UBE2C-mediated Autophagy Inhibition via Ubiquitination of SIRT1 Contributes to Endometrial Cancer Progression.

Unlabelled: Recent studies have shown that autophagy plays an important role in gynecologic tumors, and ubiquitin modification of autophagy regulatory components is essential to regulate autophagic flux. In this study, we found that the ubiquitin-conjugating enzyme E2C (UBE2C) affects endometrial cancer cell apoptosis and proliferation by inhibiting autophagy. Electron microscopy observation of cell ultrastructure and experimental biochemical analysis showed that endometrial cancer cells with UBE2C expression knocked down display typical autophagic characteristics.

A universal and specific RNA biosensor via DNA circuit-mediated PAM-independent CRISPR/Cas12a and PolyA-rolling circle amplification.

Point of care testing (POCT) has important clinical significance for the diagnosis and prognosis evaluation of diseases. At present, the biosensor based on CRISPR/Cas12a has become a powerful diagnostic tool due to its high sensitivity. However, CRISPR/Cas12a requires PAM sequence to recognize target double strand and only can recognize specific sequence, so it is not universal.

Gene signature and prognostic value of ubiquitination-related genes in endometrial cancer.

Protein ubiquitination is closely related to tumor occurrence and development. The specific role of ubiquitination in endometrial cancer remains largely unclear. Therefore, we constructed a novel endometrial cancer prognostic model based on ubiquitination-related genes.

KIF4A promotes genomic stability and progression of endometrial cancer through regulation of TPX2 protein degradation.

Kinesin family member 4A (KIF4A) belongs to the kinesin superfamily proteins, which are closely associated with mitophagy. Nonetheless, the role of KIF4A in endometrial cancer (EC) remains poorly characterized. The present study showed that KIF4A not only was upregulated but also predicted poor prognosis in patients with EC.

CircRAPGEF5 interacts with RBFOX2 to confer ferroptosis resistance by modulating alternative splicing of TFRC in endometrial cancer.

Endometrial cancer (EC) is one of the most common gynecological cancers. Ferroptosis is a newly identified form of cell death characterized by iron-dependent lipid peroxide accumulation. Circular RNAs (circRNAs) have emerged as critical regulators for cancer development.

Regulation of Transcription Factor YAP-TEAD by Non-coding RNA LINC00857 and the Inhibitory Effects on Ovarian Cancer Cell Proliferation.

This study was aimed to explore the expression and mechanism of the transcription factor YAP-TEAD in the Hippo signaling pathway under the regulation of non-coding Ribonucleic Acid (RNA) LINC00857 in the proliferation of ovarian cancer cells, so as to provide a scientific research basis for clinical diagnosis and treatment of ovarian cancer. In the study, the ovarian cancer cell lines (BT 549) were rolled into a control group (normal culture-defined as BT549/NC) and a response group (transfected with non-coding RNA LINC00857 cultured cells-defined as BT 549YAP cells). The expression and proliferation ability of the transcription factor YAP-TEAD in the two groups of cancer cells were analyzed and compared.

Single-cell sequencing reveals the heterogeneity and intratumoral crosstalk in human endometrial cancer.

Background: Endometrial cancer (EC) is one of the most common gynecologic malignancies with increasing morbidity. Cell-cell and cell-matrix interactions within the tumour microenvironment (TME) exert a powerful influence over the progression of EC. Therefore, a comprehensive exploration of heterogeneity and intratumoral crosstalk is essential to elucidate the mechanisms driving EC progression and develop novel therapeutic approaches.

Human papillomavirus prevalence and genotype distribution landscapes in Shannan City, Tibet Tibetan Autonomous Region, China.

Background: Data regarding human papillomavirus (HPV) prevalence and genotype distribution are limited in Shannan City, Tibet Tibetan Autonomous Region, China. The purpose of this study is to provide reliable data for guiding women in Shannan City in cervical cancer screening and HPV vaccine innoculation.

