Analytical Cellular Pathology
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Acceptance rate17%
Submission to final decision111 days
Acceptance to publication25 days
CiteScore4.400
Journal Citation Indicator0.570
Impact Factor4.133

Bioinformatics Analysis of Molecular Interactions between Endoplasmic Reticulum Stress and Ferroptosis under Stress Exposure

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Analytical Cellular Pathology provides a forum for pathologists and medical practitioners working in the cellular pathology field. Topics covered include cytology, carcinogenesis, cell receptors, biomarkers, diagnostic pathology, and immunopathology.

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Chief Editor Professor Dimitrios Karamichos focuses on investigating corneal wound healing and dystrophies with a particular interest in the effect of transforming growth factor-β3 or TGF- β3 on corneal stromal cells and their extracellular environment.

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Research Article

Inhibition of miR-182-5p Targets FGF9 to Alleviate Osteoarthritis

Background. The pathogenesis of osteoarthritis (OA) is complex and there is no specific drug for treatment. The aim of this study was to identify the molecular targets of OA therapy, focusing on the expression and biological functions of miR-182-5p and its target genes in OA. Methods. miR-182-5p and fibroblast growth factor 9 (FGF9) were overexpressed or knocked down in IL-1β-induced chondrocytes. An OA knee model was performed by surgically destroying the medial meniscus. The gene expression of miR-182-5p and FGF9 was calculated. The protein FGF9 was tested by western blotting. Cell counting kit-8 (CCK8), plate cloning assay, and flow cytometry were conducted to evaluate cell proliferation and apoptosis. The expression of inflammatory factors, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and interleukin (IL)-8, was evaluated using enzyme-linked immunosorbent assay (ELISA). Dual-luciferase reporter assays validated the targeting relationship between miR-182-5p and FGF9. Hematoxylin–eosin (HE) and safranin O-fast Green (S–O) staining were utilized to access cartilage damage. Ki67 expression in cartilage was detected using immunohistochemistry (IHC). TdT-mediated dUTP nick-end labeling (TUNEL) assays were used to calculate the apoptosis rate of cartilage. Results. The expression of miR-182-5p was upregulated, and FGF9 was downregulated in the IL-1β-induced chondrocytes. OA chondrocytes proliferation ability in the miR-182-5p mimics group was decreased, and the apoptosis rate and inflammatory factor were increased. Transfection with miR-182-5p inhibitor increased the proliferative ability and decreased the apoptosis rate in the IL-1β-induced chondrocytes. Transfection with miR-182-5p inhibitor reversed IL-1β-induced inflammatory factor release in chondrocytes. Targeted binding sites existed between miR-182-5p and FGF9. After overexpression of FGF9, the miR-182-5p effect on OA chondrocytes was reversed. The hyaline cartilage thickness and proteoglycan content decreased in OA rats, and this was reversed by miR-182-5p inhibitor treatment. Conclusions. miR-182-5p expression levels were increased in OA chondrocytes and regulated chondrocyte proliferation, apoptosis, and inflammation by targeting FGF9. miR-182-5p is a potential gene for OA treatment.

Research Article

Effect of COP1 in Promoting the Tumorigenesis of Gastric Cancer by Down-Regulation of CDH18 via PI3K/AKT Signal Pathway

In recent years, the involvement of E3 ubiquitin ligase constitutive photomorphogenesis 1 (COP1) in the tumorigenesis of gastric cancer (GC) has been elucidated. However, the exact underlying mechanism remains to be clarified. In the present study, the expression profiles of COP1 in GC were derived from the Gene Expression Omnibus (GEO) and the Cancer Genome Atlas (TCGA) databases, followed by verification via immunohistochemical staining (IHC), Western blotting (WB), and quantitative real-time polymerase chain reaction (qRT-PCR) reaction assays on clinical samples. In vitro, the gain- and loss-of-function experiments of COP1 protein were conducted to explore its role in GC cell lines HGC-27 and SGC-7901. Furthermore, we screened the interaction protein of COP1 by yeast two-hybrid experiment and verified their combination by co-immunoprecipitation (co-IP). We preliminary explored the possible underlying mechanisms of COP1 protein in GC cell lines via WB. COP1 was upregulated in GC tissues compared with the corresponding non-carcinoma tissues. In vitro, the upregulation of COP1 protein promoted the proliferation and migration of GC cells. The yeast two-hybrid experiment and co-IP indicated that Cadherin 18 (CDH18) could constitute a complex with COP1. Moreover, cells with COP1 over-expression showed low levels of CDH18 expression, with the intracellular PI3K/AKT pathway activated and the malignancy of GC cell lines enhanced. Our findings demonstrated that COP1 promoted the GC tumorigenesis by downregulated CDH18 with the involvement of PI3K/AKT signaling pathway in cell lines, suggesting the potential of COP1 as a prognostic biomarker and therapeutic target for GC.

