JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献

{"title":"iPSCs-derived iMSCs prevent osteoporotic bone loss and affect bone metabolites in ovariectomized mice","authors":"Wei-Zhou Wang,&nbsp;Yang-Hao Wang,&nbsp;Sha-Sha Bao,&nbsp;Fei He,&nbsp;Guoyu Li,&nbsp;Guang Yang,&nbsp;Jing Chen,&nbsp;Xin-Yu Yang,&nbsp;Ya Xiao,&nbsp;Ya-Shuang Tong,&nbsp;Xue-Ting Zhao,&nbsp;Jun Hu,&nbsp;Ding-You You","doi":"10.1111/jcmm.70200","DOIUrl":"https://doi.org/10.1111/jcmm.70200","url":null,"abstract":"<p>Osteoporosis is a metabolic bone disease that seriously jeopardizes the health of middle-aged and elderly people. Mesenchymal stem cell-based transplantation for osteoporosis is a promising new therapeutic strategy. Induced mesenchymal stem cells (iMSCs) are a new option for stem cell transplantation therapy. Acquired mouse skin fibroblasts were transduced and reprogrammed into induced pluripotent cells and further induced to differentiate into iMSCs. The iMSCs were tested for pluripotency markers, trilineage differentiation ability, cell surface molecular marker tests, and gene expression patterns. The iMSCs were injected into the tail vein of mice by tail vein injection, and the distribution of cells in various organs was observed. The effect of iMSCs on the bone mass of mice was detected after injection into the mouse osteoporosis model. The effects of iMSCs infusion on metabolites in femoral tissue and peripheral blood plasma were detected based on LC–MS untargeted metabolomics. iMSCs have similar morphology, immunophenotype, in vitro differentiation potential, and gene expression patterns as mesenchymal stem cells. The iMSCs were heavily distributed in the lungs after infusion and gradually decreased over time. The iMSCs in the femoral bone marrow cavity gradually increased with time. iMSCs infusion significantly avoided bone loss due to oophorectomy. The results of untargeted metabolomics suggest that amino acid and lipid metabolic pathways are key factors involved in iMSCs bone protection and prevention of osteoporosis formation. iMSCs obtained by reprogramming-induced differentiation had cellular properties similar to those of bone marrow mesenchymal stem cells. The iMSCs could promote the remodelling of bone structure in ovariectomy-induced osteoporotic mice and affect the changes of several key metabolites in bone and peripheral blood. Some of these metabolites can serve as potential biomarkers and therapeutic targets for iMSCs intervention in osteoporosis. Investigating the effects of iMSCs on osteoporosis and the influence of metabolic pathways will provide new ideas and methods for the clinical treatment of osteoporosis.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 22","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70200","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142708271","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 and analysis of a cell communication prognostic signature for oral squamous cell carcinoma at bulk and single-cell levels","authors":"Xingwei Zhang,&nbsp;Fan Yang,&nbsp;Chen Dong,&nbsp;Baojun Li,&nbsp;Shuo Zhang,&nbsp;Xiaohui Jiao,&nbsp;Dong Chen","doi":"10.1111/jcmm.70166","DOIUrl":"https://doi.org/10.1111/jcmm.70166","url":null,"abstract":"<p>Head and neck squamous cancer (HNSC) is a heterogenous malignant tumour disease with poor prognosis and has become the current major public health concern worldwide. Oral squamous cell carcinoma (OSCC) is the majority of HNSC. It is still in lack of comprehensive tumour immune microenvironment analysis and prognostic model development for OSCC's clinic practice. Single-cell sequencing data analysis was conducted to identify immune cell subtypes and illustrate cell–cell interaction status in OSCC via R package ‘Seurat’, ‘Harmony’, ‘elldex’ and ‘CellChat’. Base on the bulk sequencing data, WGCNA analysis was employed to identify the CD8⁺ T cell related gene module. XGBoost was used to construct the gene prognostic model for OSCC. Validation sets and immunotherapy data sets were analysed to further evaluate the model's effectiveness and immunotherapy responsiveness predicting potential. siRNA was used to down regulate FCRL4 expression. Real-time PCR and Western blot were used to validate target gene expression. The effects of FCRL4 on OSCC cells were detected by wound healing, Trans well and clone formation assays. Communication between epithelial cells and tissue stem cells may be the potential key regulators for OSCC progression. By integrating single-cell sequencing data analysis and bulk sequencing data analysis, we constructed a novel immune-related gene prognostic model. The model can effectively predict the prognosis and immunotherapy responsiveness of OSCC patients. In addition, the effects of FCRL4 on OSCC cells were validated. We comprehensively interpreted the immune microenvironment pattern of OSCC based on the single-cell sequencing data and bulk sequencing data analysis. A robust immune feature-based prognostic model was developed for the precise treatment and prognosis evaluation of OSCC.