International Journal of Immunopathology and Pharmacology最新文献

{"title":"Pentagalloyl glucose induces anti-inflammatory macrophage polarization - suppressing macrophage mediated vascular cell dysfunction and TGF-β secretion.","authors":"Gregory Halsey, Fatema-Tuj Zohora, Shivani Arora, Holly Zimmerman, Naren Vyavahare","doi":"10.1177/03946320241276894","DOIUrl":"10.1177/03946320241276894","url":null,"abstract":"<p><p><b>Background:</b> Pentagalloyl glucose (PGG) is a polyphenol with vasoprotective properties. Targeted delivery of PGG reversed aortic aneurysm growth in several rodent models associated with decreased number of macrophages and transforming growth factor-β (TGF-β) expression. Thus, we sought to determine cellular mechanisms by which PGG reduces macrophage-induced aortic pathogenicity and its relationship to TGF-β. <b>Methods:</b> Using THP-1 cells, primary human aortic cells, and explanted rat aortas, we assessed the anti-inflammatory effect of PGG. Expression of pro/anti-inflammatory macrophage markers was analyzed. Adhesion of monocytes as well as oxidative stress status, viability, and TGF-β expression after primary aortic cell exposure to macrophage-conditioned medium with and without PGG were assessed. The release of TGF-β was also examined in elastase-treated cultured rat aortas. <b>Results:</b> PGG pre-treatment of human aortic cell monolayers reduced the adhesion of THP-1 monocytes. PGG enhanced the expression of anti-inflammatory markers in THP-1-derived macrophages, and increased mitochondrial reactive oxygen species as well as mitochondrial polarization. Conditioned medium from THP-1-derived macrophages induced reactive oxygen species, cell death, and TGF-β release from human aortic cells, which was suppressed by PGG. In explanted rat aortas, PGG reduced elastase mediated TGF-β release. <b>Conclusions:</b> Combining anti-inflammatory, cytotoxic, and oxidative effects, PGG has high cardiovascular therapeutic potential. We confirmed previous in vivo observations whereby PGG suppressed TGF-β response associated with disease resolution.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241276894"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11320691/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141972125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence of cutaneous manifestations and myositis-specific antibodies in COVID-19 patients and Anti-PL7 antibodies association with pulmonary radiological severity: A retrospective study.","authors":"Giorgio Alberto Oddenino, Paola Canepa, Emanuele Cozzani, Giulia Gasparini, Alessandro Garlaschi, Luca Roccatagliata, Irene Schiavetti, Aurora Parodi","doi":"10.1177/03946320241260295","DOIUrl":"10.1177/03946320241260295","url":null,"abstract":"<p><strong>Background: </strong>Dermatomyositis (DM) is an idiopathic immune-mediated myopathy, and may involve many organs, including muscles, skin and lungs. Myositis-specific autoantibodies (MSAs) are a useful aid in diagnosis DM and identifying its clinical subtype. During the COVID-19 pandemic, several studies found clinical similarities regarding lung involvement in both COVID-19 and DM. Such similarities have prompted speculation of a common pathogenetic mechanism. Indeed, viral infections are well-known triggers of autoimmune diseases. This prompted us to investigate whether circulating MSAs could be markers of the severity of lung involvement and of clinical outcome in COVID-19 patients. Moreover, we investigated the presence of cutaneous signs of DM in COVID-19 patients.</p><p><strong>Methods: </strong>We conducted a retrospective cohort study on 178 hospitalized patients affected by COVID-19. The diagnosis was confirmed by naso-pharyngeal swab positivity for SARS-CoV-2. The severity of lung involvement was assessed by assigning to each patient a radiological score ranging from 1 to 4, based on chest imaging (chest X-rays or CT scans). Serum samples were tested for MSAs.</p><p><strong>Results: </strong>Anti-PL-7 antibodies were detected in 10.1% of patients and were found to be associated with an increased risk of severe pulmonary involvement (<i>p</i> = 0.019) and a worse prognosis in COVID-19 patients. Cutaneous lesions were observed in 26.4% of patients. However, none were cutaneous manifestations of DM.</p><p><strong>Conclusions: </strong>The detection of anti-PL7 antibodies might predict severe pulmonary involvement and a worse prognosis in COVID-19 patients.