Biochemistry and Biophysics Reports最新文献

{"title":"Construction and evaluation of a prognostic model of autophagy-related genes in hepatocellular carcinoma","authors":"Yutao He ,&nbsp;Bin Du ,&nbsp;Weiran Liao ,&nbsp;Wei Wang,&nbsp;Jifeng Su,&nbsp;Chen Guo,&nbsp;Kai Zhang,&nbsp;Zhitian Shi","doi":"10.1016/j.bbrep.2024.101893","DOIUrl":"10.1016/j.bbrep.2024.101893","url":null,"abstract":"<div><h3>Background</h3><div>Hepatocellular carcinoma (HCC) is a globally prevalent disease. Our article evaluates risk models based on autophagy- and HCC-related genes and their prognostic value by bioinformatics analytical methods to provide a scientific basis for clinical treatment.</div></div><div><h3>Methods</h3><div>Prognostic genes were identified by univariate and multivariate Cox analyses, and risk scores were calculated. The value of risk models was analysed by receiver operating characteristic curve (ROC), immune microenvironment and drug sensitivity. Prognostic gene-related regulatory mechanisms based on network database.</div></div><div><h3>Results</h3><div>We screened four prognosis-related genes (SQSTM1, GABARAPL1, CDKN2A, HSPB8) for model construction. The AUC for 1-, 2- and 3-year survival was higher than 0.6 in both the training and validation sets. The nomogram constructed based on risk scores, pathologic_T predicted the outcome better. There were differences in the tumour microenvironment between the high and low risk groups, as evidenced by differences in the distribution of immune cells and differences in the expression of immune checkpoints.</div></div><div><h3>Conclusion</h3><div>Our results illustrate that models, nomograms and risk scores were valuable for tumour progression.</div></div><div><h3>Clinical trial number</h3><div>Not applicable.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101893"},"PeriodicalIF":2.3,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structure/function of ATP sulfurylase domain of human 3′-phosphoadenosine 5′-phosphosulfate synthase (hPAPSS)","authors":"K.V. Venkatachalam ,&nbsp;Dhiraj Sinha ,&nbsp;Chris Soha ,&nbsp;Rudi H. Ettrich","doi":"10.1016/j.bbrep.2024.101892","DOIUrl":"10.1016/j.bbrep.2024.101892","url":null,"abstract":"<div><div>3′-phosphoadenosine 5′-phosphosulfate (PAPS) is synthesized by PAPS synthase (PAPSS) in two steps. In the first step ATP sulfurylase (ATPS) transfers sulfate group onto adenylyl moiety of ATP to form adenosine 5′-phosphosulfate (APS) and PPi. APS-kinase (APSK) then transfers the gamma-phosphoryl from ATP onto 3′-OH of APS to form PAPS and ADP. Mutations of histidine's (H₄₂₅/H₄₂₈) of hPAPSS isoform1 knocked out ATPS and not APSK. <em>In silico</em> ATP binding and molecular dynamics experiments exhibited an unfavorable binding energy for mutant enzymes. Thus, requirements of H₄₂₅NGH₄₂₈ motif for ATPS is established. The N₄₂₆ residue in various organisms is substituted with R. We mutated hPAPSS1 with basic residue K. The N₄₂₆ to K₄₂₆ (N–K) mutant exhibited slightly lower Km (3.7 mM) and higher Vmax (3X) for ATP compared to wildtype (WT, Km 4.3 mM). The Km for sulfate for N–K mutant was nearly same as WT but the Vmax was ∼4X higher for N–K. The catalytic efficiency (Vmax/Km) of N–K was ∼3 fold higher than WT. The full length hPAPSS1 evinced bimodal response against ATP, a paradigm that was deduced to be a trait of PAPSS that requires 2 mol of ATP/PAPS formed. This bimodal kinetics with ATP was lost when the N-terminal APSK was deleted from the C-terminal ATPS domain. The C-terminal domain contained ATPS activity, exhibited Km of 2.2 mM for ATP and Km of 0.53 mM for Sulfate and much higher catalytic efficiency compared to full length hPAPSS1. Thus, fused ATPS-APSK must be structurally and kinetically different than individual domains influenced by inter-domain residues.