Methods: HPV testing was performed on women aged 16-109 years (mean age 44.

Development and Validation of a Novel Prognostic Model for Endometrial Cancer Based on Clinical Characteristics.

Objective: Existing prognostic models for endometrial cancer are short of facility and effective validation. In this study, we aim to develop and validate a novel prognostic model for endometrial cancer based on clinical characteristics.

Methods: The clinical data such as age, BMI (body mass index), FIGO stage, surgical approach, myometrial invasion, grade, lymph node metastasis, pathology and menopause status were collected for constructing and validating the prognostic model from The Cancer Genome Atlas (TCGA) and Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, respectively.

N6-Methyladenosine-Related Long Noncoding RNAs as Potential Prognosis Biomarkers for Endometrial Cancer.

Purpose: Endometrial cancer (EC) is a common gynaecologic malignancy with an increasing incidence rate and mortality in recent years. N6-methylandenosine (m6A)-related long noncoding RNA (lncRNA) plays a vital role in EC, emerging as one of the most abundant RNA modifications.

Materials And Methods: The Cancer Genome Atlas (TCGA) database and UCSC Xena were used to download data related to EC.

KIF2C Is a Novel Prognostic Biomarker and Correlated with Immune Infiltration in Endometrial Cancer.

Endometrial cancer (EC) is commonly diagnosed cancer in women, and the prognosis of advanced types of EC is extremely poor. Kinesin family member 2C (KIF2C) has been reported as an oncogene in cancers. However, its pathophysiological roles and the correlation with tumor-infiltrating lymphocytes in EC remain unclear.

LncRNA LINC00857 regulates the progression and glycolysis in ovarian cancer by modulating the Hippo signaling pathway.

Ovarian cancer is one of the most common gynecological cancers with high morbidity and mortality, which seriously endangers women's health and quality of life. Long noncoding RNAs (lncRNAs) can regulate the progression of cancers, including ovarian cancer. LINC00857 (long intergenic non-protein coding RNA 857) has been discovered to be a crucial factor in the regulation of cancer development.

Protein kinase CK2 participates in estrogen-mediated endothelial progenitor cell homing to endometriotic lesions through stromal cells in a stromal cell-derived factor-1- CXCR4-dependent manner.

Objective: To explore the possible mechanism of protein kinase CK2, which participates in estrogen recruitment of endothelial progenitor cells (EPCs), and its role in the angiogenesis of endometriosis lesions.

Design: Laboratory study.

Setting: University.

NLRP3 inflammasome activation by estrogen promotes the progression of human endometrial cancer.

Background: Activation of NLPR3 inflammasome is associated with the development and progression of some types of malignant tumors, but its role in endometrial cancer is unclear. This study aimed to investigate the expression and function of NLRP3 inflammasome in endometrial cancer.

Materials And Methods:  The expression levels of NLRP3, its inflammasome components and estrogen receptor β in endometrial cancer and paired non-tumor tissues were detected.

Knockdown of long non-coding HOTAIR enhances the sensitivity to progesterone in endometrial cancer by epigenetic regulation of progesterone receptor isoform B.

Purpose: Progesterone, particularly medroxyprogesterone acetate (MPA) has been mainly used for young endometrial carcinoma (EC) patients with conservative treatment. However, its treatment benefits are limited by insensitivity or acquired resistance. In this study, we aim to investigate the effect of long non-coding RNA HOTAIR on progesterone sensitivity in endometrial cancer, as well as the underlying mechanisms.

Estrogen‑related receptor γ promotes the migration and metastasis of endometrial cancer cells by targeting S100A4.

S100 calcium binding protein A4 (S100A4) is a well‑established tumor metastasis mediator in various malignancies, including endometrial cancer (EC). However, the regulatory mechanism underlying S100A4 expression remains elusive. In the present study, by analyzing public datasets and clinical samples, we found that estrogen‑related receptor γ (ERRγ) was upregulated and positively correlated with S100A4 transcription in EC.