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241260295"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11282529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141761894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curcumin suppresses metastasis, invasion, and proliferation in osteosarcoma cells by regulating the EGFR/Src signaling axis.","authors":"Huiying Liu, Zhiqiang Li, Binwu Xu, Zhipeng Li, Xili Yang, Jun Luo","doi":"10.1177/03946320241308082","DOIUrl":"10.1177/03946320241308082","url":null,"abstract":"<p><p>We explored the biological mechanisms by which curcumin (Cur) confronts osteosarcoma (OS) tumorigenesis and potential drug gene targets based on network pharmacology and in vitro cell experiments. Cur has been recognized for its significant role in combating various types of tumors. However, the intrinsic molecular mechanisms through which it affects OS remain uncharted. In this study, we performed network pharmacology methods including protein-protein interaction (PPI) and core target screening, Functional Enrichment Analysis and Network Construction, Molecular Docking, which obtained the potential target of Cur. Meanwhile, cell experiments (wound healing assay, Transwell assay, Western blots, immunofluorescence, et al.) in vitro were performed to verify the targets, and reveal the biological mechanisms. A total of 18 hub genes were identified through our network pharmacological analysis. In vitro studies show that Cur inhibits the proliferation, migration, invasion capabilities of MG63 and U2OS cells. Western blot reveals a down-regulation of p-PI3K, PI3K, p-Akt, Akt, EGFR, Src, p-Src (Tyr416) and STAT3 expression when treated with Cur. Additionally, Cur upregulated epithelial proteins (E-cadherin and Occludin) while decreasing the expression of the mesenchymal protein (N-cadherin). In addition, Cur treatment decreases the EGFR/Src signaling pathway in the presence of active Src overexpression. Cur inhibits the proliferation, migration, invasion, epithelial-mesenchymal transition (EMT) by down-regulating EGFR/Src signaling axis, also resulting in coordinated weakening of its downstream regulatory genes, including Akt, STAT3, Bcl2, ERK1/2, among others signal axis (PI3K/Akt signaling pathway).</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241308082"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11663267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142873014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retinol dehydrogenase 10 promotes epithelial-mesenchymal transition in spinal cord gliomas via PI3K/AKT pathway.","authors":"Zijun Zhao, Zihan Song, Zairan Wang, Fan Zhang, Ze Ding, Zongmao Zhao, Liqiang Liu, Tao Fan","doi":"10.1177/03946320241276336","DOIUrl":"10.1177/03946320241276336","url":null,"abstract":"<p><p><b>Background:</b> Spinal cord glioma (SCG), a rare subset of central nervous system (CNS) glioma, represents a complex challenge in neuro-oncology. There has been research showing that Retinol Dehydrogenase 10 (RDH10) may be a tumor promoting factor in brain glioma, but the biological effects of RDH10 remain undefined in SCG. <b>Methods:</b> We performed gene set enrichment analysis (GSEA) and unsupervised clustering analysis to investigate the roles of EMT (epithelial-mesenchymal transition) in glioma. DEG (differently expressed gene) screening and correlation analysis were conducted to filter the candidate genes which were closely associated with EMT process in SCG. Enrichment analysis and GSVA (Gene Set Variation Analysis) were conducted to investigate the potential mechanism of RDH10 for SCG. Trans-well and healing assay were performed to explore the role of RDH10 in the invasion of SCG. Western blotting was performed to evaluate the levels of markers in PI3K-AKT and EMT pathway. In vivo tests were conducted to verify the role of RDH10 in EMT process. <b>Results:</b> Bioinformatic analysis demonstrated the EMT pathway was associated with dismal prognosis of glioma. Further analysis demonstrated that RDH10 showed the strongest correlation with the EMT process. Retinol Dehydrogenase 10 expression was significantly increased in SCG tissues, correlating with advanced tumor grade and unfavorable prognosis. Functional analysis indicated that decreasing RDH10 levels impeded the invasive and migratory abilities of SCG cells, whereas increasing RDH10 levels augmented them. Enrichment analysis and western blot revealed that RDH10 regulated EMT process of SCG by PI3K-AKT pathway. We observed that the enhanced invasion ability and increased EMT-related protein induced by RDH10 overexpression can be suppressed by PI3K-AKT pathway inhibitor (LY294002). <b>Conclusion:</b> Our research found that RDH10 was an effective biomarker associated with tumor grade and prognosis of SCG. RDH10 could regulate EMT process of SCG through PI3K-AKT pathway.