HPV prevalence and distribution characteristics in postmenopausal women from Nanjing, China.

BACKGROUND: Cervical cancer is strongly associated with human papillomavirus (HPV) infection. In this retrospective study, we analyzed the data of postmenopausal women who were tested for HPV in Nanjing First Hospital from 2019 to 2021. METHODS: We retrospectively analyzed the data of 14,608 postmenopausal women aged 45-90 years, who underwent HPV examination in Nanjing First Hospital between January 2019 and December 2021. All participants were tested for 23 HPV genotypes. We subsequently analyzed the infection rate and evaluated the distribution of HPV using the chi-square test. RESULTS: Our results showed that the HPV infection rate in postmenopausal women in Nanjing, China was 22.36%. In terms of age group, the infection rate was 19.54%, 24.30%, 26.58%, and 14.99% in those aged ≤ 50, 51-60, 61-70, and ≥ 71 years, respectively. The most common HPV subtypes were HPV52 (22.1 3%), HPV58 (15.86%), HPV53 (14.17%), HPV16 (12.61%), and HPV81 (11.66%), in that order. The single-HPV infection rate was 14.23%, and the multiple-genotype infection rate was 8.14% (1189/14,608). CONCLUSIONS: This study showed that in Nanjing, China, the different age groups of post-menopausal women could have different rates of HPV infection, and the most common types were HPV52, HPV58, HPV53, HPV16 and HPV81. These findings highlighted the importance of understanding the epidemiology of HPV infection in specific populations, such as postmenopausal women in Nanjing, China. The results could provide valuable information for healthcare professionals and policymakers to develop targeted prevention and screening strategies for reducing the burden of HPV-related diseases in this population.

[Retracted] Upregulation of miR­183­5p is responsible for the promotion of apoptosis and inhibition of the epithelial­mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin.

Following the publication of this article, a concerned reader drew to the Editor's attention that, in Fig. 9C on p. 2478 showing the results of Transwell invasion assay experiments, unexpected areas of similarity were identified in terms of the cellular patterns revealed both within the data panels for the six different experiments portrayed in this figure, and comparing among them. After having conducted an internal investigation, the Editor of International Journal of Molecular Medicine has reached the conclusion that the overlapping sections of data shown in this figure were unlikely to have arisen by coincidence. Therefore, on the grounds of a lack of confidence in the integrity of these data, the Editor has decided that the article should be retracted from the publication. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused, and thanks the interested reader for drawing this matter to our attention. [International Journal of Molecular Medicine 42: 2469­2480, 2018; DOI: 10.3892/ijmm.2018.3853].

Clinical Performance of a Dedicated Urine-Based Assay for the Detection of Human Papillomavirus and Cervical Intraepithelial Neoplasia.

Objective: The objective of this study is to assess the clinical performance of a urine-based high-risk human papillomavirus (hrHPV) test for the detection of cervical intraepithelial neoplasia grade 2 or higher (CIN2+). Methods: Between September and December 2021, women aged 20 to 65 years referred to colposcopy clinic were prospectively recruited at three clinical centers in China. Paired urine and cervical specimens from all enrolled women were obtained for hrHPV DNA fluorescence quantitative PCR test. The results of liquid-based cytology (LBC), colposcopy and diagnostic biopsies were collected. We evaluated the sensitivity and specificity for CIN and assessed the agreement/kappa value. Results: A total of 732 women (median age, 40 years) with valid results were included in the study, and 130 (17.8%) women were histologically confirmed as CIN2+. The sensitivity of urine and cervical test for CIN2+ and CIN3+ were 87.69% and 85.45%, respectively. The specificity of urine test performed better than cervical test in women with

Immunity-and-matrix-regulatory cells enhance cartilage regeneration for meniscus injuries: a phase I dose-escalation trial.