The suppressive role of calcium sensing receptor in endometrial cancer.

Studies have shown that calcium sensing receptor (CaSR) is involved in the progressions of several human cancers. However, the role of CaSR in endometrial cancer remains unknown. This study provides a preliminary analysis of the CaSR effect on endometrial cancer development.

S100A4 promotes endometrial cancer progress through epithelial-mesenchymal transition regulation.

Epithelial-mesenchymal transition (EMT) is a major cause of endometrial cancer (EC) to initiate invasion and metastasis. S100A4, a calcium-binding protein, is implicated in multistage of tumorigenesis and tumor progression. The correlation between S100A4 and EMT in EC is still unclear.

Luminal epithelium in endometrial fragments affects their vascularization, growth and morphological development into endometriosis-like lesions in mice.

In endometriosis research, endometriosis-like lesions are usually induced in rodents by transplantation of isolated endometrial tissue fragments to ectopic sites. In the present study, we investigated whether this approach is affected by the cellular composition of the grafts. For this purpose, endometrial tissue fragments covered with luminal epithelium (LE(+)) and without luminal epithelium (LE(-)) were transplanted from transgenic green-fluorescent-protein-positive (GFP(+)) donor mice into the dorsal skinfold chamber of GFP(-) wild-type recipient animals to analyze their vascularization, growth and morphology by means of repetitive intravital fluorescence microscopy, histology and immunohistochemistry during a 14-day observation period.

Vascular disrupting effects of combretastatin A4 phosphate on murine endometriotic lesions.

Objective: To study the effect of combretastatin A4 phosphate (CA4P) on the vascularization of endometriotic lesions.

Design: Intravital microscopic, histologic, and immunohistochemical study.

Setting: University institute.

Inhibition of angiogenesis: a novel antitumor mechanism of the herbal compound arctigenin.

Arctigenin, a functional ingredient of several traditional Chinese herbs, has been reported to have potential antitumor activity. However, its mechanisms of action are still not well elucidated. Because the establishment and metastatic spread of tumors is crucially dependent on angiogenesis, here we investigated whether arctigenin inhibits tumor growth by disturbing blood vessel formation.

Protein kinase CK2 is a regulator of angiogenesis in endometriotic lesions.

Endometriosis is a frequent gynecological disease, which is crucially dependent on the process of angiogenesis. However, the underlying regulatory mechanisms of blood vessel development are still poorly understood. CK2 is a pleiotropic protein kinase, which is implicated in the regulation of various cellular processes including angiogenesis.

Ovarian cancer-associated fibroblasts contribute to epithelial ovarian carcinoma metastasis by promoting angiogenesis, lymphangiogenesis and tumor cell invasion.

Cancer-associated fibroblasts (CAFs) are thought to play an essential role in cancer initiation and development. However, little research has been done to evaluate the role of CAFs in epithelial ovarian cancer (EOC) development. To address this issue, ninety-one specimens were immunostained with α-smooth muscle actin (α-SMA) and fibroblast activation protein (FAP) antibodies to quantify CAFs, and antibodies D2-40 and CD34 to evaluate the lymphatic vessel density (LVD) and microvessel density (MVD) of the lesions.

Elevated vascular endothelia growth factor-A in the serum and peritoneal fluid of patients with endometriosis.

There has been emergence of evidence suggesting that specific variants of the vascular endothelia growth factor (VEGF) family, based on their ability to regulate angiogenesis, would be pivotal in the pathogenesis of endometriosis. This study was aimed at determining whether high levels of VEGF-A could be found in the serum and peritoneal fluid (PF) of patients with endometriosis. VEGF-A levels were measured by enzyme-linked immunosorbent assay (ELISA) in serum and PF from 46 patients with surgically confirmed endometriosis, and 40 controls with no clinical evidence of the disease or detectable endometriotic lesions at the time of surgical examination.