Experimental cell research最新文献

{"title":"Dual role of microRNA-31 in human cancers; focusing on cancer pathogenesis and signaling pathways","authors":"Paul Rodrigues ,&nbsp;Jasur Alimdjanovich Rizaev ,&nbsp;Ahmed Hjazi ,&nbsp;Farag M.A. Altalbawy ,&nbsp;Malathi H ,&nbsp;Kirti Sharma ,&nbsp;Satish Kumar Sharma ,&nbsp;Yasser Fakri Mustafa ,&nbsp;Mohammed Abed Jawad ,&nbsp;Ahmed Hussein Zwamel","doi":"10.1016/j.yexcr.2024.114236","DOIUrl":"10.1016/j.yexcr.2024.114236","url":null,"abstract":"<div><p>Widespread changes in the expression of microRNAs in cancer result in abnormal gene expression for the miRNAs that control those genes, which in turn causes changes to entire molecular networks and pathways. The frequently altered miR-31, which is found in a wide range of cancers, is one cancer-related miRNA that is particularly intriguing. MiR-31 has a very complicated set of biological functions, and depending on the type of tumor, it may act both as a tumor suppressor and an oncogene. The endogenous expression levels of miR-31 appear to be a key determinant of the phenotype brought on by aberrant expression. Varied expression levels of miR-31 could affect cell growth, metastasis, drug resistance, and other process by several mechanisms like targeting BRCA1-associated protein-1 (BAP1), large tumor suppressor kinase 1 (LATS1) and protein phosphatase 2 (PP2A). This review highlights the current understanding of the genes that miR-31 targets while summarizing the complex expression patterns of miR-31 in human cancers and the diverse phenotypes brought on by altered miR-31 expression.</p></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"442 2","pages":"Article 114236"},"PeriodicalIF":3.3,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased m6A RNA methylation and METTL3 expression may contribute to the synovitis progression of rheumatoid arthritis","authors":"Yazhen Su ,&nbsp;Zewen Wu ,&nbsp;Yang Liu ,&nbsp;Xinling Liu ,&nbsp;Jie Kang ,&nbsp;Junqing Jia ,&nbsp;Liyun Zhang","doi":"10.1016/j.yexcr.2024.114237","DOIUrl":"10.1016/j.yexcr.2024.114237","url":null,"abstract":"<div><h3>Objective</h3><p>Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial hyperplasia and progressive bone destruction. The tumor-like growth of fibroblast-like synoviocytes (FLSs) plays a crucial role in the pathogenesis of RA. The N6 methyladenine (m6A) mRNA methylation modification, regulated by methyltransferases (METTL3) and demethylation enzymes, is a novel epigenetic regulator in the development of RA. However, there is limited research on m6A methylation modifications in RA synovitis and a lack of mechanistic studies on their impact on the function of RA-FLSs.</p></div><div><h3>Methods</h3><p>This study utilized clinical synovial tissue specimens and FLSs as research subjects. The m6A methylation level and the expression of methyltransferases and demethylation enzymes were detected. RNA interference and gene overexpression methods were employed to investigate the mechanism of METTL3 in RA-FLSs. The study also examined the proliferation, apoptosis, migration, invasion, and cytokine levels of RA-FLSs, as well as the expression of METTL3 in RA animal models.</p></div><div><h3>Results</h3><p>In this study, we found that m6A methylation levels were elevated in synovial tissues and FLSs of RA patients. Immunohistochemical staining showed that METTL3 and METTL14 levels were up-regulated in synovial tissues of RA, the mRNA levels of <em>METTL3</em>, <em>METTL14</em>, <em>WTAP</em>, <em>FTO</em>, and <em>ALKBH5</em> were significantly higher in synovial tissues and FLSs of RA patients. Overexpression of METTL3 could promote the proliferation, migration, and secretion of IL-6, RANKL of RA-FLSs; inhibition of METTL3 expression could inhibit the abnormal proliferation, migration, invasion, and secretion of IL-6, RANKL, at the same time promoted the apoptosis and secretion of OPG, thus inhibited RA-FLSs tumor-like growth. In CIA mice, the use of MTX and STM2457 reduced METTL3 expression, synovial hyperplasia and bone destruction.</p></div><div><h3>Conclusion</h3><p>Abnormal modification of m6A methylation exists in synovial tissues and FLSs of RA patients, and inhibition of METTL3 can reduce synovitis and bone destruction. Our findings suggest that m6A methylation might control FLS-mediated tumor-like phenotype, and be a novel target for RA treatment.