Histology and histopathology Vol.37,nº10 (2022)
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- PublicationOpen AccessCircRNF220 plays a pathogenic role to facilitate cell progression of AML in vitro via sponging miR-330-5p to induce upregulation of SOX4(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Zhang, Zewen; Lin, Shujun; Yin, Jun; Yu, Wenjun; Xu, ChengweiBackground: Circular RNAs (circRNAs) are a specific family of non-coding RNAs (ncRNAs) with important function in disease progression. This research is performed to study circRNA Ring Finger Protein 220 (circRNF220) in acute myeloid leukemia (AML). Methods: CircRNF220, microRNA-330-5p (miR330-5p) and sex-determining region Y-related highmobility group box 4 (SOX4) were measured via quantitative real-time polymerase chain reaction (qRTPCR). 3-(4, 5-dimethylthiazol-2-y1)-2, 5- diphenyl tetrazolium bromide (MTT) and EdU assays were used to assess cell proliferation. Cell cycle and apoptosis were detected using flow cytometry. Cell invasion was determined by transwell assay. Glycolytic metabolism was assessed by glucose consumption and lactate production. The target interaction was implemented via dual-luciferase reporter and RNA pull-down assays. SOX4 protein detection was conducted by western blot. Results: Expression detection identified that circRNF220 was overexpressed in AML. In vitro experiments showed that silence of circRNF220 promoted cell apoptosis but impeded proliferation, cell cycle progression, invasion and glycolytic metabolism in AML cells. Target analysis indicated that circRNF220 directly targeted miR-330-5p, and the effects of sicircRNF220 were abrogated by miR-330-5p inhibitor. Moreover, circRNF220 targeted miR-330-5p to increase the expression of SOX4 and SOX4 promoted cell progression of AML. Conclusion: All these findings revealed that circRNF220 contributed to AML cell development in vitro via upregulating SOX4 expression by targeting miR-330-5p.
- PublicationOpen AccessSignificance of Anoctamin 6 in progression and prognostic prediction of gastric adenocarcinoma(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Li, Bin; Fan, Qiong; Zheng, Li; Liu, Peng; Fang, NianBackground. Gastric cancer is one of the most lethal malignancies worldwide with surgery as the only curative therapy. However, postoperative overall survival of gastric cancer is far from satisfactory although significant improvement has been made in adjuvant therapies. Gastric cancer is characterized as highly heterogeneous and illustrating the molecular mechanisms is invaluable for both identification of novel prognostic biomarkers and development of therapeutic drugs. Here we aimed to investigate the participation of Anoctamin 6 (ANO6) in gastric adenocarcinoma. Methods. Immunohistochemical (IHC) staining was used to explore the expression pattern of ANO6 in tumor tissues from gastric adenocarcinoma patients (n=108). Clinicopathological data was subjected to Kaplan-Meier survival and Cox multivariate analyses to evaluate prognostic predictors. Overexpression and silencing procedures were performed on gastric cancer cell lines to investigate the functional mechanisms of ANO6 in regulating tumor development. Results. Higher ANO6 expression showed a positive correlation with advanced tumor stage of gastric cancer. Univariate and multivariate analyses revealed that ANO6 was an independent prognostic factor for overall survival of gastric cancer. An in vitro study demonstrated that ANO6 can promote cell proliferation while silencing ANO6 significantly downregulated cell viability. Conclusion. High ANO6 expression in gastric cancer indicates poor clinical outcomes, and ANO6 may act as a potential target for novel therapy development targeting gastric cancer.
- PublicationOpen AccessInvestigation of clinical application of claudin 18 isoform 2 in pancreatic ductal adenocarcinoma: A retrospective analysis of 302 chinese patients(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Zhang, Zhiwei; Liu, Xiaoding; Zhou, Liangrui; Zhang, Mu; Liang, ZhiyongThe malignancy of pancreatic ductal adenocarcinoma (PDAC) results from high frequency of recurrence and limited effective therapies. Targeted therapy is a promising treatment in multiple solid tumours. A new target, claudin 18 isoform 2 (CLDN18.2) was discovered in gastric and pancreatic adenocarcinoma, but more clinical evaluations of CLDN18.2 are still needed. Several CLDN18.2-targeted drugs have already been in procedure of clinical trials. Therefore, the present study aimed to explore the expression and clinical value of CLDN18.2 in PDAC by immunohistochemistry. A microarray cohort of 302 PDAC specimens and a whole-slide cohort of randomized 84 PDAC specimens were constructed. In total, 56.52% (171/302) of PDAC patients showed diverse positivity for CLDN18.2, especially in highly differentiated PDAC. About eighty-two percent (62/75) highly- and 62.61% (72/115) intermediate-differentiated PDAC showed positive for CLDN18.2, while only 10.16% (6/59) low differentiated PDAC was positive for CLDN18.2. Besides, CLDN18.2 positivity was associated with several clinicopathological characteristics, including sex (P=0.001), smoking (P=0.006), abdominal pain (P=0.021), jaundice (P=0.010), pathological differentiation (P=0.001), common bile duct invasion (P=0.010), and M stage (P=0.003). CLDN18.2-positive expression also predicts an improved survival (P=0.032) but not progression free survival (P=0.460). However, CLDN18.2 is not an independent prognostic predictor. In conclusion, CLDN18.2 may be a potential therapeutic target for PDAC and the study supplies persuasive pathological evidence for CLDN18.2-targeted therapy on PDAC patients.