Research Article

Classification of Signature-Based Phenotypes of Aging-Related Genes to Identify Prognostic and Immune Characteristics in HCC

Hepatocellular carcinoma (HCC), which has become one of the most significant malignancies causing cancer-related mortality, presents genetic and phenotypic heterogeneity that makes predicting prognosis challenging. Aging-related genes have been increasingly reported as significant risk factors for many kinds of malignancies, including HCC. In this study, we comprehensively dissected the features of transcriptional aging-relevant genes in HCC from multiple perspectives. We applied public databases and self-consistent clustering analysis to classify patients into C1, C2, and C3 clusters. The C1 cluster had the shortest overall survival time and advanced pathological features. Least absolute shrinkage and selection operator (LASSO) regression analysis was adopted to build the prognostic prediction model based on six aging-related genes (HMMR, S100A9, SPP1, CYP2C9, CFHR3, and RAMP3). These genes were differently expressed in HepG2 cell lines compared with LO2 cell lines measured by the mRNA expression level. The high-risk score group had significantly more immune checkpoint genes, higher tumor immune dysfunction and exclusion score, and stronger chemotherapy response. The results indicated that the age-related genes have a close correlation with HCC prognosis and immune characteristics. Overall, the model based on six aging-associated genes demonstrated great prognostic prediction ability.

Research Article

Suppression of lncRNA OIP5-AS1 Attenuates Apoptosis and Inflammation, and Promotes Proliferation by Mediating miR-25-3p Expression in Lipopolysaccharide-Induced Myocardial Injury

Purpose. Long non-coding RNAs (LncRNAs) OIP5-AS1 and miR-25-3p play important roles in myocardial injury, whereas their roles in lipopolysaccharide (LPS)-induced myocardial injury remain unknown. The purpose of our study was to investigate the functional mechanisms of OIP5-AS1 and miR-25-3p in LPS-induced myocardial injury. Methods. Rats and H9C2 cells were treated with LPS to establish the model of myocardial injury in vivo and in vitro, respectively. The expression levels of OIP5-AS1 and miR-25-3p were determined by quantitative reverse transcriptase-polymerase chain reaction. Enzyme-linked immunosorbent assay was performed to measure the serum levels of IL-6 and TNF-α. The relationship between OIP5-AS1 and miR-25-3p/NOX4 was determined by luciferase reporter assay and/or RNA immunoprecipitation assay. The apoptosis rate was detected by flow cytometry, and cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. Western blot was performed to detect the protein levels of Bax, Bcl-2, caspase3, c-caspase3, NOX4, and p-NF-κB p65/NF-κB p65. Results. OIP5-AS1 was up-regulated, and miR-25-3p was down-regulated in myocardial tissues of LPS-induced rats and LPS-treated H9C2 cells. Knockdown of OIP5-AS1 relieved the myocardial injury in LPS-induced rats. Knockdown of OIP5-AS1 also inhibited the inflammation and apoptosis of myocardial cells in vivo, which was subsequently confirmed by in vitro experiments. In addition, OIP5-AS1 targeted miR-25-3p. MiR-25-3p mimics reversed the effects of OIP5-AS1 overexpression on promoting cell apoptosis and inflammation and on inhibiting cell viability. Besides, miR-25-3p mimics blocked the NOX4/NF-κB signalling pathway in LPS-induced H9C2 cells. Conclusion. Silencing of lncRNA OIP5-AS1 alleviated LPS-induced myocardial injury by regulating miR-25-3p.

