RHPN2 Promotes Malignant Cell Behaviours in Ovarian Cancer by Activating STAT3 Signalling.

BACKGROUND: Ovarian cancer is the fifth most common cause of cancer-related deaths and accounts for 3% of cancer cases occurring in women. Therefore, determining the underlying genes that can promote ovarian cancer progression is of great urgency. It has been reported that RHPN2 promotes tumour progression in various types of cancer, but its role in ovarian cancer pathogenesis remains unknown. MATERIALS AND METHODS: In this study, bioinformatic datasets were used to predict the expression of RHPN2 in clinical samples and determine the relationship between RHPN2 and the prognosis of ovarian cancer patients. Clinical samples were used to verify the prediction. RHPN2-targeting shRNA was used to investigate the effect of RHPN2 on ovarian cancer cells, and following RHPN2 knockdown, the proliferative and migratory capacities of ovarian cancer cells were tested. To determine the downstream signalling target of RHPN2, a luciferase reporter assay was conducted, and an animal experiment was carried out to confirm the effect of RHPN2 in vivo. RESULTS: The public datasets indicated that ovarian cancer tissues showed significantly higher RHPN2 expression than para-cancer normal tissues, and poor prognosis was observed in patients with higher RHPN2 expression, which was further confirmed in clinical samples. After RHPN2 was knocked down, the proliferation and migration of ovarian cancer cells were significantly impaired; a luciferase reporter assay indicated that the STAT3 signalling pathway was the most highly affected, and RHPN2 downregulation inhibited STAT3 nuclear translocation. STAT3 inhibitors partially rescued the tumour-promoting effect induced by RHPN2 overexpression, which was further confirmed by animal experiments. CONCLUSION: Collectively, our results indicate that RHPN2 promotes malignant behaviours in ovarian cancer by activating STAT3 signalling.

Loop electrosurgical excision procedure followed by 5-aminolevulinic acid photodynamic therapy for cervical intraepithelial neoplasia, a report of six cases.

BACKGROUND: Cervical intraepithelial neoplasia (CIN) may progress to cervical cancer if left untreated. The loop electrosurgical excision procedure (LEEP) of the transitional zone of the cervix is a standard form of treatment. However, human papillomavirus (HPV)-induced CIN may recur after LEEP. The purpose of this case report is to describe the successful use of 5-aminolevulinic acid photodynamic therapy (ALA-PDT) as an adjunct to LEEP, in preventing the recurrence of CIN. METHODS: The effectiveness of this combined treatment was evaluated in six women. The diagnosis of HPV-induced CIN was determined using HPV DNA tests and liquid-based cervical cytology. Lesion removal was performed 3 h after application of ALA using a 635 nm light density of 80 mw/cm2. RESULTS: We treated 6 women aged 31-62 years who had persistent CIN following LEEP, with ALA-PDT (range, 4-7 treatments). Five of the 6 women were HPV negative on retesting 6-7 months after ALA-PDT. Most patients showed no signs of recurrence during the follow-up period. CONCLUSIONS: Use of ALA-PDT following LEEP may prevent the recurrence of CIN. Monitoring HPV status by means of DNA testing and liquid-based cytology may be used as a standard for clinical diagnosis and treatment. Post-treatment care should be carefully considered because improper post-treatment care might directly lead to relapse.

Insufficient peroxiredoxin-2 expression in uterine NK cells obtained from a murine model of abortion.

The CBA/J × DBA/2 mouse mating combination is prone to spontaneous embryo loss, in contrast to the MHC-identical CBA/J × BALB/c mating combination, which yields successful pregnancies. The underlying mechanisms for these observations are unclear. In this study, multi-vision immunohistochemical staining (IHC), flow cytometry and Western blot analysis were used to detect peroxiredoxin-2 (PRX-2) expression in the uterine natural killer (uNK) cells from CBA/J × DBA/2 and CBA/J × BALB/c mice. In IHC analysis, co-localization of PRX-2 and lectin from Dolichos biflorus agglutinin (DBA-lectin) was confirmed and the frequency of PRX-2(+) DBA-lectin(+) cells was significantly lower in CBA/J × DBA/2 than CBA/J × BALB/c. In flow cytometry and Western blotting, PRX-2 was found expressed at a significantly lower level in CBA/J × DBA/2 mice. PRX-2 inhibition with a neutralizing antibody significantly decreased PRX-2 expression, increased the cytotoxicity of uNK cells, and increased the percentage of embryo loss in CBA/J × DBA/2J mice. Our data suggest that PRX-2 may be involved in the modulation of maternal-fetal tolerance and that insufficient expression of this protein may correlate with increased embryo loss in CBA/J × DBA/2J mice.

Increased prevalence of T helper 17 (Th17) cells in peripheral blood and decidua in unexplained recurrent spontaneous abortion patients.

T helper 17 (Th17) cells and regulatory T (Treg) cells are two distinct subsets of CD4(+) T cells which have opposite effects on inflammation, autoimmunity and immunological rejection of foreign tissue. Treg cells have been shown to be important in maintaining materno-fetal tolerance, but the role of Th17 cells in human pregnancy and pathological pregnancy, especially in relation to unexplained recurrent spontaneous abortion (RSA), has not been investigated. In this study, we showed that the proportion of Th17 cells in the peripheral blood and decidua was significantly higher in unexplained RSA patients compared to normal, early pregnant women. Meanwhile, there was an inverse relationship between Th17 cells and Treg cells in the peripheral blood lymphocytes (PBL) and decidua in unexplained RSA. The expression of Th17 related factors, IL-17, IL-23 and retinoid orphan nuclear receptor (RORC), in PBL and decidua in unexplained RSA patients was significantly higher than normal, early pregnant women. This study is the first to define the occurrence of Th17 cells in unexplained RSA patients and in normal, early pregnant women. We suggest that these highly pro-inflammatory cells contribute to unexplained RSA, and the balance between Th17 cells and Treg cells may be critical to pregnancy outcomes.