Benign Brenner tumor of the ovary: two-dimensional and contrast-enhanced ultrasound features-a retrospective study from a single center.

Objective: Benign Brenner tumor (BBT) is a rare ovarian tumor, and there are few discrete reports about its manifestation in an ultrasound. This study sought to investigate the two-dimensional (2D) and contrast-enhanced ultrasound (CEUS) features of this entity. Methods: This is a retrospective single-center study. The clinical manifestations, laboratory examination, and ultrasound data of 25 female patients with BBT were confirmed by pathology when they underwent 2D and/or CEUS examination at Ningbo First Hospital from January 2012 to June 2023. The ultrasound findings of the patients were analyzed using the terminology of the International Organization for the Analysis of Ovarian Tumor and were read by two senior sonographers who reached an agreement. Results: Among the all 25 patients, most of them were unilateral, and only one patient was bilateral. Thus, 26 lesions were found: 44.0% (11/25) were in the left and 52.0% (13/25) were in the right. Moreover, 53.84% (14/26) were solid lesions, 15.38% (4/26) were mixed lesions, and 26.92% (7/26) were cystic lesions. Among the solid-type patients, 42.85% (6/14) of the cases were with calcification. Upon laboratory examination, 12.0% (3/25) of the patients had high carbohydrate antigen 125 (CA-125) level, and 19.04% (4/21) of the patients had an elevated carbohydrate antigen724 (CA-724) level in the serum tumor markers. In the hormone test, 14.28% (3/21) were found to have a high postmenopausal estrogen level and 14.28%(3/21) were found to have a high level of follicle-stimulating hormone (FSH). One patient with complex manifestations and three with solid manifestations were examined by CEUS to observe the microcirculation perfusion of the tumor. One with solid and cystic separation was rapidly hyperenhanced and cleared, and the filling subsided faster than the uterus. The postoperative pathological diagnosis was benign Brenner tumor with mucinous cystadenoma. The other three cases were solid adnexal lesions, which showed isoenhancement on CEUS and disappeared slowly, synchronizing with the uterus. The CEUS results were considered as benign tumors and confirmed by pathology. Conclusions: BBT can show ovarian cystic, mixed cystic and solid type, and solid echo in 2D ultrasound. Unilateral ovarian fibrosis with punctate calcification is an important feature of BBT in 2D ultrasound. However, for solid adnexal masses and mixed cystic and solid masses with unclear diagnosis, if CEUS shows isoenhancement or hyperenhancement, the possibility of BBT cannot be excluded.

Regulatory mechanism of GPER in the invasion and migration of ectopic endometrial stromal cells in endometriosis.

Endometriosis (EMS) is a chronic inflammatory disorder of high incidence that causes serious reproductive consequences. High estrogen production is a consistently observed endocrine feature of EMS. The present study aims to probe the molecular mechanism of G protein-coupled estrogen receptor 1 (GPER) in the invasion and migration of ectopic endometrial stromal cells (Ect-ESCs) and provides a new rationale for EMS treatment. Eutopic and ectopic endometrial tissues were collected from 41 EMS patients, and primary ESCs were separated. GPER, miR-16-5p, and miR-103a-3p levels in cells and tissues were determined by qRT-PCR or Western blot assay. Cell viability, proliferation, invasion, and migration were evaluated by CCK-8, colony formation, and Transwell assays. The upstream miRNAs of GPER were predicted by databases, and dual-luciferase assay was performed to validate the binding of miR-16-5p and miR-103a-3p to GPER 3'UTR. GPER was highly expressed in EMS tissues and Ect-ESCs. Inhibition of GPER mitigated the proliferation, invasion, and migration of Ect-ESCs. GPER was regulated by miR-16-5p and miR-103a-3p. Overexpression of miR-16-5p and miR-103a-3p negatively regulated GPER expression and inhibited the invasion and migration of Ect-ESC. In conclusion, GPER promoted the invasion and migration of Ect-ESCs, which can be reversed by upstream miR-16-5p and miR-103a-3p.

Evodiamine inhibits malignant progression of ovarian cancer cells by regulating lncRNA-NEAT1/miR-152-3p/CDK19 axis.