Research Article

The Protective Role of Nrf2 in Renal Tubular Cells in Oxidised Low-Density Lipoprotein-Induced Fibrosis

Background: CD36 is the receptor of oxidised low-density lipoprotein (OxLDL) in renal tubular epithelial cells. Nuclear factor erythroid 2-related factor 2 (Nrf2) is the key factor in the activation of the Nrf2 signalling pathway and the regulation of oxidative stress. Kelch-like ECH-associated protein 1 (Keap1) is known as an Nrf2 inhibitor. Methods: We used OxLDL and Nrf2 inhibitors at different concentrations and durations to treat renal tubular epithelial cells; the expression of CD36 and cytoplasmic and nucleic Nrf2 and E-cadherin in those cells were observed by Western blot and reverse-transcription polymerase chain reaction. Results: The protein levels of Nrf2 decreased in expression after 24 hours of OxLDL treatment. At the same time, the Nrf2 protein level in the cytoplasm did not change significantly compared with that of the control group, and the Nrf2 protein level expression in the nucleus increased. Both the messenger ribonucleic acid (mRNA) and protein expression of CD36 decreased following the treatment of cells with the Nrf2 inhibitor Keap1. Kelch-like ECH-associated protein 1 was overexpressed, and CD36 mRNA and protein expression were decreased in OxLDL-treated cells. Following the overexpression of Keap1, E-cadherin expression was reduced in NRK-52E cells. Conclusion: Nuclear factor erythroid 2-related factor 2 can be activated by OxLDL; however, it can only alleviate OxLDL-induced oxidative stress by transferring from the cytoplasm to the nucleus. Additionally, Nrf2 may play a protective role by upregulating CD36.

Research Article

Association between CHFR and PARP-1, and Their Roles in Regulation of Proliferation and Apoptosis of B Cell Lymphoma

Background. Aberrant methylation of checkpoint with forkhead and ring finger domains (CHFR) was found in B-cell non-Hodgkin lymphoma (NHL), whereas its role in carcinogenesis is not clear. CHFR can control poly (ADP-ribose) polymerase levels by causing its degradation. The study was aimed to explore the roles and mechanisms of CHFR in the pathogenesis of B-cell NHL. Methods. Short hairpin ribonucleic acid (ShRNAs) targeting CHFR and poly (ADP-ribose) polymerase 1 (PARP-1) were transduced into Raji cells, and real-time polymerase chain reaction (PCR) and western blotting were carried out to determine their expression. Afterwards, the CCK-8 assay and flow cytometry were used to evaluate the cell growth and apoptosis. Tumor size and weight were determined using a xenograft model, and decitabine (5-Aza-dC) was used to further determine the methylation status of CHFR through a methylation specificity-PCR assay. Results. 5-Aza-dC-treatment promoted the expression of CHFR and decreased the expression of PARP-1 at both messenger ribonucleic acid (mRNA) and protein levels. 5-Aza-dC also accelerated Raji-cell apoptosis and restrained its growth in vitro and in vivo (). These results were contrary to those observed in the shRNA-CHFR group but consistent with those observed in the shRNA-PARP-1 group. The expression profiles of CHFR and PARP-1 in the xenograft model were consistent with those in the cellular model. Treatment with 5-Aza-dC led to demethylation of CHFR in nude mice. Besides, there may be a negative correlation between CHFR and PARP-1 in B-cell NHL cells. Conclusion. Our findings indicated that 5-Aza-dC could lead to the demethylation of the CHFR promoter and suppress Raji cell growth.

Analytical Cellular Pathology
 Journal metrics
See full report
Acceptance rate17%
Submission to final decision111 days
Acceptance to publication25 days
CiteScore4.400
Journal Citation Indicator0.570
Impact Factor4.133
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Article of the Year Award: Outstanding research contributions of 2021, as selected by our Chief Editors. Read the winning articles.