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 22","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70166","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142708226","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":"Associations of genetic variation and mRNA expression of PDGF/PDGFRB pathway genes with coronary artery disease in the Chinese population","authors":"Pengfei Wei,&nbsp;Hankun Xie,&nbsp;Junxiang Sun,&nbsp;Qian Zhuang,&nbsp;Jichao Xie,&nbsp;Yunjie Yin,&nbsp;Fangyuan Liu,&nbsp;Wen Li,&nbsp;Changying Chen,&nbsp;Feifan Wang,&nbsp;Xu Han,&nbsp;Liang Xu,&nbsp;Xianghai Zhao,&nbsp;Yanchun Chen,&nbsp;Song Yang,&nbsp;Chong Shen","doi":"10.1111/jcmm.70193","DOIUrl":"10.1111/jcmm.70193","url":null,"abstract":"<p>Platelet-derived growth factors (PDGFs) and receptors (PDGFR) play a key role in the process of coronary atherosclerosis. We aimed to investigate the association of genetic variations and mRNA expressions of PDGF/PDGFRB pathway genes with coronary artery disease (CAD). In this case–control study (3139 CAD vs. 3270 controls), 13 single nucleotide polymorphisms (SNPs) at five pathway genes were genotyped and combined to construct a weighted genetic risk score (wGRS). Three hundred and six pairs of cases and controls were selected for mRNA quantification. Restricted cubic spline (RCS) analyses were conducted for the dose–response relationship between wGRS, mRNAs and CAD. Area under the curve (AUC) was estimated to evaluate the discrimination of wGRS, mRNAs, and traditional risk factors (TRF) for CAD. The wGRS exhibited a positive linear relationship with CAD (<i>p</i> for linearity &lt;0.001), and the medium and high wGRS had 37% and 50% increased risk of CAD compared to the low wGRS group (<i>p</i> = 1.5 × 10⁻⁴; <i>p</i> = 5.7 × 10⁻⁵). mRNA expression levels of five genes in peripheral blood leukocytes were all lower among patients at admission than controls (<i>p</i> &lt; 0.001). The PDGF/PDGFRB mRNA expressions had significant non-linear correlations with AMI, with “U”-shaped trend for <i>PDGFA</i>, <i>PDGFB</i> and “L”-shaped trend for <i>PDGFC</i>, <i>PDGFD</i> and <i>PDGFRB</i>. Adding wGRS and mRNAs to the TRF model significantly improved the discrimination for CAD with an AUC of 0.921 (95% CI, 0.898–0.943). Genetic variations in the PDGF/PDGFRB pathway contribute to CAD susceptibility with a significantly joint effect. The down-regulated PDGF/PDGFRB mRNAs in peripheral leukocytes have the potential as blood-based biomarkers for CAD with high discriminative value.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 22","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11579943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681872","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":"Exploring the Immune Landscape of ccRCC: Prognostic Signatures and Therapeutic Implications","authors":"Minjie Pan,&nbsp;Xinchi Xu,&nbsp;Dong Zhang,&nbsp;Wei Cao","doi":"10.1111/jcmm.70212","DOIUrl":"10.1111/jcmm.70212","url":null,"abstract":"<p>The tumour immunological microenvironment is involved in the development of clear cell renal cell carcinoma (ccRCC). Nevertheless, the role of the immunological microenvironment in ccRCC has not been thoroughly investigated. In this study, we combined six ccRCC cohorts into a large cohort and quantified the expression matrix into 53 immunological terms using the ssGSEA algorithm. Five immune terms related to prognosis were screened through 1000 iterations of L1-penalised (lasso) estimation and Cox regression analysis for immune-related risk score (IRS) calculation. The IRS showed satisfactory prognosis prediction efficacy in ccRCC. We then compared the clinical and genomic characteristics of two IRS subgroups. Patients with low IRS showed a high level of tumour mutational burden (TMB) and a low level of copy number variation (CNV), indicating that low IRS group patients have a higher probability of responding to immunotherapy. We employed TIDE and subclass mapping analyses to corroborate our results, and the findings demonstrated that patients with a low IRS had a significantly greater percentage of immunotherapy response. According to the Genomics of Drug Sensitivity in Cancer (GDSC), patients with a high IRS had a decreased IC50 for sunitinib, which is the first-line treatment for ccRCC patients. As a result, the immune characteristics of the microenvironment of ccRCC tumours have been explored, and a signature has been constructed. Analysis demonstrated that our signature could effectively predict prognosis and immunotherapy response rate.