Evodiamine (EVO) has been demonstrated to promote apoptosis of ovarian cancer cells, and upregulate miR-152-3p level in colorectal cancer. Here, we explore part of the network mechanism of EVO and miR-152-3p in ovarian cancer. The bioinformatics website, dual luciferase reporter assay, and quantitative real-time polymerase chain reaction were applied to analyze the network among EVO, lncRNA, miR-152-3p, and mRNA. The effect and mechanism of EVO on ovarian cancer cells were determined using cell counting kit-8, flow cytometry, TUNEL, Western blot, and rescue experiments. As a result, EVO dose-dependently attenuated cell viability, induced G2/M phase arrest and apoptosis, promoted miR-152-3p level (4.5- or 2-fold changes), and inhibited expressions of NEAT1 (0.225- or 0.367-fold changes), CDK8 (0.625- or 0.571-fold changes), and CDK19 (0.25- or 0.147-fold changes) in OVCAR-3 and SKOV-3 cells. In addition, EVO decreased Bcl-2 expression, but increased the expressions of Bax and c-caspase-3. NEAT1 targeted miR-152-3p which bound to CDK19. The impacts of EVO on cell viability, cycle, apoptosis, and apoptosis-related proteins were partially reversed by miR-152-3p inhibitor, NEAT1 overexpression, or CDK19 overexpression. Furthermore, miR-152-3p mimic offset the effects of NEAT1 or CDK19 overexpression. The role of NEAT1 overexpression in the biological phenotype of ovarian cancer cells was counteracted by shCDK19. In conclusion, EVO attenuates ovarian cancer cell progression via the NEAT1-miR-152-3p-CDK19 axis.

MiR-486-5p Act as a Biomarker in Endometrial Carcinoma: Promotes Cell Proliferation, Migration, Invasion by Targeting MARK1.

BACKGROUND: miRNA expression acts as a potential biomarker in many diseases including endometrial carcinoma (EC). miR-486-5p dysregulation is observed in several tumor types, but the roles of miR-486-5p in EC are hardly ever studied. OBJECTIVE: This study aimed to analyze the expression profile of miR-486-5p in tumor tissues and serum samples of patients with EC and explore the target prediction, function analysis and validation in immortal cell lines. PATIENTS AND METHODS: A total of 42 freshly paired EC tissues, the corresponding adjacent non-neoplastic tissues and serum samples were also collected from patients with EC, and 42 matched normal serum samples were included as control group. The level of miR-486-5p expression was tested by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was determined by colony formation assay and CCK-8 assay. Furthermore, functional evaluation of miR-486-5p on migration was performed by wound-healing assay and invasion was estimated by transwell invasion assay. qRT-PCR, luciferase reporter assay and Western blotting (WB) were performed to verify the targeting of MARK1 by miR-486-5p. RESULTS: miR-486-5p was significantly up-regulated in EC tissues and serum samples, promoting the proliferation, migration and invasive activities of EC cells by targeting MARK1. CONCLUSION: These data indicated miR-486-5p as a novel molecular biomarker for diagnosing and treating EC, and MARK1 might act as a critical and functional target of miR-486-5p with the implications on cell proliferation, migration and invasiveness of EC tumor cells.

Effects of CD44 and E-cadherin overexpression on the proliferation, adhesion and invasion of ovarian cancer cells.

CD44 is a prognostic indicator of shorter survival time in ovarian cancer. E-cadherin fragmentation promotes the progression of ovarian cancer. However, the effects of CD44 and E-cadherin overexpression on ovarian cancer cells have remained elusive. The present study aimed to investigate the effects of overexpression of CD44 and E-cadherin on cell proliferation, adhesion and invasion of SKOV-3 and OVCAR-3 ovarian cancer cells. Overexpression of CD44 and E-cadherin was achieved by transfecting SKOV-3 and OVCAR-3 cells with viruses carrying the CD44 or E-cadherin gene, respectively. Expression of CD44 and E-cadherin was detected by western blot analysis. The proliferation of SKOV-3 and OVCAR-3 cells was measured by a Cell Counting Kit-8 at 0, 24 and 48 h after viral transfection. The adhesion ability of SKOV-3 and OVCAR-3 cells to the endothelial layer was detected. A Transwell invasion assay was utilized to assess the invasion ability of the cells. Overexpression of CD44 and E-cadherin in SKOV-3 and OVCAR-3 cells was confirmed by western blot. Compared with the blank or negative control groups, the CD44 overexpression groups of SKOV-3 and OVCAR-3 cells exhibited an increased cell proliferation rate at 24 and 48 h, whereas overexpression of E-cadherin did not alter the proliferation of these cells. Furthermore, compared with the blank and negative control groups, the cell adhesion and invasion ability in the CD44 overexpression groups of SKOV-3 and OVCAR-3 cells was markedly higher. There were no significant differences in adhesion ability between the E-cadherin overexpression group and the blank/negative control group. Of note, overexpression of E-cadherin decreased the invasive ability of SKOV-3 and OVCAR-3 cells. In conclusion, Overexpression of CD44 increased the proliferation, adhesion and invasion of ovarian cancer cells, while overexpression of E-cadherin decreased the invasion of ovarian cancer cells.