Immunity-and-matrix-regulatory cells (IMRCs) derived from human embryonic stem cells have unique abilities in modulating immunity and regulating the extracellular matrix, which could be mass-produced with stable biological properties. Despite resemblance to mesenchymal stem cells (MSCs) in terms of self-renew and tri-lineage differentiation, the ability of IMRCs to repair the meniscus and the underlying mechanism remains undetermined. Here, we showed that IMRCs demonstrated stronger immunomodulatory and pro-regenerative potential than umbilical cord MSCs when stimulated by synovial fluid from patients with meniscus injury. Following injection into the knees of rabbits with meniscal injury, IMRCs enhanced endogenous fibrocartilage regeneration. In the dose-escalating phase I clinical trial (NCT03839238) with eighteen patients recruited, we found that intra-articular IMRCs injection in patients was safe over 12 months post-grafting. Furthermore, the effective results of magnetic resonance imaging (MRI) of meniscus repair and knee functional scores suggested that 5 × 107 cells are optimal for meniscus injury treatment. In summary, we present the first report of a phase I clinical trial using IMRCs to treat meniscus injury. Our results demonstrated that intra-articular injection of IMRCs is a safe and effective therapy by providing a permissive niche for cartilage regeneration.

Recurrent Chemotherapy Treated Indeterminate Dendritic Cell Tumor: Case Report and Literature Review.

Indeterminate dendritic cell tumor (IDCT) is an extremely uncommon histiocytic and dendritic neoplasms subtype that presents as single or multiple papules. There is currently no standard method for diagnosis and treatment, and the selection of therapeutic approaches is mainly based on successful examples of folk medicine. We describe a case of a pathology diagnosed indeterminate dendritic cell tumor, which shows the presence of CD1a, S100, and CD68, but lack langerin. She was treated with multi-chemotherapy regimens used to treat lymphoma and gained good results short term but was easy to recur. In addition, we reviewed the literature on the effectiveness and safety of chemotherapy in IDCT patients.

Systemic immune-inflammation index associated with contrast-induced nephropathy after elective percutaneous coronary intervention in a case-control study.

Elevated systemic immune-inflammation index (SII) has associated with coronary heart disease and poor clinical outcomes. However, the relationship between SII and contrast-induced nephropathy (CIN) in patients who underwent elective percutaneous coronary intervention (PCI) is still unclear. We aimed to investigate the association of SII with the development of CIN in elective PCI patients. A retrospective study with 241 participants was performed from March 2018 to July 2020. CIN was defined as any of the following: increase in serum creatinine (SCr) level by ≥0.5 mg/dl (≥44.2 mol/L) or increase in SCr to ≥25% over the baseline value within 48-72 h after PCI. The SII levels in patients with CIN ( n = 40) were significantly higher than those without. In correlation analysis, SII positively correlated to uric acid but negatively with the estimated glomerular filtration rate. Increased log2(SII) levels were independent risk factors for patients with CIN [odds ratio (OR) = 2.686; 95% confidence interval (CI), 1.457-4.953]. In the subgroup analysis, increased log2(SII) was strongly associated with the presence of CIN in male participants (OR = 3.669; 95% CI, 1.925-6.992; P < 0.05), whereas no association was found in females (OR = 1.552; 95% CI, 0.533-4.515; P > 0.05). Receiver operating characteristic analysis demonstrated that in a cutoff of 586.19, SII showed 75% sensitivity and 54.2% specificity for predicting CIN in patients undergoing elective PCI, respectively. In conclusion, elevated SII was an independent risk factor of CIN development in patients undergoing elective PCI, particularly in male people.

Prediction of the development of contrast­induced nephropathy following percutaneous coronary artery intervention by machine learning.