</p></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"442 2","pages":"Article 114237"},"PeriodicalIF":3.3,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014482724003288/pdfft?md5=26b849d4a271c3e174cbd9949c4bcd58&pid=1-s2.0-S0014482724003288-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142153526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deubiquitinase USP18 inhibits hepatic stellate cells activation and alleviates liver fibrosis via regulation of TAK1 activity","authors":"Yan Zhang ,&nbsp;Jing Gao ,&nbsp;Yi Liu,&nbsp;Li Zhong,&nbsp;Song He,&nbsp;Chan Qiu","doi":"10.1016/j.yexcr.2024.114235","DOIUrl":"10.1016/j.yexcr.2024.114235","url":null,"abstract":"<div><h3>Background &amp; aims</h3><p>Activation of hepatic stellate cells (HSCs) is the key process underlying liver fibrosis. Unveiling its molecular mechanism may provide an effective target for inhibiting liver fibrosis. Protein ubiquitination is a dynamic and reversible process. Deubiquitinases (DUBs) catalyze the removal of ubiquitin chains from substrate proteins, thereby inhibiting the biological processes regulated by ubiquitination signals. However, there are few studies revealing the role of deubiquitination in the activation of HSCs.</p></div><div><h3>Methods &amp; results</h3><p>Single-cell RNA sequencing (scRNA-seq) revealed significantly decreased USP18 expression in activated HSCs when compared to quiescent HSCs. In mouse primary HSCs, continuous activation of HSCs led to a gradual decrease in USP18 expression whilst restoration of USP18 expression significantly inhibited HSC activation. Injection of USP18 lentivirus into the portal vein of a CCl₄-induced liver fibrosis mouse model confirmed that overexpression of USP18 can significantly reduce the degree of liver fibrosis. In terms of mechanism, we screened some targets of USP18 in mouse primary HSCs and found that USP18 could directly bind to TAK1. Furthermore, we demonstrated that USP18 can inhibit TAK1 activity by interfering with the K63 ubiquitination of TAK1.</p></div><div><h3>Conclusions</h3><p>Our study demonstrated that USP18 inhibited HSC activation and alleviated liver fibrosis via modulation of TAK1 activity; this may prove to be an effective target for inhibiting liver fibrosis.</p></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"442 2","pages":"Article 114235"},"PeriodicalIF":3.3,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The miRNA Landscape in Crohn's disease: Implications for novel therapeutic approaches and interactions with Existing therapies","authors":"Hebatallah Ahmed Mohamed Moustafa ,&nbsp;Elsayed G.E. Elsakka ,&nbsp;Ahmed I. Abulsoud ,&nbsp;Shereen Saeid Elshaer ,&nbsp;Ahmed A. Rashad ,&nbsp;Walaa A. El-Dakroury ,&nbsp;Al-Aliaa M. Sallam ,&nbsp;Nehal I. Rizk ,&nbsp;Mohamed Bakr Zaki ,&nbsp;Rania M. Gomaa ,&nbsp;Ahmed E. Elesawy ,&nbsp;Osama A. Mohammed ,&nbsp;Sherif S. Abdel Mageed ,&nbsp;Ali M.S. Eleragi ,&nbsp;Jasmine A. ElBoghdady ,&nbsp;Shaimaa H. El-Fayoumi ,&nbsp;Mustafa Ahmed Abdel-Reheim ,&nbsp;Ahmed S. Doghish","doi":"10.1016/j.yexcr.2024.114234","DOIUrl":"10.1016/j.yexcr.2024.114234","url":null,"abstract":"<div><p>MicroRNAs (miRNAs), which are non-coding RNAs consisting of 18–24 nucleotides, play a crucial role in the regulatory pathways of inflammatory diseases. Several recent investigations have examined the potential role of miRNAs in forming Crohn's disease (CD). It has been suggested that miRNAs serve as diagnostics for both fibrosis and inflammation in CD due to their involvement in the mechanisms of CD aggravation and fibrogenesis. More information on CD pathophysiology could be obtained by identifying the miRNAs concerned with CD and their target genes. These findings have prompted several in vitro and in vivo investigations into the putative function of miRNAs in CD treatment. Although there are still many unanswered questions, the growing body of evidence has brought miRNA-based therapy one step closer to clinical practice. This extensive narrative study offers a concise summary of the most current advancements in CD. We go over what is known about the diagnostic and therapeutic benefits of miRNA mimicry and inhibition so far, and we see what additional miRNA family targets could be useful for treating CD-related inflammation and fibrosis.