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101892"},"PeriodicalIF":2.3,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11697783/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142929961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The consequences of climate change and male reproductive health: A review of the possible impact and mechanisms","authors":"R.E. Akhigbe ,&nbsp;P.A. Oyedokun ,&nbsp;T.M. Akhigbe ,&nbsp;M.A. Hamed ,&nbsp;F.B. Fidelis ,&nbsp;A.I. Omole ,&nbsp;A.E. Adeogun ,&nbsp;M.D. Akangbe ,&nbsp;A.A. Oladipo","doi":"10.1016/j.bbrep.2024.101889","DOIUrl":"10.1016/j.bbrep.2024.101889","url":null,"abstract":"<div><div>A global decline in male fertility has been reported, and climate change is considered a major cause of this. Climate change refers to long-term shifts in temperatures and weather patterns, and results from greenhouse gas emissions like carbon dioxide and methane that act as a blanket wrapped around the earth, trapping heat and elevating temperatures. Sad to say, the consequences of climatic variation are beyond the dramatic elevated temperature, they include cold stress, increased malnutrition, air pollution, cardiovascular diseases respiratory tract infections, cancer, sexually transmitted infections, mental stress, and heat waves. These negative effects of climate change impair male reproductive function through multiple pathways, like ROS-sensitive signaling, suppression of steroidogenic markers, and direct damage to testicular cells. The present study aimed to describe the impact of the consequences of climate change on male reproductive health with details of the various mechanisms involved. This will provide an in-depth understanding of the pathophysiological and molecular basis of the possible climatic variation-induced decline in male fertility, which will aid in the development of preventive measures to abate the negative effects of climate change on male reproductive function.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101889"},"PeriodicalIF":2.3,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11664087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An integrated machine learning framework for developing and validating a prognostic risk model of gastric cancer based on endoplasmic reticulum stress-associated genes","authors":"Gang Wei ,&nbsp;Yan Wang ,&nbsp;Ru Liu ,&nbsp;Lei Liu","doi":"10.1016/j.bbrep.2024.101891","DOIUrl":"10.1016/j.bbrep.2024.101891","url":null,"abstract":"<div><h3>Background</h3><div>Gastric cancer (GC), a prevalent and deadly malignancy, demonstrates poor survival outcomes. Evidence has emerged indicating that disruptions in endoplasmic reticulum homeostasis are significantly implicated in the onset and progression of various oncological conditions. This study was designed to construct a prognostic model based on genes related to endoplasmic reticulum stress(ERS) to predict survival outcomes in patients with GC.</div></div><div><h3>Methods</h3><div>Expression profiling data for GC samples were extracted and analyzed from TCGA-STAD, revealing 214 genes related to endoplasmic reticulum stress that show differential expression when compared with normal gastric tissue. Building on these insights, a prognostic model was formulated using data from TCGA-STAD and validated through subsequent analyses of GEO datasets. The tumor immune dysfunction and exclusion(TIDE) algorithm was applied to determine the susceptibility of individuals in high- and low-risk categories to immunotherapy. The presence of immune and stromal cells within the tumor microenvironment was assessed with the aid of the ESTIMATE algorithm. Sensitivity variations to prevalent anticancer drugs between the risk groups were evaluated using the Genomics of Drug Sensitivity in Cancer(GDSC) database, and prospective therapeutic agents were confirmed through molecular docking techniques.</div></div><div><h3>Results</h3><div>Thirty-one endoplasmic reticulum stress (ERS)-related differentially expressed genes (DEGs) crucial for prognosis in GC were pinpointed. These DEGs were then used to construct a prognostic model and were considered as independent prognostic factors for GC patients. This risk model proved to have a good predictive performance for estimating the overall survival of these patients. The patients placed into the high-risk group showed worse results and lower sensitivity to immunotherapy. Moreover, five specific targeted therapy drugs, namely BMS-754807, Dasatinib, JQ1, AZD8055 and SB505124, produced better results in the treatment of the high-risk group of patients.</div></div><div><h3>Conclusions</h3><div>A new molecular prognostic model associated with ERS was established and validated for GC and showed relatively good discriminative and predictive ability. This model greatly expands the collection of weapons in the armoury of prognostic analysis in GC.