Contrast-induced nephropathy (CIN) is associated with increased mortality and morbidity in patients with coronary artery disease undergoing elective percutaneous coronary intervention(PCI). We developed a machine learning-based risk stratification model to predict contrast-induced nephropathy after PCI. A study retrospectively enrolling 240 patients eligible for PCI from December 2017 to May 2020 was performed. CIN was defined as a rise in serum creatinine levels ≥0.5 mg/dL or ≥25% from baseline within 72 h after surgery. Eight machine learning methods were performed based on clinical variables. Shapley Additive exPlanation values were also used to interpret the best-performing prediction models. Development of CIN was found in 37 patients(16.5%) after PCI. There were 11 significant predictors of CIN, including uric acid, peripheral vascular disease, cystatin C, creatine kinase-MB, haemoglobin, N-terminal pro-brain natriuretic peptide, age, diabetes, systemic immune-inflammatory index, total protein, and low-density lipoprotein. Regarding the efficacy of the machine learning model that accurately predicted CIN, SVM exhibited the most outstanding AUC value of 0.784. The SHAP and radar plots were used to illustrate the positive and negative effects of the 11 features attributed to the SVM. Machine learning models have the potential to identify the risk of CIN for elective PCI patients.

LncRNA H19 Contributes to Smoke-Related Chronic Obstructive Pulmonary Disease by Targeting miR-181/PDCD4 Axis.

Chronic obstructive pulmonary disease (COPD) kills more than 3 million people worldwide every year. Despite progress in the treatment of symptoms and prevention of acute exacerbations, few advances have been made to ameliorate disease progression or affect mortality. Exercise plays a positive role in the prevention and treatment of diaphragm dysfunction in COPD, and the changes in diaphragm structure and function induced by exercise are closely related to the regulation of oxidative stress. But the mechanism remains unclear. So the aim of this study was to reveal the therapeutic mechanism of exercise to COPD using both in vivo and in vitro experiments. In this study, cigarette smoke (CS) induced COPD mice model, treadmill aerobic training for COPD mice were constructed and cigarette smoke extract (CSE) induced bronchial epithelial cells (BECs) model were used for COPD study. Bioinformatics analysis, luciferase reporting analysis, and RT-qPCR detection were used to clarify the interacted relationship among lncRNA, miRNA, and mRNA. ROS, inflammatory cytokines expression, and EMT relative protein α-SMA were detected using immunofluorescence and ELISA detection. The result shows that exercise ameliorates COPD induced lung injury by inhibit ROS, inflammation, and epithelial-mesenchymal transition (EMT) relative protein α-SMA expression. RT-qPCR detection shows that lnc-H19 expression was increased in lung tissues of COPD mice. Exercise decreased COPD induced lnc-H19 expression. Downregulation lnc-H19 inhibits COPD mediated lung injury. Bioinformatics analysis and luciferase reporting analysis confirmed that miR-181 and PDCD4 were downstream targets of lnc-H19. Upregulation of PDCD4 or downregulation of miR-181 reversed the protective effect of si-lnc-H19 to BECs after exposure to CSE. In conclusion, lncRNA H19 contributes to smoke-related chronic obstructive pulmonary disease by targeting miR-181/PDCD4 Axis.

Simulated Microgravity Alters P-Glycoprotein Efflux Function and Expression via the Wnt/ß-Catenin Signaling Pathway in Rat Intestine and Brain.

The drug efflux transporter permeability glycoprotein (P-gp) plays an important role in oral drug absorption and distribution. Under microgravity (MG), the changes in P-gp efflux function may alter the efficacy of oral drugs or lead to unexpected effects. Oral drugs are currently used to protect and treat multisystem physiological damage caused by MG; whether P-gp efflux function changes under MG remains unclear. This study aimed to investigate the alteration of P-gp efflux function, expression, and potential signaling pathway in rats and cells under different simulated MG (SMG) duration. The altered P-gp efflux function was verified by the in vivo intestinal perfusion and the brain distribution of P-gp substrate drugs. Results showed that the efflux function of P-gp was inhibited in the 7 and 21 day SMG-treated rat intestine and brain and 72 h SMG-treated human colon adenocarcinoma cells and human cerebral microvascular endothelial cells. P-gp protein and gene expression levels were continually down-regulated in rat intestine and up-regulated in rat brain by SMG. P-gp expression was regulated by the Wnt/ß-catenin signaling pathway under SMG, verified by a pathway-specific agonist and inhibitor. The elevated intestinal absorption and brain distribution of acetaminophen levels also confirmed the inhibited P-gp efflux function in rat intestine and brain under SMG. This study revealed that SMG alters the efflux function of P-gp and regulates the Wnt/ß-catenin signaling pathway in the intestine and the brain. These findings may be helpful in guiding the use of P-gp substrate drugs during spaceflight.