- PublicationOpen AccessCircular RNA circSDHC (hsa_circ_0015004) regulates tumor growth and angiogenesis via regulating centrosomal protein 55 expression in renal cell carcinoma(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Pei, Long; Dong, Chunhui; Wang, Yanchao; Lv, Xianqiang; Jia, Gaopei; Zhang, AiliBackground. Renal cell carcinoma (RCC) is the main aggressive subtype of kidney cancer. Circular RNAs have been shown to exert critical roles in RCC. However, little is known about the regulatory mechanism of hsa_circ_0015004 (circSDHC) in RCC. Methods. 35 patients with RCC were recruited in the research. Expression changes of circSDHC were determined by real-time quantitative polymerase chain reaction (RT-qPCR). The effects of circSDHC inhibition on cell proliferation, apoptosis, angiogenesis, migration, and invasion were analyzed. The regulation mechanism of circSDHC was surveyed by bioinformatics analysis. The effect of circSDHC on tumorigenesis was validated by xenograft assay. Results. We observed an observable elevation in circSDHC expression in RCC tissues and cell lines. Functionally, circSDHC silencing decreased xenograft tumor growth and induced RCC cell apoptosis, repressed RCC cell proliferation, angiogenesis, migration, and invasion in vitro. Mechanically, circSDHC modulated centrosomal protein 55 (CEP55) expression by functioning as a miR-130a-3p sponge. Also, miR-130a3p silencing offset circSDHC knockdown-mediated impacts on malignant phenotypes and angiogenesis of RCC cells. Furthermore, exogenetic expression of CEP55 counteracted miR-130a-3p overexpressionmediated effects on malignant phenotypes and angiogenesis of RCC cells. Conclusion. Silencing of circSDHC restrained cell malignant phenotypes and angiogenesis via reducing CEP55 expression by releasing miR-130a-3p in RCC, providing a new mechanism for understanding the progression of RC
- PublicationOpen AccessEarly structural alterations of intrinsic cardiac ganglionated plexus in spontaneously hypertensive rats(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Ranceviene, Dalia; Rysevaite Kyguoliene, Kristina; Inokaitis, Hermanas; Saburkina, Inga; Plekhanova, Khrystyna; Sabeckiene, Deimante; Sabeckis, Ignas; Azukaite, Joana; Pauza, Dainius H; Pauziene, NeringaPersistent arterial hypertension leads to structural and functional remodeling of the heart resulting in myocardial ischemia, fibrosis, hypertrophy, and eventually heart failure. Previous studies have shown that individual neurons composing the intracardiac ganglia are hypertrophied in the failing human, dog, and rat hearts, indicating that this process involves changes in cardiac innervation. However, despite a wealth of data on changes in intrinsic cardiac ganglionated plexus (GP) in late-stage disease models, little is known about the effects of hypertension on cardiac innervation during the early onset of heart failure development. Thus, we examined the impact of early hypertension on the structural organization of the intrinsic cardiac ganglionated plexus in juvenile (8-9 weeks) and adult (12-18 weeks) spontaneously hypertensive (SH) and age-matched Wistar-Kyoto (WKY) rats. GP was studied using a combination of immunofluorescence confocal microscopy and transmission electron microscopy in whole-mount preparations and tissue sections. Here, we report intrinsic cardiac GP of SH rats to display multiple structural alterations: (i) a decrease in the intracardiac neuronal number, (ii) a marked reduction in axonal diameters and their proportion within intracardiac nerves, (iii) an increased density of myocardial nerve fibers, and (iv) neuropathic abnormalities in cardiac glial cells. These findings represent early neurological changes of the intrinsic ganglionated plexus of the heart introduced by early-onset arterial hypertension in young adult SH rats.