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241276336"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11344904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142047351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protocatechuic aldehyde attenuates chondrocyte senescence via the regulation of PTEN-induced kinase 1/Parkin-mediated mitochondrial autophagy.","authors":"Lishi Jie, Xiaoqing Shi, Junfeng Kang, Houyu Fu, Likai Yu, Di Tian, Wei Mei, Songjiang Yin","doi":"10.1177/03946320241271724","DOIUrl":"10.1177/03946320241271724","url":null,"abstract":"<p><p>This study aimed to investigate whether the beneficial effects of PCA on chondrocyte senescence are mediated through the regulation of mitophagy. Chondrocyte senescence plays a significant role in the development and progression of knee osteoarthritis (OA). The compound protocatechuic aldehyde (PCA), which is abundant in the roots of <i>Salvia miltiorrhiza</i>, has been reported to have antioxidant properties and the ability to protect against cellular senescence. To achieve this goal, a destabilization of the medial meniscus (DMM)-induced mouse OA model and a lipopolysaccharide (LPS)-induced chondrocyte senescence model were used, in combination with PINK1 gene knockdown or overexpression. After treatment with PCA, cellular senescence was assessed using Senescence-Associated β-Galactosidase (SA-β-Gal) staining, DNA damage was evaluated using Hosphorylation of the Ser-139 (γH2AX) staining, reactive oxygen species (ROS) levels were measured using Dichlorodihydrofluorescein diacetate (DCFH-DA) staining, mitochondrial membrane potential was determined using a 5,5',6,6'-TETRACHLORO-1,1',3,3'-*. TETRAETHYBENZIMIDA (JC-1) kit, and mitochondrial autophagy was examined using Mitophagy staining. Western blot analysis was also performed to detect changes in senescence-related proteins, PINK1/Parkin pathway proteins, and mitophagy-related proteins. Our results demonstrated that PCA effectively reduced chondrocyte senescence, increased the mitochondrial membrane potential, facilitated mitochondrial autophagy, and upregulated the PINK1/Parkin pathway. Furthermore, silencing PINK1 weakened the protective effects of PCA, whereas PINK1 overexpression enhanced the effects of PCA on LPS-induced chondrocytes. PCA attenuates chondrocyte senescence by regulating PINK1/Parkin-mediated mitochondrial autophagy, ultimately reducing cartilage degeneration.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241271724"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11311163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141908055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Bibliometric and visual analyses of trends in the field of T cell exhaustion research: Findings from 2000 to 2022\".","authors":"","doi":"10.1177/03946320241226506","DOIUrl":"10.1177/03946320241226506","url":null,"abstract":"","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241226506"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10804896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139513920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of the protective effect of coenzyme Q₁₀ on hepatotoxicity caused by acute phosphine poisoning.","authors":"Mohammad Reza Hooshangi Shayesteh, Zahra Hami, Mohsen Chamanara, Mohammad Reza Parvizi, Alireza Golaghaei, Ehsan Nassireslami","doi":"10.1177/03946320241250286","DOIUrl":"10.1177/03946320241250286","url":null,"abstract":"<p><p><i>Background</i>: Aluminum phosphide (AlP) poisoning is prevalent in numerous countries, resulting in high mortality rates. Phosphine gas, the primary agent responsible for AlP poisoning, exerts detrimental effects on various organs, notably the heart, liver and kidneys. Numerous studies have documented the advantageous impact of Coenzyme Q₁₀ (CoQ₁₀) in mitigating hepatic injuries. The objective of this investigation is to explore the potential protective efficacy of CoQ₁₀ against hepatic toxicity arising from AlP