Anti-inflammatory effect of Danhong injection through inhibition of GSDMD-mediated pyroptosis.

BACKGROUND: Pyroptosis is an inflammatory form of cell death that has been implicated in various infectious and non-infectious diseases. Gasdermin family proteins are the key executors of pyroptotic cell death, thus they are considered as novel therapeutic targets for inflammatory diseases. However, only limited gasdermin specific inhibitors have been identified to date. Traditional Chinese medicines have been applied in clinic for centuries and exhibit potential in anti-inflammation and anti-pyroptosis. We attempted to find candidate Chinese botanical drugs which specifically target gasdermin D (GSDMD) and inhibit pyroptosis. METHODS: In this study, we performed high-throughput screening using a botanical drug library to identify pyroptosis specific inhibitors. The assay was based on a cell pyroptosis model induced by lipopolysaccharides (LPS) and nigericin. Cell pyroptosis levels were then evaluated by cell cytotoxicity assay, propidium iodide (PI) staining and immunoblotting. We then overexpressed GSDMD-N in cell lines to investigate the direct inhibitory effect of the drug to GSDMD-N oligomerization. Mass spectrometry studies were applied to identify the active components of the botanical drug. Finally, a mouse model of sepsis and a mouse model of diabetic myocardial infarction were constructed to verify the protective effect of the drug in disease models of inflammation. RESULTS: High-throughput screening identified Danhong injection (DHI) as a pyroptosis inhibitor. DHI remarkably inhibited pyroptotic cell death in a murine macrophage cell line and bone marrow-derived macrophages. Molecular assays demonstrated the direct blockade of GSDMD-N oligomerization and pore formation by DHI. Mass spectrometry studies identified the major active components of DHI, and further activity assays revealed salvianolic acid E (SAE) as the most potent molecule among these components, and SAE has a strong binding affinity to mouse GSDMD Cys192. We further demonstrated the protective effects of DHI in mouse sepsis and mouse myocardial infarction with type 2 diabetes. CONCLUSION: These findings provide new insights for drug development from Chinese herbal medicine like DHI against diabetic myocardial injury and sepsis through blocking GSDMD-mediated macrophage pyroptosis.

Long-term results of synovectomy in total knee arthroplasty: a prospective, randomized controlled trial.

BACKGROUND: Synovectomy has been introduced into total knee arthroplasty (TKA) with the aim of relieving pain and inflammation of the synovium. However, there are no long-term, comparative data to evaluate the effect of synovectomy in TKA. This study was aimed at assessing pain, function, and complications in patients undergoing synovectomy during TKA for osteoarthritis (OA) at long-term follow-up. METHODS: This was a prospective randomized controlled trial of 42 consecutive patients who underwent staged bilateral TKA. Patients undergoing the first-side TKA were allocated to receive TKA with or without synovectomy followed by a 3-month washout period and crossover to the other strategy for the opposite-side TKA. The overall efficacy of both strategies was evaluated by determination of blood loss, the Knee Society score (KSS), and knee inflammation conditions during a 3-month postoperative period. The postoperative pain, range of motion (ROM), and complications were sequentially evaluated to compare the two groups until 10 years after surgery. RESULTS: At the 10-year follow-up, both groups had a similarly significantly improved ROM (114.88 ±â€Š9.84° vs. 114.02 ±â€Š9.43°, t  = 0.221, P  = 0.815) and pain relief with no differences between the two groups (1.0 [1.0] vs. 1.0 [1.5], U  = 789.500, P  = 0.613). Similar changes in total blood loss, KSS, and knee inflammation were found in both groups during 3 months postoperatively ( P  > 0.05). Additionally, there was no significant difference regarding complications and satisfaction between the two groups ( P  > 0.05). CONCLUSIONS: Synovectomy in conjunction with TKA for primary OA does not seem to provide any benefit regarding postoperative pain, ROM, and satisfaction during a 10-year follow-up. In addition, it may not result in more blood loss and increased incidence of long-term complications. Based on our long-term findings, it should not be performed routinely. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR-INR-16008245; https://www.chictr.org.cn/showproj.aspx?proj=13334 .