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101891"},"PeriodicalIF":2.3,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11653156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142852229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of the effect of LMO2 on indicating CD8+ T-lymphocyte infiltration in pan-cancers","authors":"Yanhong Yu ,&nbsp;Mei Yuan ,&nbsp;Zhao Zhang ,&nbsp;Dan Wang ,&nbsp;Wei Sun","doi":"10.1016/j.bbrep.2024.101890","DOIUrl":"10.1016/j.bbrep.2024.101890","url":null,"abstract":"<div><div>LMO2 is a critical factor in hematopoiesis but widely expressed in kinds of epithelia and solid tumors as well, and it has been demonstrated that increased LMO2 level in some tumor cells exhibits an effect on promoting CD8⁺ T-lymphocyte infiltration in tumor microenvironment. Herein we expanded the investigation of such effect in pan-cancer spectrum, and the transcriptome data analysis revealed extensively positive associations between LMO2 and CD8⁺ T-lymphocyte infiltration in pan-cancers. Meanwhile, tissue staining revealed variable expression level and consistently cytosolic localization of LMO2 in different tissues and their tumor counterparts, and further indicated that high LMO2 expression in malignant cells was strongly associated with positive CD8⁺ T-lymphocyte infiltration selectively in digestive tract, breast and kidney tumors. Taken together, this study depicted an overall view of LMO2 functional linkage with tumor immunology in pan-cancers and provided novel insight of LMO2 significance in the field of tumor immune therapy.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101890"},"PeriodicalIF":2.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142757651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The high-risk model associated with SYTL4 predicts poor prognosis and correlates with immune infiltration in AML","authors":"Ke Shi ,&nbsp;Dan Li ,&nbsp;Bo-Hui Peng ,&nbsp;Qiang Guo","doi":"10.1016/j.bbrep.2024.101859","DOIUrl":"10.1016/j.bbrep.2024.101859","url":null,"abstract":"<div><div>Acute myeloid leukemia (AML) currently lacks a definitive cure. Studies have highlighted the involvement of SYTL4 expression levels in neoplasms, yet its specific roles in AML remain unexplored in the literature. Utilizing the TCGA and XENA databases, this study investigated SYTL4 expression levels in AML and identified associations between SYTL4 overexpression and clinicopathological features, prognosis, and immune infiltration in AML patients through genomic analysis. ROC analysis demonstrated the diagnostic value of SYTL4 overexpression in AML. Kaplan-Meier survival, Cox regression, and Lasso analyses were employed to explore SYTL4-coexpressed long non-coding RNAs linked to AML patient prognosis, alongside the construction of nomograms and risk models. SYTL4 expression was significantly elevated in AML and correlated with FAB classification, cytogenetic risk, IDH1 R140 mutation, and NPM1 mutation in cancer patients. SYTL4 overexpression signaled a poor prognosis, serving as a risk indicator for assessing adverse outcomes in AML patients. SYTL4 expression levels also correlated with AML immune cell levels and markers. COX regression analysis revealed that LINC01700, CPNE8-AS1, HOXA10-AS, LINC00899, and SYTL4 influenced adverse AML prognosis. Patients in the high-risk group for these factors experienced significantly poor outcomes, which were closely associated with aDC, CD8 T cells, and TH17 cells. In summary, SYTL4 overexpression is linked to poor prognosis and immune infiltration in AML, with the constructed risk model intended as a prognostic evaluation tool for AML patients.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101859"},"PeriodicalIF":2.3,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142743792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KLF14 inhibits tumor progression via FOSL1 in glioma","authors":"Xiaohua Wang ,&nbsp;Xinjuan Qu ,&nbsp;Xuelai Liu ,&nbsp;Kaiyue Wang ,&nbsp;Yongfang Yang ,&nbsp;Yujuan Zhang ,&nbsp;Zhenguo Wang ,&nbsp;Guangjian Fan ,&nbsp;Yuming Li ,&nbsp;Yuanyuan Zeng ,&nbsp;Hongwei Chen ,&nbsp;Ting Zhu","doi":"10.1016/j.bbrep.2024.101885","DOIUrl":"10.1016/j.bbrep.2024.101885","url":null,"abstract":"<div><h3>Background</h3><div>Glioma, the most frequent central nervous system malignancy, is often promoted by the overexpression of Fos-like antigen 1 (FOSL1). However, the regulation of FOSL1 remains unexplored. The present study aimed to investigate the regulatory mechanism of FOSL1 to identify potential therapeutic targets for glioblastoma.