poisoning. <i>Method</i>: The study encompassed distinct groups receiving almond oil, normal saline, exclusive CoQ₁₀ (at a dosage of 100 mg/kg), AlP at 12 mg/kg; LD₅₀ (lethal dose for 50%), and four groups subjected to AlP along with CoQ₁₀ administration (post-AlP gavage). CoQ₁₀ was administered at 10, 50, and 100 mg/kg doses via Intraparietal (ip) injections. After 24 h, liver tissue specimens were scrutinized for mitochondrial complex activities, oxidative stress parameters, and apoptosis as well as biomarkers such as aspartate transaminase (AST) and alanine transaminase (ALT). <i>Results</i>: AlP induced a significant decrease in the activity of mitochondrial complexes I and IV, as well as a reduction in catalase activity, Ferric Reducing Antioxidant Power (FRAP), and Thiol levels. Additionally, AlP significantly elevated oxidative stress levels, indicated by elevated reactive oxygen species (ROS) production, and resulted in the increment of hepatic biomarkers such as AST and ALT. Administration of CoQ₁₀ led to a substantial improvement in the aforementioned biochemical markers. Furthermore, phosphine exposure resulted in a significant reduction in viable hepatocytes and an increase in apoptosis. Co-treatment with CoQ₁₀ exhibited a dose-dependent reversal of these observed alterations. <i>Conclusion</i>: CoQ₁₀ preserved mitochondrial function, consequently mitigating oxidative damage. This preventive action impeded the progression of heart cells toward apoptosis.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241250286"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11104032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141065768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phillygenin rescues impaired autophagy flux by modulating the PI3K/Akt/mToR signaling pathway in a rat model of severe acute pancreatitis.","authors":"Jiaxing Li, Jiming Duan, Yiwen Sun, Ruifeng Yang, Hong Yang, Wenxing Li","doi":"10.1177/03946320241309260","DOIUrl":"10.1177/03946320241309260","url":null,"abstract":"<p><p>To investigate the mechanism of pancreatic alveolar cell autophagy in rats with severe acute pancreatitis (SAP) by phillygenin (PHI) based on the PI3K/Akt/mToR pathway. Rats were randomly divided into control group (CON group), SAP model group (SAP group) and PHI treatment group (SAP+PHI group), with 10 rats in each group. 5% sodium taurocholate was injected retrogradely into the biliopancreatic duct to establish a SAP rat model, and PHI was injected intraperitoneally into the pancreas after successful establishment of the model. The colorimetric assay was used to determine serum amylase and lipase activity levels. Pancreatic morphology and histological changes were assessed by H&E staining. Autophagy-related indices were determined by immunohistochemistry: LC3-II, P62, LAMP. Autophagy pathway-related indices were determined by western blotting assay: p-PI3K, PI3K, p-Akt, Akt, p-mToR, mToR. Autophagy vesicle alteration. Compared with the SAP group, the SAP+PHI group showed a decrease in amylase, lipase and pathological score, an increase in the expression of LAMP-2, and a decrease in the expression of p62, p-PI3K, p-Akt and p-mToR, with a statistically significant difference (<i>p</i> < 0.05). Electron microscopy showed that autophagic flux was restored and accumulated autophagic vehicles were relatively reduced by PHI intervention. PHI can rescue the impaired autophagic flux by inhibiting the PI3K/Akt/mToR pathway, allowing abnormal autophagic vesicles to complete autophagy to protect the rat.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"38 ","pages":"3946320241309260"},"PeriodicalIF":3.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11653457/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142839863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study of the possible effect of sacubitril/valsartan combination versus valsartan on the cognitive function in Alzheimer's disease model in rats.","authors":"Abdallah Salah El-Din Hussein,&nbsp;Rahma Kamal El-Din Abou-El Nour,&nbsp;Omayma A Khorshid,&nbsp;Afaf S Osman","doi":"10.1177/03946320231161469","DOIUrl":"https://doi.org/10.1177/03946320231161469","url":null,"abstract":"<p><p><b>Objectives:</b> Alzheimer's disease (AD) is an irreversible, progressive neurodegenerative disorder. The proportion of elderly individuals at risk for AD and cardiovascular problems increases by raising life expectancy. The