Wnt3a/YTHDF1 Regulated Oxaliplatin-Induced Neuropathic Pain Via TNF-α/IL-18 Expression in the Spinal Cord.

Oxaliplatin is widely used in cancer treatment, however, many patients will suffer from neuropathic pain (NP) induced by it at the same time. Therefore exploring the mechanism and founding novel target for this problem are needed. In this study, YTHDF1 showed upregulation in oxaliplatin treated mice. As m6A is known as conserved and it widely functions in numerous physiological and pathological processes. Therefore, we focused on exploring the molecular mechanism of whether and how YTHDF1 functions in NP induced by oxaliplatin. IHC and western blotting were conducted to measure proteins. Intrathecal injection for corresponding siRNAs in C57/BL6 mice or spinal microinjection for virus in YTHDF1flox/flox mice were applied to specially knockdown the expression of molecular. Von Frey, acetone test and ethyl chloride (EC) test were applied to evaluate NP behavior. YTHDF1, Wnt3a, TNF-α and IL-18 were increased in oxaliplatin treated mice, restricted the molecular mentioned above respectively can significantly attenuate oxaliplatin-induced NP, including the mechanical allodynia and cold allodynia. Silencing YTHDF1 and inhibiting Wnt3a and Wnt signaling pathways can reduce the enhancement of TNF-α and IL-18, and the decreasing of the upregulation of YTHDF1 can be found when inhibiting Wnt3a and Wnts signaling pathways in oxaliplatin treated mice. Our study indicated a novel pathway that can contribute to oxaliplatin-induced NP, the Wnt3a/YTHDF1 to cytokine pathway, which upregulating YTHDF1 functioned as the downstream of Wnt3a signal and promoted the translation of TNF-α and IL-18 in oxaliplatin treated mice.

The Role of Hypoxia-Inducible Factor-1 Alpha in Renal Disease.

Partial pressure of oxygen (pO2) in the kidney is maintained at a relatively stable level by a unique and complex functional interplay between renal blood flow, glomerular filtration rate (GFR), oxygen consumption, and arteriovenous oxygen shunting. The vulnerability of this interaction renders the kidney vulnerable to hypoxic injury, leading to different renal diseases. Hypoxia has long been recognized as an important factor in the pathogenesis of acute kidney injury (AKI), especially renal ischemia/reperfusion injury. Accumulating evidence suggests that hypoxia also plays an important role in the pathogenesis and progression of chronic kidney disease (CKD) and CKD-related complications, such as anemia, cardiovascular events, and sarcopenia. In addition, renal cancer is linked to the deregulation of hypoxia pathways. Renal cancer utilizes various molecular pathways to respond and adapt to changes in renal oxygenation. Particularly, hypoxia-inducible factor (HIF) (including HIF-1, 2, 3) has been shown to be activated in renal disease and plays a major role in the protective response to hypoxia. HIF-1 is a heterodimer that is composed of an oxygen-regulated HIF-1α subunit and a constitutively expressed HIF-1ß subunit. In renal diseases, the critical characteristic of HIF-1α is protective, but it also has a negative effect, such as in sarcopenia. This review summarizes the mechanisms of HIF-1α regulation in renal disease.

A modified xanthine oxidase cell model for screening of antihyperuricemic functional compounds.

