Histology and histopathology Vol.37, nº3 (2022)
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- 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 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 AccessDownregulation of KIF15 inhibits the tumorigenesis of non-small-cell lung cancer via inactivating Raf/MEK/ERK signaling(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Luo, Yingbin; Zhang, Bo; Xu, Lili; Li, Minghua; Wu, Jianchun; Zhou, Yiyang; Li, YanBackground. Lung cancer is one of the most common causes of cancer-associated mortality worldwide. Upregulation of kinesin family member 15 (KIF15) expression has been observed in non-small cell lung cancer (NSCLC), and high expression levels of KIF15 are associated with a poor prognosis in patients with NSCLC. However, to the best of our knowledge, the mechanisms by which KIF15 regulates apoptosis, migration and invasion in NSCLC remain unclear. Methods. Cell Counting Kit-8, flow cytometry and Transwell assays were performed to determine the proliferation, apoptosis and invasion of NSCLC cells, respectively. In addition, western blotting was used to detect the levels of phosphorylated (p-)c-Raf, p-ERK and p-MEK in NSCLC cells. Results. Downregulation of KIF15 expression markedly inhibited the proliferation, migration and invasion of NSCLC cells through mediation of MMP2 and MMP9. In addition, downregulation of KIF15 markedly induced apoptosis and cell cycle arrest in NSCLC cells through regulation of active caspase 3, p27 Kip1 and cyclin D1. Furthermore, KIF15 knockdown notably decreased the levels of activating transcription factor 2, p-c-Raf, p-ERK and p-MEK in A549 and NCIH460 cells. Finally, KIF15 knockdown notably inhibited the tumor growth of NSCLC in vivo. Conclusion. In conclusion, the present study indicated that downregulation of KIF15 expression was able to inhibit the tumorigenesis of NSCLC by inactivating Raf/MEK/ERK signaling. These findings may help improve the diagnosis and treatment of NSCLC.
- 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.
- 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 AccessAdenosine deaminase, not immune to a mechanistic rethink in central nervous system disorders?(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Hall, Benjamin; George, Jonathan G.; Allen, Scott P.Adenosine deaminase (ADA) is a purine metabolism enzyme that catalyses the breakdown of adenosine and deoxyadenosine. The enzyme is important in several cellular processes, including the innate immune response and cellular differentiation, and it is also an important enzyme for the maintenance of brain homeostasis, in part due to its regulation of adenosine. Aberrant regulation of ADA enzyme activity has been linked to several neurodegenerative diseases and diseases that can result in neurological impairment. However, the mechanisms behind altered ADA regulation and how this leads to the development of neurological dysfunction are poorly characterised. This review summarises the current research on ADA and its role and regulation in disease pathology, with a focus on the central nervous system (CNS) and the neurodegenerative disease, amyotrophic lateral sclerosis (ALS)
- PublicationOpen AccessSphingosine 1-phosphate and its regulatory role in vascular endothelial cells(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Qiu, Yan; Shen, Junyi; Jiang, Wenli; Yang, Yi; Liu, Xiaoheng; Zeng, YeSphingosine 1-phosphate (S1P) is a bioactive metabolite of sphingomyelin. S1P activates a series of signaling cascades by acting on its receptors S1PR1-3 on endothelial cells (ECs), which plays an important role in endothelial barrier maintenance, anti-inflammation, antioxidant and angiogenesis, and thus is considered as a potential therapeutic biomarker for ischemic stroke, sepsis, idiopathic pulmonary fibrosis, cancers, type 2 diabetes and cardiovascular diseases. We presently review the levels of S1P in those vascular and vascularrelated diseases. Plasma S1P levels were reduced in various inflammation-related diseases such as atherosclerosis and sepsis, but were increased in other diseases including type 2 diabetes, neurodegeneration, cerebrovascular damages such as acute ischemic stroke, Alzheimer's disease, vascular dementia, angina, heart failure, idiopathic pulmonary fibrosis, communityacquired pneumonia, and hepatocellular carcinoma. Then, we highlighted the molecular mechanism by which S1P regulated EC biology including vascular development and angiogenesis, inflammation, permeability, and production of reactive oxygen species (ROS), nitric oxide (NO) and hydrogen sulfide (H2S), which might provide new ways for exploring the pathogenesis and implementing individualized therapy strategies for those diseases
- PublicationOpen AccessThe potential adverse effect of 2.45 GHz microwave radiation on the testes of prenatally exposed peripubertal male rats(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Andrašková, Sandra; Holovská, Katarína; Ševčíková, Zuzana; Andrejčáková, Zuzana; Tóth, Štefan; Martončíková, Marcela; Račeková, Enikö; Almášiová, VieraIn utero development of organs is easily influenced by many environmental factors. The aim of this study was to elucidate the effect of microwave radiation (MR) at a frequency of 2.45 GHz and a specific absorption rate of 1.73 W/kg on intrauterine development of testis. Pregnant albino rats were exposed to whole-body MR for 2 hours per day throughout the pregnancy. Male offspring (n=12, age 35 days) were not exposed to MR after birth. The study revealed that MR applied in utero induced apparent structural changes in the testes, such as irregular shape of seminiferous tubules, significant decrease in the diameter of seminiferous tubules (p<0.05) and in the height of the germinal epithelium (p<0.01), disorganisation of germ cells, desquamations of immature germ cells, formation of giant multinucleated cells, and significant (p<0.01) expansion of the interstitium. At the level of transmission electron microscopy, there were observed basement membrane irregularities in seminiferous tubules, vacuolation of the cytoplasm and adversely affected organelles in Sertoli cells, germ cells, Leydig cells, peritubular and endothelial cells. The tight junctions between adjacent Sertoli cells were often incomplete, and necrotizing germ cells were more numerous in experimental animals compared to controls. Enhanced necrotizations of germ cells proved by a Fluoro Jade C method, and declined germ cells proliferation confirmed by proliferating cell nuclear antigen analysis, were detected in MR exposed animals. Our results revealed that the prenatal exposure to MR had an adverse effect on the postnatal testicular development in rats.