
endometrial cancer, providing a foundation for MIS/AMH as a
biological modifier for treatment of
endometrial hyperplasia and
endometrial cancer. The present study included healthy endometrial tissues (n=20),
simple endometrial hyperplasia tissues without atypia (n=17),
complex endometrial hyperplasia tissues without atypia (n=24) and
endometrial cancer tissues (n=8). The location and variation of MIS/AMHRII
protein expression was observed by immunohistochemistry. The expression was graded by two pathologists and was categorized as follows: Negative, weakly positive, moderately positive or strongly positive. Reverse transcription-quantitative polymerase chain reaction was used to quantify MIS/AMHRII
mRNA expression. The expression of MIS/AMHRII
protein was observed in the cytoplasm of healthy human endometria,
endometrial hyperplasia and
endometrial cancer cells. The frequency of MIS/AMHRII
protein expression was 20.22±10.35% in the proliferative phase of the healthy endometrium and 24.09±11.73% in the secretory phase of the healthy endometrium. However, no differences were observed in the menstrual cycle phases. The frequency was 54.50±16.59% in
endometrial hyperplasia without atypia, 55.10±15.87% in
endometrial hyperplasia with atypia and 73.88±15.70% in
endometrial cancer, indicating that expression was enhanced as the disease progressed from healthy to malignant status. In
endometrial hyperplasia, MIS/AMHRII
protein expression was significantly associated with histological complexity compared with atypia status. The present study demonstrated that MIS/AMHRII is present in healthy endometria,
endometrial hyperplasia and
endometrial cancer. The low expression frequency of MIS/AMHRII was not significantly different among normal endometrial tissues, however, the
protein expression was elevated in
endometrial hyperplasia and
endometrial cancer. These findings indicated that the study of bioactive MIS/AMH, as a possible treatment for
tumors expressing the MIS/
AMH receptor, is essential.