Hyperuricemia is a purine metabolism disorder, with increasing prevalence worldwide. Here, a high throughput cell model for screening of antihyperuricemic compounds was set up. Human kidney cells (HK2 cells) were stimulated with adenosine and the resulting supernatant and lysate were then analyzed using high performance liquid chromatography (HPLC). The results showed that hypoxanthine content was increased in both HK2 cells supernatant and xanthine oxidase (XO)-overexpressing HK2 cells lysate, but no uric acid was detected due to lower endogenous XO content in these cells. Exogenous XO was added to the supernatant, and then used to evaluate the antihyperuricemic activity of Febuxostat and two the previously identified peptides, Pro-Gly-Ala-Cys-Ser-Asn (PGACSN) and Trp-Met-Leu (WML). By adding exogenous XO, this combined-adenosine-XO-induced hyperuricemia model was optimized and established, and the Febuxostat and peptides were confirmed to significantly reduce uric acid production in the HK2 cells supernatant (p < 0.05). Therefore, this cell model could be recommended for screening potential bioactive antihyperuricemic compounds.

COA3 overexpression promotes non-small cell lung cancer metastasis by reprogramming glucose metabolism.

Recent advances in cancer research have revealed a close relationship between mitochondrial dysfunction and cancer development. Human COX assembly factor 3 (COA3), also known as CCDC56, is a mitochondrial transmembrane protein responsible for cytochrome c oxidase (COX) protein complex assembly. However, the clinical implication and biological functions of COA3 remain unexplored in human cancers, including non-small cell lung cancer (NSCLC). Here, we found that COA3 is overexpressed at both mRNA and protein levels in human NSCLC cells, mainly as a result of decreased miR-338-3p level. The protein expression level of COA3 is positively associated with lymph node metastasis and predicts poor survival in patients with NSCLC. Silencing of COA3 significantly attenuated, while forced COA3 expression enhanced the migration and invasiveness of NSCLC cells. Mechanistically, we found that aerobic glycolysis, induced at least in part by dynamic-related protein 1 (DRP1) phosphorylation-mediated mitochondrial fragmentation, contributed to COA3-promoted NSCLC metastasis. Together, our study illustrates that COA3 plays a crucial role in NSCLC carcinogenesis, implying COA3 as a prognostic marker and treatment target in NSCLC.

Integrated bioinformatics data analysis reveals a risk signature and PKD1 induced progression in endometrial cancer patients with postmenopausal status.

BACKGROUND: Endometrial cancer (EC) is one of the most common type of female genital malignancies. The purpose of the present study was to reveal the underlying oncogene and mechanism that played a pivotal role in postmenopausal EC patients. METHODS: Weighted gene co-expression network analysis (WGCNA) was conducted using the microarray dataset and clinical data of EC patients from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to identify significant gene modules and hub genes associated with postmenopausal status in EC patients. LASSO regression was conducted to build and validate the risk model. Finally, expression of hub gene was validated in pre- and post-menopausal EC patients in our center. RESULTS: 1240 common genes were used to construct the WGCNA model. According to the WGCNA results, we identified a brown module with 471 genes which was significantly associated with postmenopausal status in EC patients. Furthermore, we constructed an 11-gene risk signature to predict the overall survival of EC patients. The Kaplan-Meier curve and area under the ROC curve (AUC) of this model showed high accuracy in prediction. We also validate the risk model in patients in our center and it also has a high accuracy. Among the 11 genes, PKD1 was recognized as a potential biomarker in the progression of EC patients with postmenopausal status. CONCLUSION: Taken together, we uncovered a common PKD1-mediated mechanism underlying postmenopausal EC patients' progression by integrated analyses. This finding may improve targeted therapy for EC patients.

Osteoporosis in COPD patients: Risk factors and pulmonary rehabilitation.

