Histology and histopathology Vol.37, nº3 (2022)
Ir a Estadísticas
Permanent URI for this collection
Browse
Recent Submissions
- PublicationOpen AccessGPBAR1 promotes proliferation and is related to poor prognosis of high-grade glioma via inducing MAFB expression(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Sun, Suohui; Guo, Hui; Liang, Nan; Wu, Tao; Zhang, Chunpu; Li, HuaqingBackground. Glioma is the most prevalent brain tumors with extremely poor prognosis, but the prognostic biomarkers of high-grade (grade III and IV) gliomas (HGG) are still insufficient. Materials and methods. In our study, we investigated the expression of GPBAR1 in HGG by qRT-PCR and immunohistochemistry (IHC), and evaluated the clinical significance of GPBAR1 with univariate and multivariate analyses. By retrieving the data from TCGA, we screened the genes significantly associated with GPBAR1, and identified the correlation between GPBAR1 and MAFB. By experiments in vitro, we showed the pivotal role of MAFB in GPBAR1-induced proliferation of HGG. Results. GPBAR1 expression in HGGs was significantly higher than that in normal brain tissues. GPBAR1 was an independent prognostic biomarker of HGG. GPBAR1 promoted the proliferation of HGG by inducing MAFB expression. MAFB was also a prognostic biomarker of HGG, and patients with coexpression of MAFB and GPBAR1 had worse prognosis. Conclusions. GPBAR1 promoted the proliferation of HGG by inducing MAFB expression. Both GPBAR1 and MAFB were prognostic biomarkers of HGG, and patients with co-expression of MAFB and GPBAR1 had worse prognosis than those with only GPBAR1 or MAFB expression.
- PublicationOpen AccessHigh Annexin A10 expression is correlated with poor prognosis in pancreatic ductal adenocarcinoma(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Ishikawa, Akira; Kuraoka, Kazuya; Zaitsu, Junichi; Saito, Akihisa; Yamaguch, Atsushi; Kuwai, Toshio; Sudo, Takeshi; Hadano, Naoto; Tashiro, Hirotaka; Taniyama, Kiyomi; Yasui, WataruPancreatic ductal adenocarcinoma (PDAC) is the third-leading cause of cancer-related death. Owing to its poor prognosis, new molecular biomarkers for PDAC are needed. Annexin A10 (ANXA10) is a calcium- /phospholipid-binding protein belonging to the annexin family of proteins. ANXA10 is not only associated with gastric phenotypes, but also acts an independent prognostic factor in several cancers. However, the role of ANXA10 in PDAC remains unknown. Therefore, we examined the relationship between ANXA10 and the prognosis of PDAC. We analyzed the expression of ANXA10 using data from public databases, and performed immunohistochemistry analysis for 81 PDAC cases. We then investigated the relationship between ANXA10 expression and clinicopathological features. ANXA10 was detected in 47 of 81 PDAC cases (58%). High expression of ANXA10 was significantly related to poor overall survival (OS; p=0.011). Univariate analysis of OS revealed three prognostic parameters: tumor grade (p=0.046), perineural invasion (p=0.017), and ANXA10 expression (p=0.012). Multivariate analysis indicated that ANXA10 expression (p<0.01) alone was a prognostic factor in PDAC cases. Our findings suggest that ANXA10 expression is an independent prognostic factor in PDAC cases and shows promise as a new biomarker in PDAC.