</div></div><div><h3>Methods</h3><div>This study's initial investigation utilized dual-luciferase reporter gene assays and quantitative polymerase chain reaction (qPCR) assays to establish that Kruppel-like factor 14 (KLF14) inhibits the transcription of FOSL1. Subsequent immunohistochemistry and western blotting (WB) assays on glioma tissues confirmed a negative association between FOSL1 and KLF14. This study generated KLF14 knockdown cells and double knockdown cells of KLF14 and FOSL1 and further assessed cell growth through various experimental methods. The impact of KLF14 on tumor cell migration via FOSL1 was determined using qPCR and WB assays. A xenograft tumor model was utilized to verify tumor growth suppression by KLF14.</div></div><div><h3>Results</h3><div>The present study demonstrated that KLF14 restrains FOSL1 transcription and is inversely correlated with FOSL1 in glioma tissues. KLF14 overexpression was found to counteract FOSL1's effect on cell migration and epithelial-to-mesenchymal transition in glioma cells, which coincided with decreased Snail2 and cluster of differentiation 44 (CD44) expressions. Further, KLF14 overexpression was shown to hinder tumor progression in vivo.</div></div><div><h3>Conclusion</h3><div>This study highlights that FOSL1 is negatively regulated by KLF14 in glioblastoma and suggests that KLF14 overexpression can mitigate tumor growth by inhibiting FOSL1, thus identifying KLF14 as a novel molecular target for treating glioblastoma. Further research into the interplay and regulatory dynamics between KLF14 and FOSL1 under varying stress conditions can enhance the precision of glioblastoma treatment.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101885"},"PeriodicalIF":2.3,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142719775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of calcium ions on the aggregation of highly phosphorylated tau","authors":"Toru Tanaka ,&nbsp;Sachiyo Ohashi ,&nbsp;Akihiko Takashima ,&nbsp;Shunsuke Kobayashi","doi":"10.1016/j.bbrep.2024.101887","DOIUrl":"10.1016/j.bbrep.2024.101887","url":null,"abstract":"<div><div>Tau is typically an axonal protein, but in neurons of brains affected by Alzheimer's disease (AD), aggregation of hyperphosphorylated tau in the somatodendritic compartment causes neuronal death. We have previously demonstrated that tau mRNA is transported within dendrites and undergoes immediate translation and hyperphosphorylation of AD epitopes in response to NMDA receptor stimulation. Although this explains the emergence of hyperphosphorylated tau in dendrites, the relationship between tau hyperphosphorylation and aggregation is not well understood. In this study, we found that recombinant highly phosphorylated tau purified from NG108-15 rodent neuroblastoma/glioma cells transfected with both tau and GSK3β expression vectors bound calcium ions and formed sarkosyl-insoluble aggregates. In addition, thioflavin T analysis revealed that this highly phosphorylated tau tended to aggregate on its own, further facilitated by calcium ions. When NG108-15 cells expressing the highly phosphorylated tau were treated with calcium ionophore, sarkosyl-insoluble tau was generated. Interestingly, these cells exhibited resistance to both calcium ionophore-induced cytotoxicity and glutamate-induced excitotoxicity. We further found that sarkosyl-insoluble phosphorylated tau was increased in cultured hippocampal neurons due to glutamate-induced hyperactivity. Our data suggest that hyperphosphorylated tau synthesized in response to NMDA receptor stimulation contributes to regulation of neuronal activity by binding calcium ions, but that this calcium binding may cause tau to adopt an aggregated form.