OBJECTIVES: To present a review on the pathogenesis, risk factor and treatment of chronic obstructive pulmonary disease complicated with osteoporosis and provide new ideas for the diagnosis and treatment. DATA SOURCE: A systematic search is carried out using keywords as chronic obstructive pulmonary disease, osteoporosis, risk factors, and pulmonary rehabilitation. RESULTS: Patients with chronic obstructive pulmonary disease have a high prevalence of osteoporosis and a high risk of fracture. The mechanisms of osteoporosis in COPD patients are associated with general risk factors, such as smoking, reduced physical activity, low weight, and disease-specific risk factors, such as systemic inflammatory, Vitamin D deficiency, use of glucocorticoid, anemia, hypoxemia, and hypercapnia. The treatment of osteoporosis in COPD emphasizes comprehensive intervention, which mainly include basic treatment and anti-osteoporosis drugs. Noticeably, pulmonary rehabilitation program is an important part of treatment. CONCLUSIONS: This work summarizes the pathogenesis, risk factor, prevention, and treatment of chronic obstructive pulmonary disease complicated with osteoporosis, and the latest progress of studies on chronic obstructive pulmonary disease and osteoporosis is discussed.

Superior cervical ganglionectomy alters gut microbiota in rats.

The diversity and complexity of sympathetic function highlight the importance of fundamental research. Little is known about the interaction of superior cervical sympathetic ganglion (SCG) and gut microbiota. In this study, the engagement of the sympathetic ganglia with gut microbiota was investigated. Bilateral superior cervical ganglionectomy (SCGx) significantly altered the microbiota composition in rats 14 days post-surgery, and these microbiotas may participate in several biological pathways in the host, suggesting the vital role of the cervical sympathetic ganglion in regulating the microbiome-brain axis, and further confirming that the sympathetic nervous system (SNS) regulates the microbiome-brain axis.

CircRNA hsa_circ_0018289 exerts an oncogenic role in cervical cancer progression through miR-1294/ICMT axis.

BACKGROUND: circRNA hsa_circ_0018289-mediated growth and metastasis of CC cells were investigated, as well as the mechanistic pathway. METHODS: Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) was carried out to examine the expression of hsa_circ_0018289, microRNA (miR)-1294, and isoprenylcysteine carboxyl methyltransferase (ICMT). CC cell proliferation, migration, and invasion were evaluated by 5-ethynyl-2'-deoxyuridine (EdU) incorporation, colony formation, transwell assays, Western blot analysis of ICMT, and glycolysis-associated proteins. Dual-luciferase reporter or RNA pull-down analysis of the target interaction between miR-1294 and hsa_hsa_circ_0018289 or ICMT. Xenograft model assay was implemented to assess the role of hsa_circ_0018289 in vivo. Immunofluorescence (IHC) was employed to detect the level of Ki-67. RESULTS: Hsa_circ_0018289 was elevated in CC tissues and cells, its deficiency could repress growth, metastasis, and glycolysis of CC cells in vitro, as well as hamper tumor growth in vivo. Hsa_circ_0018289 sponged miR-1294 while miR-1294 bound with ICMT, and the inhibition of miR-1294 or addition of ICMT could partially relieve the effect caused by hsa_circ_0018289 depletion. CONCLUSION: Hsa_circ_0018289 contributes to malignant development by regulating the miR-1294/ICMT axis, affording novel insight into CC therapy.

Detection of Parental Contribution to Molar Genome Leads to Diagnosis of Recurrent Hydatidiform Mole in a Family with NLRP7 Variants.

Introduction: Genetically, complete hydatidiform mole (CHM) is androgenetic diploid, containing two sets of paternal chromosomes. In most cases, recurrent HM (RHM) is CHM but has diploid biparental chromosome constitution. Case report: We report a mother with RHM, both with biparental diploidy. The mother was compound heterozygous for two variants, c.1720dup, p.(C574Lfs*4) and c.2165A > G, p.(D722G) of the NLRP7 gene, as was a brother who fathered 2 normal pregnancies. Conclusion: The genotype study should be obtained for patients of CHM, even in their first pregnancy, followed by genetic screening for maternal-effect variants in those with biparental moles. This strategy will identify patients in their first pregnancy with HM that have a decreased chance for a normal pregnancy, to allow genetic counseling, perhaps utilizing a donor egg.