- PublicationOpen AccessThe importance of vascular epithelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) in rhinitis medicamentosa pathogenesis: An experimental rat model study(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Cumbul, Alev; Bulut, FuatObjective. Our aim in this study is to reveal the expression of Vascular Endothelial Growth Factor (VEGF) and inducible Nitric Oxide Synthase (iNOS) in the pathogenesis of rhinitis medicamentosa (RM), which occurs as a result of the overdose and long-term use of topical nasal decongestants. Methods. In this study, 24 Wistar albino rats were divided into two groups as experimental and control groups. In the experimental group, 50 µl of 0.05% oxymetazoline (iliadin® merck) was applied intranasally to each nostril three times a day for 2 months with the help of a micropipette. 50 µl saline was applied to the control group. At the end of the second month, the rats were examined. RM was detected in the experimental group. Then the nasal tissues of the rats were removed and fixed with 10% phosphate buffered neutral formaldehyde (pH=7.4). Nasal tissues were decalcified in Morse's solution (10% sodium citrate and 22.5% formic acid). Histopathological evaluations of the preparations were stained using Masson Trichrome (TCM) and Hematoxylin Eosin (H&E) techniques and immunohistochemical examinations of the preparations were stained with VEGF and iNOS antibodies and photographed using the Leica DM6000B microscope and the Leica Application Suite Program. Results. In the RM group, we found a significant increase in VEGF and iNOS expression in the nasal mucosa compared to the control group (p<0.001). We also observed the main histopathological changes in the nasal mucosa under a light microscope, including squamous metaplasia in the epithelium of the tunica mucosa, submucosal perivascular edema and degeneration of the submucosal glands. Conclusions. According to these results, increased expression levels of VEGF and iNOS play an important role in rebound swelling in RM pathogenesis.
- PublicationOpen AccessCircAKT3 promotes cell proliferation, survival and glutamine metabolism of gastric cancer by activating SLC1A5 expression via targeting miR-515-5p(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Li, Fei; Zhang, Lixiao; Sun, QiBackground. Gastric cancer (GC) is a common disorder in the population. Numerous studies have reported that the pathogenesis of GC is implicated in the dysregulation of circular RNAs (circRNAs). The aim of this study was to investigate the role and functional mechanism of circ_0000199 (circAKT3) in GC. Methods. The expression of circAKT3, miR-515-5p and solute carrier family 1 member 5 (SLC1A5) mRNA was measured by quantitative real-time PCR (qPCR). Cell proliferation was assessed by cell counting kit-8 (CCK-8) assay, colony formation assay and 5-ethynyl-2'- deoxyuridine (EdU) assay. Cell apoptosis was determined by flow cytometry assay and caspase 3/7 activity. The protein levels of glutaminase (GLS), proliferating cell nuclear antigen (PCNA) and cleavedcaspase3 were detected by western blot. The binding relationship between miR-515-5p and circAKT3 or SLC1A5 was verified by dual-luciferase reporter assay or RIP assay. The role of circAKT3 in vivo was investigated by establishing animal models. The abundance of Ki-67 and PCNA was detected by IHC assay. Results. The expression of circAKT3 in GC tissues and cells was enhanced. The knockdown of circAKT3 inhibited GC cell proliferation, survival and glutamine metabolism, as well as tumor growth in animal models. MiR-515-5p was a target of circAKT3, and miR-515-5p suppressed the expression of SLC1A5 by binding to SLC1A5 3'UTR. CircAKT3 relieved the inhibition of miR-515-5p on SLC1A5 expression by targeting miR515-5p. The effects of circAKT3 knockdown were reversed by miR-515-5p depletion, and the effects of miR-515-5p restoration were abolished by SLC1A5 overexpression. Conclusion. CircAKT3 promotes the malignant development of GC by activating SLC1A5 expression via targeting miR-515-5p.
- PublicationOpen AccessMiR-194-3p modulates the progression of colorectal cancer by targeting KLK10(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Liu, Tao; Fang, YuejunBackground. A rich history of studies have manifested the importance of miRNAs to cancer progression, while miR-194-3p has been seldom explored. Objective. The purpose of this study is to unearth the way the miR-194-3p/KLK10 axis modulates colorectal cancer (CRC). Methods. Differentially expressed genes of CRC in TCGA database were analyzed. Western blot and qRTPCR were employed to test protein and mRNA expressions of two researched genes. Their targeting was confirmed using dual-luciferase. Biological behaviors of cells were tested by a series of cellular functional assays. Result. Remarkably low miR-194-3p expression and high KLK10 expression were observed in cancer cells. Overexpressing miR-194-3p hindered the progression of CRC cells. Overexpression of miR-194-3p significantly weakened the promoting effect of upregulated KLK10 on cell migration, invasion and proliferation. Their targeting was verified by dual -luciferase assay. Therefore, miR-194-3p hindered cell behaviors of CRC through KLK10. Conclusion. This investigation casts new light on the treatment of CRC through the miR-194-3p/KLK10 axis.