Retraction Notice to: lncRNA PVT1/MicroRNA-17-5p/PTEN Axis Regulates Secretion of E2 and P4, Proliferation, and Apoptosis of Ovarian Granulosa Cells in PCOS.

[This retracts the article DOI: 10.1016/j.omtn.2020.02.007.].

lncRNA PVT1/MicroRNA-17-5p/PTEN Axis Regulates Secretion of E2 and P4, Proliferation, and Apoptosis of Ovarian Granulosa Cells in PCOS.

Recently, the roles of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) were identified in polycystic ovary syndrome (PCOS). In the present study, we investigated the role of the lncRNA PVT1/miR-17-5p/PTEN axis in PCOS ovarian granulosa cells. Expression of PVT1, miR-17-5p and PTEN in PCOS ovarian granulosa cells and follicular fluid was detected, and homeostatic model assessment of insulin resistance (HOMA-IR) and the levels of fasting plasma glucose (FPG), fasting insulin (FINS), and sex hormones were assessed. Then, the proliferation, apoptosis, and colony formation ability of ovarian granulosa cells were evaluated. The binding relationship between PVT1 and miR-17-5p as well as the target relationship between miR-17-5p and PTEN were determined by bioinformatics analysis, luciferase activity assay, RNA-induced silencing complex assay, and RNA pull-down assay. The levels of sex hormone-binding globulin and follicle-stimulating hormone were abated and the levels of luteinizing hormone, testosterone, FINS, FPG, and HOMA-IR were increased in PCOS serum. PVT1 and PTEN were overexpressed and miR-17-5p was reduced in PCOS ovarian granulosa cells and follicular fluid. Overexpressed miR-17-5p and inhibited PVT1 could decelerate apoptosis while accelerating colony formation ability and proliferation of ovarian granulosa cells in PCOS. Moreover, overexpression of PVT1 and reduced miR-17-5p could reverse these results. There existed target relation among PVT1, miR-17-5p, and PTEN, and PVT1 could inhibit miR-17-5p, thereby elevating PTEN. Our study suggests that inhibited PVT1 and overexpressed miR-17-5p result in downregulation of PTEN and promotion of cell proliferation, as well as inhibition of apoptosis of ovarian granulosa cells in PCOS.

LncRNA LOXL1-AS1 promotes endometrial cancer progression by sponging miR-28-5p to upregulate RAP1B expression.

BACKGROUND: Increasing lncRNAs are found to be involved in the biological process of multiple cancer types. Herein, we aimed to reveal the role of LOXL1-AS1 in endometrial cancer (EC) progression. METHODS: Tumor and corresponding normal tissues were obtained from EC patients. Si-LOXL1-AS1 and miR-28-5p inhibitor were transfected to downregulate the expressions of LOXL1-AS1 and miR-28-5p, while miR-28-5p mimics were used to upregulate the miR-28-5p expression. CCK-8 and colony assays were applied to estimate the cell proliferation. Flow cytometry was performed to measure the cell apoptosis. Wound healing and transwell assays were conducted to assess the cell migration and invasion abilities. Informatics analysis was used to explore the relationship among LOXL1-AS1, miR-28-5p and RAP1B. RESULTS: LOXL1-AS1 was found markedly up-regulated in EC tissues and cell lines. LOXL1-AS1 knockdown displayed evident suppression in cell proliferation, migration and invasion, as well as promotion in cell apoptosis. Moreover, the LOXL1-AS1 induced regulatory effects on EC cells were partially reversed by miR-28-5p inhibitor. Mechanistically, LOXL1-AS1 competitively bond to miR-28-5p, resulting in upregulation of RAP1B. Additionally, in vivo study confirmed the findings discovered in vitro. CONCLUSIONS: In summary, LOXL1-AS1 exerted oncogenic roles in EC progression by sponging miR-28-5p and thereby upregulating RAP1B. This finding might provide potential targets for EC therapy.

Role of interleukin-10 polymorphisms and haplotypes in polycystic ovary syndrome risk.

Polycystic ovary syndrome (PCOS) is one of the most frequently encountered endocrine malfunctions. The etiology of PCOS is complex and unclear. We aimed to investigate the role of three common SNPs (rs1800896, rs1800871 and rs1800872) of IL-10 in the development of PCOS in a Chinese population. We recruited 360 patients with PCOS and 360 healthy controls in this study. SNP genotyping of IL-10 rs1800896, rs1800871 and rs1800872 was implemented in a 384-well plate format on the Sequenom MassARRAY® System (Sequenom, San Diego, USA). Individuals carrying the GG genotype of rs1800872 were associated with an increased risk of PCOS when compared with the AA genotype (OR = 3.04, 95% CI = 1.62-5.69). No linkage disequilibrium was observed among IL-10 rs1800896, rs1800871 and rs1800872. The C-T-A (OR = 1.53, 95% CI = 1.05-2.35) haplotype indicated an increased risk of PCOS, while the A-C-G (OR = 0.72, 95% CI = 0.53-0.98) showed a reduced risk of PCOS. In summary, this study firstly estimates the association between IL-10 polymorphisms and haplotype and PCOS risk in the Chinese population.