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101887"},"PeriodicalIF":2.3,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cyclosporine and fedratinib combination therapy via modulating Th17/Treg balance in Rat model of membranous glomerulonephritis","authors":"Ali Ghassabi ,&nbsp;Maryam Hosseini ,&nbsp;Hemayat Abdoli Goungormaz ,&nbsp;Mohammad Sadegh Soltani-Zangbar ,&nbsp;Mahsa Beomidehagh ,&nbsp;Davoud Rostamzadeh ,&nbsp;Mohammadbagher Pirouzpanah ,&nbsp;Arshad Ghaffari-Nasab ,&nbsp;Arash Khaki ,&nbsp;Leili Aghebati-Maleki ,&nbsp;Elham Badihi ,&nbsp;Farshid Afandideh ,&nbsp;Reihane Shahabirad ,&nbsp;Ali Akbar Shekarchi ,&nbsp;Javad Ahmadian Heris ,&nbsp;Leila Roshangar ,&nbsp;Jalal Etemadi ,&nbsp;Mehdi Yousefi","doi":"10.1016/j.bbrep.2024.101874","DOIUrl":"10.1016/j.bbrep.2024.101874","url":null,"abstract":"<div><div>A progressive kidney disease associated with inflammation and the immune system is called membrane glomerulonephritis (MGN). The present study investigatedthe combination of cyclosporine and fedratinib on Th17/regulatory T cells (Tregs) in rat models of MGN. Rats were given several doses of anti-Fx1A to induce MGN, and the resultant five groups of rats were fedratinib-cyclosporin receiving PHN rats, fedratinib, cyclosporin, and healthy rats. Following that, the blood's biochemistry was ascertained, and splenocytes were separated to use flow cytometry to look into the proportion of Th17 and Treg cells in the blood. A real-time PCR test was used to assess the corresponding Tregs and Th17 cell transcription factors andtheir related cytokine gene expressions. Finally, serum analysis was employed to indicate serum cytokines signatures of Th17 cells and Tregs through ELISA. The combination of cyclosporine-fedratinib induced noticeably diminished levels of serum total protein, albumin, and urea in rats versus the PHN group. Th17 cell frequency and its related transcription factors and cytokines genes showed increased expression in the PHN model compared to the control group and PHN groups with different treatments.</div><div>In contrast, Tregs frequency and its related transcription factors and cytokines genes showed decreased expression in the PHN model compared to the control group and PHN groups with different treatments. Serum cytokine assay confirmed gene expression results. The combination of cyclosporine and fedratinib was capable of reducing Th17 cells in favor of Tregs enhancement in PHN rats, suggesting a novel combination therapy in the treatment of MGN.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101874"},"PeriodicalIF":2.3,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of gastric cancer biomarkers through in-silico analysis of microarray based datasets","authors":"Arbaz Akhtar ,&nbsp;Yasir Hameed ,&nbsp;Samina Ejaz ,&nbsp;Iqra Abdullah","doi":"10.1016/j.bbrep.2024.101880","DOIUrl":"10.1016/j.bbrep.2024.101880","url":null,"abstract":"<div><div>Gastric cancer is among the most prevalent cancers worldwide including in Pakistan. Late diagnosis of gastric cancer leads to reduced survival. The present study aimed to investigate biomarkers for early diagnosis and prognosis of gastric cancer. For this purpose, the ten microarray-based gene expression datasets (GSE54129, GSE79973, GSE161533, GSE103236, GSE33651, GSE19826, GSE118916, GSE112369, GSE13911, and GSE81948) were retrieved from GEO database and analyzed by GEO2R to identify differentially expressed genes. Datasets were arranged in subsets of different dataset combinations to identify common DEGs. The gene ontology and functional pathway enrichment analysis of common DEGs was performed by DAVID tool. Pan-cancer analysis was conducted by UALCAN database. Survival analysis of common DEGs was done by Kaplan-Meier plotter. A total of 71 common DEGs were identified in different combinations of datasets. Among them, only 5 DEGs namely ATP4B, ATP4A, CCKBR, KCNJ15, and KCNJ16 were detected to be common in all the datasets. The GO and pathway analysis represented that the identified DEGs are involved in gastric acid secretion and collecting duct acid secretion pathways. Further expression validation of these five genes using three additional datasets (GSE31811, GSE26899, and GSE26272) confirmed their differential expression in gastric cancer samples. The pan-cancer analysis also revealed aberrant expression of DEGs in various cancers. The survival analysis showed the association of these 5 DEGs with poor survival of gastric cancer patients. To conclude, this study revealed a panel of 5 genes, which can be employed as diagnostic and prognostic biomarkers of gastric cancer patients.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"40 ","pages":"Article 101880"},"PeriodicalIF":2.3,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142699922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}