present study was designed to investigate the effect of the sacubitril/valsartan combination compared to that of valsartan alone in a rat model of AD. <b>Methods:</b> 72 male adult Wistar rats were divided into seven groups; control untreated rats received saline, control valsartan-treated rats received valsartan orally, control sacubitril/valsartan treated rats received sacubitril/valsartan orally, model rats received aluminum chloride i.p., model valsartan treated rats received aluminum chloride i.p. and valsartan orally and model sacubitril/valsartan treated rats received aluminum chloride i.p. and sacubitril/valsartan combination orally. All previous treatments continued on a daily basis for 6 weeks. At the second, fourth, and sixth weeks of the experiment, behavioral changes were evaluated using the Morris water maze and novel object recognition tests, and systolic blood pressure was measured. In the end, rat brain malondialdehyde and amyloid-beta 1-42 levels were measured, and the isolated hippocampus was evaluated histopathologically. <b>Results:</b> Valsartan improved AD symptoms in the aluminum-induced rat model, while the sacubitril/valsartan combination significantly worsened all tested parameters in both control and model rats compared with untreated and valsartan-treated animals. <b>Conclusion:</b> Based on the current study's findings, valsartan did not increase the risk for AD development in control rats and improved AD symptoms in a rat model, while sacubitril/valsartan combination increased the risk of AD in control rats and worsened the condition in a rat model.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"37 ","pages":"3946320231161469"},"PeriodicalIF":3.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ee/17/10.1177_03946320231161469.PMC9996744.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9085070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Down-regulation of S1PR2 is correlated with poor prognosis and immune infiltrates in cervical squamous cell carcinoma and endocervical adenocarcinoma.","authors":"Yu Zhang,&nbsp;Haichuan Wang,&nbsp;Jie Lu,&nbsp;Qiang Lv,&nbsp;Bei Yun,&nbsp;Zhiru Ge,&nbsp;Li Yan","doi":"10.1177/03946320231178131","DOIUrl":"10.1177/03946320231178131","url":null,"abstract":"<p><p><b>Objectives:</b> Cervical squamous cell carcinoma and cervical adenocarcinoma (CESC) are the second leading cause of deaths from malignant tumors in women, while their therapeutic and diagnostic aims are still finited. A growing body of evidence indicated that sphingosine-1-phosphate receptor 2 (S1PR2) plays essential roles in the occurrence and development about several human cancers. Nevertheless, the key mechanism and role mechanism of S1PR2 in CESC are still unclear.<b>Methods:</b> We first used Tissue Expression (GTEx) and Genotypic Cancer Genome Atlas (TCGA) data to perform pan-cancer analysis on the expression and prognosis of S1PR2, and found that S1PR2 may have a potential impact on CESC. To generate a protein-protein interaction (PPI) network using the STRING database. The clusterProfiler package is used for feature-rich analysis. The Tumor IMmune Estimation Resource was used to determine the connection between S1PR2 mRNA expression and immune infiltrates. <b>Results:</b> S1PR2 expression in CESC tissues was down-regulated compared with adjacent normal tissues. Kaplan-Meier analysis indicated that compared with patients with high expression of S1PR2, CESC patients with low S1PR2 expression had a worse prognosis. Reduced S1PR2 expression is associated with patients with high clinical stage, more histological types of squamous cell carcinoma, and poor primary treatment outcomes. The receiver operating characteristic curve of S1PR2 was 0.870. Correlation analysis showed that the mRNA expression of S1PR2 was related to immune infiltrates and tumor purity.<b>Conclusion:</b> Down-regulated S1PR2 expression is related to poor survival and immune infiltration in CESC. S1PR2 is a potential biomarker for poor prognosis and as a potential target for CESC immune therapy.</p>","PeriodicalId":48647,"journal":{"name":"International Journal of Immunopathology and Pharmacology","volume":"37 ","pages":"3946320231178131"},"PeriodicalIF":3.5,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4e/e8/10.1177_03946320231178131.PMC10226337.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9915889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}