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 22","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11573483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142668104","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 oncogenic functions of SPARCL1 in bladder cancer","authors":"Changjiu Li,&nbsp;Hui Yuan,&nbsp;Jun Chen,&nbsp;Kun Shang,&nbsp;Huadong He","doi":"10.1111/jcmm.70196","DOIUrl":"10.1111/jcmm.70196","url":null,"abstract":"<p>Secreted protein, acidic and rich in cysteine-like 1 (SPARCL1) belongs to the SPARC family of matricellular proteins. However, underlying functions of SPARCL1 in bladder cancer (BCa) remain understudied. We performed an integrated search for the expression patterns of SPARCL1 in relation to various clinicopathological features of BCa. We then carried out Gene Ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and gene set enrichment analysis (GSEA). Furthermore, we investigated the correlations between SPARCL1 and immunological features, such as tumour mutation burden (TMB), immune activation processes, immune checkpoint expression, tumour immune dysfunction and exclusion (TIDE) scores, and chemotherapeutic sensitivity in BCa. Our analysis revealed that SPARCL1 was downregulated across multiple cancers. In BCa, elevated SPARCL1 was linked with advanced histopathologic stage, higher T and N stage, and poorer prognosis in the clinical cohort. In vitro experiments demonstrated that increased SPARCL1 expression inhibited cell proliferation, migration, and invasion. Additionally, highly expressed SPARCL1 was linked to elevated immune, stromal and ESTIMATE scores, as well as an increase in naive B cells, M2 macrophages, and resting mast cells. We observed a moderate correlation between SPARCL1 expression and CD163, VSIG4 and MS4A4A, which are markers of M2 macrophages. Furthermore, SPARCL1 expression was positively related to TMB, immune activation processes, TIDE scores, immune checkpoint expression, and chemotherapeutic sensitivity in BCa. Our study highlights the potential involvement of SPARCL1 in macrophage recruitment and polarization and suggests its utility as a biomarker for prognosis in BCa.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 22","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11567778/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142638724","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":"Repurposing flubendazole for glioblastoma ferroptosis by affecting xCT and TFRC proteins","authors":"Wei Teng,&nbsp;Yuanguo Ling,&nbsp;Niya Long,&nbsp;Wu Cen,&nbsp;Hongzhi Zhang,&nbsp;Lishi Jiang,&nbsp;Jian Liu,&nbsp;Xingwang Zhou,&nbsp;Liangzhao Chu","doi":"10.1111/jcmm.70188","DOIUrl":"10.1111/jcmm.70188","url":null,"abstract":"<p>New uses of old drugs hold great promise for clinical translation. Flubendazole, an FDA-approved antiparasitic drug, has been shown to target p53 and promote apoptosis in glioblastoma (GBM) cells. However, its damaging mechanism in GBM remains elusive. Herein, we explored the ferroptosis-inducing ability of flubendazole on GBM cells. After treating glioma cell lines U251 and LN229 with the flubendazole (DMSO &lt;1‰), cell viability was inhibited in a concentration-dependent manner (IC₅₀ for LN229 = 0.5331 μM, IC₅₀ for U251 = 0.6809 μM), attributed to the induction of ferroptosis, as evidenced by increased MDA levels, accumulation of ROS and lipid peroxides, change in mitochondrial membrane potential and structure. Protein analysis related to ferroptosis showed upregulation of TFRC, DMT1 and p53, alongside downregulation of xCT, FHC and GPX4 (<i>p</i> &lt; 0.05). All-atom docking studies demonstrated that flubendazole bound closely with xCT, and TFRC, validating its role in inducing glioma ferroptosis via modulation of these proteins. Notably, flubendazole could damage the glioblastoma stem cells (GSC) that are typically resistant to other therapies, thereby possessing advantages in stopping glioma recurrence. This study delved into the mechanisms of flubendazole-induced ferroptosis in glioma, broadening its application and providing new ideas for new uses of other old drugs.