[Expression of suppressor of cytokine signaling-3 and caspase-3 in endometriosis and their correlation].

OBJECTIVE: To investigate the expression of suppressor of cytokine signaling(SOCS)-3 and caspase-3 and their correlative significance in endometriosis. METHODS: Immunohistochemical EnVision method was used to detect the SOCS-3 and caspase-3 protein expression in ectopic and eutopic endometrium (n = 32) of patients with endometriosis, as well as normal endometrium (n = 30) of women without endometriosis. RESULTS: SOCS-3 and caspase-3 proteins were expressed in all three groups and not affected by the menstrual cycles. The expression of SOCS-3 in ectopic endometrium (5.54 ± 2.12) was significantly lower than that in eutopic (7.39 ± 1.09, P = 0.001) and control group (7.48 ± 1.26, P < 0.01), but without difference between the eutopic and control group (P = 0.756). SOCS-3 expression in ectopic and eutopic endometrium was significantly lower in III/IV stages than that in I/II stages of endometriosis (P < 0.05). Significantly lower expression of caspase-3 protein was found in ectopic (3.20 ± 1.24) and eutopic endometrium (3.88 ± 1.93) as compared with the control group (6.49 ± 1.85, P < 0.01), however ectopic and eutopic endometrium showed no significant difference (t = 1.66, P = 0.10). There was no significant difference of the expression of caspase-3 in ectopic and eutopic endometrium at different disease stages (P > 0.05). Positive correlation was found between the expression of SOCS-3 and caspase-3 proteins in ectopic endometrium (r = 0.655, P < 0.01). CONCLUSION: SOCS-3 may be involved in the development of endometriosis through inhibition of apoptosis of ectopic endometrial cells.

[Effects of PRL-3 siRNA on the migration of endometriotic stromal cells].

OBJECTIVE: To evaluate the effects of PRL-3 siRNA (small interfering RNA) on the migration of endometriotic stromal cells. METHODS: Primary endometriotic stromal cells were cultured in vitro. Then PRL-3 (phosphatase of regenerating liver-3) siRNA was transfected to silence the PRL-3 gene. And the PRL-3 protein expression was analyzed by Western blot. The changes of cell migration were detected by cell pseudopod formation, scratch test and transwell cell migration test. RESULTS: The expression of PRL-3 protein significantly decreased in the experimental group versus two other control groups (P < 0.05). The formation of cell pseudopod was much less in experimental group than that in control groups. Within the same time, the number of migration cells was 0.87 ± 0.21 in experimental group. It was less than 1.75 ± 0.28 in blank control group and 1.63 ± 0.39 in negative control group (P < 0.05). CONCLUSION: PRL-3 siRNA can down-regulate the PRL-3 gene and decrease the migratory capacity of endometriotic stromal cells. And PRL-3 may be a promising target in the therapeutics of endometriosis.