Prenatal features and postnatal follow-up of congenital ventricular outpouching: A retrospective study of two centers in China.

OBJECTIVES: Congenital ventricular outpouching (CVO) is a rare cardiac malformation that can manifest as congenital ventricular aneurysm (CVA) and/or congenital ventricular diverticula (CVD). In this study, we describe the prenatal features and postnatal follow-up of 27 cases of CVO. METHODS: The clinical data of 27 patients with CVO who attended Sir Run Run Shaw Hospital Affiliated to the Medical College of Zhejiang University (Zhejiang Province, China) and Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University (Zhejiang Province, China) from April 2013 to October 2022 were retrospectively analyzed. The patients were also followed up by telephone. The prenatal characteristics and postnatal outcomes of the patients with CVO were evaluated. RESULTS: CVO was detected in 26 cases prenatally, 14 (51.85%) were diagnosed with CVA, nine (33.33%) were diagnosed with CVD, three (11.11%) were equivocal for CVA/CVD, and one (3.70%) was detected with CVA postnatally. Six patients underwent follow-up fetal echocardiography approximately 4 weeks after the initial echocardiography examination, and a significant difference in CVO size was observed between the two examinations (P = .02). Eight patients (29.63%) demonstrated cardiovascular dysfunction, and the median CVO size in fetuses with and without cardiovascular dysfunction was 205 (range: 169-396) mm2 and 124 (range: 92-154.5) mm2 , respectively (P = .01). Correlation was found between CVO size and fetal cardiac dysfunction (p = .000, r = .778). Eight patients (29.63%) had cardiac/extracardiac defects. Thirteen patients were live born, 12 were terminated pregnancies, and two were lost to follow-up. The postpartum size of the CVOs remained stable in six patients, decreased in two patients, dissolved in three patients, and were surgically removed in two patients. With the exception of one patient with CVA complicated with complex congenital cardiac malformation who underwent surgical treatment after birth and who had postoperative left ventricular dysfunction (Case 1), the prognosis of all of the patients was good. CONCLUSION: CVO is often associated with cardiac malformations. The size of prenatal CVOs can increase with gestational development, and cardiovascular dysfunction is significantly related to CVO size. The postpartum prognosis of patients with CVO is good. Echocardiography plays a key role in the diagnosis of congenital ventricular outpouching. Prenatal counseling should be cautious regarding the diagnosis and the prognosis although our cases had a favorable prognosis.

Pan-cancer and single-cell analysis reveal the prognostic value and immune response of NQO1.

Background: Overexpression of the NAD(P)H: Quinone Oxidoreductase 1 (NQOI) gene has been linked with tumor progression, aggressiveness, drug resistance, and poor patient prognosis. Most research has described the biological function of the NQO1 in certain types and limited samples, but a comprehensive understanding of the NQO1's function and clinical importance at the pan-cancer level is scarce. More research is needed to understand the role of NQO1 in tumor infiltration, and immune checkpoint inhibitors in various cancers are needed. Methods: The NQO1 expression data for 33 types of pan-cancer and their association with the prognosis, pathologic stage, gender, immune cell infiltration, the tumor mutation burden, microsatellite instability, immune checkpoints, enrichment pathways, and the half-maximal inhibitory concentration (IC50) were downloaded from public databases. Results: Our findings indicate that the NQO1 gene was significantly upregulated in most cancer types. The Cox regression analysis showed that overexpression of the NQO1 gene was related to poor OS in Glioma, uveal melanoma, head and neck squamous cell carcinoma, kidney renal papillary cell carcinoma, and adrenocortical carcinoma. NQO1 mRNA expression positively correlated with infiltrating immune cells and checkpoint molecule levels. The single-cell analysis revealed a potential relationship between the NQO1 mRNA expression levels and the infiltration of immune cells and stromal cells in bladder urothelial carcinoma, invasive breast carcinoma, and colorectal cancer. Conversely, a negative association was noted between various drugs (17-AAG, Lapatinib, Trametinib, PD-0325901) and the NQO1 mRNA expression levels. Conclusion: NQO1 expression was significantly associated with prognosis, immune infiltrates, and drug resistance in multiple cancer types. The inhibition of the NQO1-dependent signaling pathways may provide a promising strategy for developing new cancer-targeted therapies.

CircSERPINA3 promoted cell proliferation, migration, and invasion of laryngeal squamous cell carcinoma by targeting miR-885-5p.

CircSERPINA3 has been shown to be upregulated in laryngeal squamous cell carcinoma (LSCC); however, whether it regulates the development of LSCC and the specific molecular mechanism remains unclear, which is to be explored in this study. Expressions of circSERPINA3, miR-885-5p, and Malic enzyme 1 (ME1) in LSCC tissues or cell lines were determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The regulation of circSERPINA3 on the biological behavior of LSCC cells was confirmed by loss and gain experiments (cell counting kit-8, transwell, and colony formation assay). The correlation between circSERPINA3/ME1 and miR-885-5p was predicted and confirmed by bioinformatics analysis, dual-luciferase reporter assay, and qRT-PCR. The effect of circSERPINA3/miR-885-5p axis on the biological behavior of LSCC cells and expressions of epithelial-mesenchymal transition-related proteins was confirmed by rescue experiments. CircSERPINA3 and ME1 was upregulated in LSCC tissues, whereas miR-885-5p was downregulated. MiR-885-5p was the target gene of circSERPINA3, whereas ME1 was the target gene of miR-885-5p. Silent circSERPINA3 suppressed viability, invasion, migration, colony formation, and expression of ME1, claudin-4, snail, and vimentin but elevated expression of miR-885-5p and E-cadherin, whereas overexpressed circSERPINA3 was the opposite. However, miR-885-5p inhibitor or mimic reversed the effects of silent circSERPINA3 or overexpressed circSERPINA3. Collectively, circSERPINA3 promotes proliferation, migration, and invasion of LSCC cells by targeting miR-885-5p.

Long noncoding RNA ZEB2-AS1 facilitates laryngeal squamous cell carcinoma progression by miR-6840-3p/PLXNB1 axis.

PURPOSE: To investigate the role of zinc finger E­box­binding homeobox 2 antisense RNA 1 (ZEB2-AS1) in regulating laryngeal squamous cell carcinoma (LSCC) progression. PATIENTS AND METHODS: In this retrospective study, we included all patients who underwent a surgical operation at The First Hospital of Qiqihaer City for LSCC. Then, we compared the expression of ZEB2-AS1 in LSCC tissues and paired healthy tissues. Besides, we also performed a series of functional assays, CCK8 assays, colony formation assays, and transwell assays to examine the functions of LSCC cells after knockdown of ZEB2-AS1. Through bioinformatics analysis, we predicted that ZEB2-AS1 binds to miR-6840-3p and targets PLXNB1. RESULTS: We indicated that the expression of ZEB2-AS1 was higher in LSCC tissues compared to the paired adjacent tissues, and ZEB2-AS1 was also highly expressed in LSCC cell lines. Furthermore, we discovered that ZEB2-AS1 promoted cell proliferation, migration and invasion and was associated with poor prognosis. To find the mechanism, we performed bioinformatics analysis. We identified that ZEB2-AS1 binds to miR-6840-3p and targets PLXNB1. Additionally, miR-6840-3p overexpression or knockdown of PLXNB1 decreased the abilities of cell migration and invasion. CONCLUSION: These findings demonstrated that overexpression of ZEB2-AS1 promotes LSCC progression. Overexpression of miR-6840-3p or downregulation of PLXNB1 can abrogate ZEB2-AS1-mediated LSCC malignant development.