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 22","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563996/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620266","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":"Esculetin rebalances M1/M2 macrophage polarization to treat sepsis-induced acute lung injury through regulating metabolic reprogramming","authors":"Feng Chen,&nbsp;Ning Wang,&nbsp;Jiabao Liao,&nbsp;Mengxue Jin,&nbsp;Fei Qu,&nbsp;Chengxin Wang,&nbsp;Min Lin,&nbsp;Huantian Cui,&nbsp;Weibo Wen,&nbsp;Fengjuan Chen","doi":"10.1111/jcmm.70178","DOIUrl":"10.1111/jcmm.70178","url":null,"abstract":"<p>Sepsis-induced acute lung injury (SALI) is characterized by a high incidence and mortality rate, which has caused a serious medical burden. The pharmacological effects of esculetin (ELT), such as antibacterial and anti-inflammatory actions, have been widely confirmed. However, the therapeutic effects and mechanisms of ELT on SALI still need to be further clarified. In this study, we first evaluated the therapeutic potential of ELT on a caecal ligation and puncture (CLP) induced septic rat model, particularly in the treatment of acute lung injury. Afterwards, we explored the effect of ELT on macrophage polarization in vivo and in vitro. Then, we investigated the anti-inflammatory mechanism of ELT based on modulating the metabolic reprogramming of macrophage (the effect on glycolysis in M1, and the effect on fatty acid β-oxidation in M2). In addition, macrophage metabolic inhibitors (glycolysis inhibitor: 2-DG, and fatty acid β-oxidation inhibitor: etomoxir) were used to verify the regulatory effect of ELT on macrophage metabolic reprogramming. Our results proved that ELT intervention could effectively improve the survival rate of SALI rats and ameliorate pathological injury. Next, we found that ELT intervention inhibited M1 polarization and promoted M2 polarization of macrophages in vivo and in vitro, including the downregulation of M1-related markers (CD86, iNOS), the decrease of pro-inflammatory factors (nitric oxide, IL-1β, IL-6, and TNF-α), the upregulation of M2-related markers (CD206, ARG-1), the increase of immunomodulatory factors (IL-4 and IL-10). Subsequently, seahorse analysis showed that ELT intervention inhibited the glycolytic capacity in M1, and promoted the ability of fatty acid β-oxidation in M2. Besides, ELT intervention inhibited the level of glycolysis product (lactic acid), and the expression of glycolysis-related genes (<i>Glut1</i>, <i>Hk2</i>, <i>Pfkfb1</i>, <i>Pkm</i> and <i>Ldha</i>) and promoted the expression of fatty acid β-oxidation related genes (<i>Cpt1a</i>, <i>Cpt2</i>, <i>Acox1</i>). In addition, we found that the inhibitory effect of ELT on M1 polarization was comparable to that of 2-DG, while intervention with etomoxir abolished the promoting effect of ELT on M2 polarization. ELT inhibited the inflammatory response in SALI by correcting macrophage polarization (inhibiting M1 and promoting M2). The mechanism of ELT on macrophage polarization was associated with regulating metabolic reprogramming (inhibiting glycolysis in M1 and promoting fatty acid β-oxidation in M2).</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 21","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11558263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621367","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":"Integration analysis using bioinformatics and experimental validation on cellular signalling for sex differences of hypertrophic cardiomyopathy","authors":"Hongyu Kuang,&nbsp;Yanping Xu,&nbsp;Guangliang Liu,&nbsp;Yuhao Wu,&nbsp;Zhiyan Gong,&nbsp;Yuehui Yin","doi":"10.1111/jcmm.70147","DOIUrl":"10.1111/jcmm.70147","url":null,"abstract":"<p>There is a paucity of research examining the molecular mechanisms underlying sex differences of clinical phenotypes and the prognosis in hypertrophic cardiomyopathy (HCM). The dataset GSE36961 was retrieved from Gene Expression Omnibus (GEO) database and comprehensive bioinformatics was employed to identify the core genes linked to sex differences in HCM patients. Additionally, gene set enrichment analysis (GSEA) was conducted to detect downstream signalling pathways. Furthermore, experimental validation was carried out using hearts from spontaneously hypertensive rats (SHRs). A comprehensive analysis revealed the identification of 208 differentially expressed genes (DEGs) in female patients with HCM with a notable downregulation of seven core genes. Notably, there were sex differences in the expression of ras dexamethasone-induced protein 1 (RASD1) and myosin 6 (MYH6) in HCM. Gene ontology (GO) analysis and GSEA demonstrated an enrichment of autophagy-related processes in disease progression in HCM females. Specifically, spearman's correlation analysis revealed a positive correlation between nicotinamide phosphoribosyl transferase (NAMPT) and RASD1 levels, particularly among female patients (<i>R</i> = 0.569, <i>p</i> &lt; 0.001). Additionally, animal models confirmed that cardiac hypertrophy was more pronounced in SHR females compared to males. SHR females exhibited lower mRNA and protein expressions of RASD1 and NAMPT, which were associated with impaired autophagy. In this study, bioinformatics and validation using external data sets and animal models of left ventricular hypertrophy suggested that the RASD1/NAMPT axis is potentially a crucial mechanism underlying the elevated risk of cardiovascular disorders in HCM females, also pointing potentially prognostic biomarkers.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 21","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11558267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621383","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":"Integrated machine learning developed a prognosis-related gene signature to predict prognosis in oesophageal squamous cell carcinoma","authors":"Peng Tang,&nbsp;Baihui Li,&nbsp;Zijing Zhou,&nbsp;Haitong Wang,&nbsp;Mingquan Ma,&nbsp;Lei Gong,&nbsp;Yufeng Qiao,&nbsp;Peng Ren,&nbsp;Hongdian Zhang","doi":"10.1111/jcmm.70171","DOIUrl":"10.1111/jcmm.70171","url":null,"abstract":"<p>The mortality rate of oesophageal squamous cell carcinoma (ESCC) remains high, and conventional TNM systems cannot accurately predict its prognosis, thus necessitating a predictive model. In this study, a 17-gene prognosis-related gene signature (PRS) predictive model was constructed using the random survival forest algorithm as the optimal algorithm among 99 machine-learning algorithm combinations based on data from 260 patients obtained from TCGA and GEO. The PRS model consistently outperformed other clinicopathological features and previously published signatures with superior prognostic accuracy, as evidenced by the receiver operating characteristic curve, C-index and decision curve analysis in both training and validation cohorts. In the Cox regression analysis, PRS score was an independent adverse prognostic factor. The 17 genes of PRS were predominantly expressed in malignant cells by single-cell RNA-seq analysis via the TISCH2 database. They were involved in immunological and metabolic pathways according to GSEA and GSVA. The high-risk group exhibited increased immune cell infiltration based on seven immunological algorithms, accompanied by a complex immune function status and elevated immune factor expression. Overall, the PRS model can serve as an excellent tool for overall survival prediction in ESCC and may facilitate individualized treatment strategies and predction of immunotherapy for patients with ESCC.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 21","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11558266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142636097","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":"RETRACTION: MiR-129-5p Inhibits Glioma Cell Progression In Vitro and In Vivo by Targeting TGIF2","authors":"","doi":"10.1111/jcmm.70174","DOIUrl":"10.1111/jcmm.70174","url":null,"abstract":"<p><b>RETRACTION</b>: Y. Diao, B. Jin, L. Huang, and W. Zhou, “MiR-129-5p Inhibits Glioma Cell Progression In Vitro and In Vivo by Targeting <i>TGIF2</i>,” <i>Journal of Cellular and Molecular Medicine</i> 22, no. 4 (2018): 2357–2367. doi: 10.1111/jcmm.13529.</p><p>The above article, published online on 12 February 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Stefan Constantinescu; The Foundation for Cellular and Molecular Medicine; and John Wiley and Sons Ltd. The retraction has been agreed following an investigation into concerns raised by a third party, which revealed inappropriate duplications of image panels (Figure 4A and 6G) between this and other articles that were either previously published or published later in the same year by different group of authors. Thus, the editors consider the conclusions of this manuscript substantially compromised. The authors and their institute were informed of the concerns and the decision to retract but they remained unresponsive.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"28 21","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620264","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}