</p></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"442 2","pages":"Article 114234"},"PeriodicalIF":3.3,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142132263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NRF2 inhibits RSL3 induced ferroptosis in gastric cancer through regulation of AKR1B1","authors":"Xin Li ,&nbsp;Jianxin Qian ,&nbsp;Jiahua Xu ,&nbsp;Haoran Bai ,&nbsp;Jinzu Yang ,&nbsp;Ling Chen","doi":"10.1016/j.yexcr.2024.114210","DOIUrl":"10.1016/j.yexcr.2024.114210","url":null,"abstract":"<div><p>Gastric cancer is a malignant tumor associated with a high mortality rate. Recently, emerging evidence has shown that ferroptosis, a regulated form of cell death induced by iron (Fe)-dependent lipid peroxidation. Nuclear factor E2 related factor 2 (NRF2) is a key regulator of intracellular oxidation homeostasis that plays a pivotal role in controlling lipid peroxidation, which is closely related to the process of ferroptosis. However, the molecular mechanism of NRF2 on ferroptosis remains to be investigated in gastric cancer. In our study, NRF 2 was found to transcriptionally activate Aldo-keto reductase 1 member B1 (AKR1B1) expression in gastric cancer. AKR1B1 is involved in the regulation of lipid metabolism by removing the aldehyde group of glutathione. We found that AKR1B1 is highly expressed in gastric cancer and is associated with a poor prognosis of the patients. In vitro experiments found that AKR1B1 has the ability to promote the proliferation and invasion of gastric cancer cells. AKR1B1 inhibited RSL3-induced ferroptosis in gastric cancer by reducing reactive oxygen species accumulation and lipid peroxidation, as well as decreasing intracellular ferrous ion and malondialdehyde expression and increasing glutathione expression. Our study demonstrated that AKR1B1 resisted RSL3-induced ferroptosis by regulating GPX4, PTGS2 and ACSL4, which was further demonstrated in a xenograft nude mouse model. Our work reveals a critical role for the AKR1B1 in the resistance to RSL3-induced ferroptosis in gastric cancer.</p></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"442 1","pages":"Article 114210"},"PeriodicalIF":3.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141999668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hemin-induced reactive oxygen species triggers autophagy-dependent macrophage differentiation and pro-inflammatory responses in THP-1 cells","authors":"Pramita Chowdhury ,&nbsp;Priyanka Dey Talukdar ,&nbsp;Pritha Mukherjee ,&nbsp;Debangana Dey ,&nbsp;Urmi Chatterji ,&nbsp;Sanghamitra Sengupta","doi":"10.1016/j.yexcr.2024.114216","DOIUrl":"10.1016/j.yexcr.2024.114216","url":null,"abstract":"<div><p>The toxic effect of oxidized-heme, also known as hemin, is implicated in developing adverse clinical outcome in various hematolytic diseases. To simulate and reconstruct the molecular events associated with hemin exposure on circulating monocytes, we employed a THP-1 cell line based <em>in vitro</em> model. Flow cytometry and Western blot analyses were subsequently applied. Hemin-treated THP-1 produced ROS in a dose-dependent manner which resulted in 10–30 % of cell death primarily through apoptosis. Surviving cells induced autophagy which too was ROS-dependent, as revealed by application of N-acetyl-L-cysteine. Hemin-mediated autophagy promoted differentiation of CD14⁺ THP-1 cells into CD11b⁺ macrophages. Application of 3-methyladenine, reinforced that differentiation of THP-1 was an autophagy-dependent process. It was revealed that despite a higher polarization towards M2-macrophage, synthesis of pro-inflammatory cytokines namely TNF-α, IL-1A, IL-2, IL-8 and IL-17A predominated. IL-6, a pleiotropic cytokine, was also elevated. It may thus be surmised that hemin-induced pro-inflammatory response in THP-1 is downstream to ROS-dependent autophagy and monocyte differentiation. This finding is translationally meaningful as hemin is already approved by FDA for amelioration of acute porphyria and is actively considered as a therapeutic agent for other diseases. This study underscores the need of further research untangling the reciprocal regulation of inflammatory signaling and autophagy under oxidative stress.</p></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"442 1","pages":"Article 114216"},"PeriodicalIF":3.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing of lncRNA NEAT1 alleviates acute myocardial infarction by suppressing miR-450–5p/ACSL4-mediated ferroptosis","authors":"Qiuting Yu ,&nbsp;Yuxue Li ,&nbsp;Ning Zhang,&nbsp;Jun Lu,&nbsp;Xiaowen Gan,&nbsp;Linglin Chen,&nbsp;Ronggan Liang,&nbsp;Jie Jian","doi":"10.1016/j.yexcr.2024.114217","DOIUrl":"10.1016/j.yexcr.2024.114217","url":null,"abstract":"<div><p>Ferroptosis is principally initiated by dysregulation of iron metabolism and excessive accumulation of ROS, which exacerbates myocardial injury during acute myocardial infarction (AMI). Previous studies have indeed demonstrated the significant involvement of long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) exerts its pleiotropic effects in the pathophysiology of myocardial infarction, heart failure and atherosclerosis by modulating inflammation, apoptosis, and oxidative stress. However, whether and how NEAT1 mediates myocardial ferroptosis remain unknown. In this study, we found that NEAT1 expression was significantly elevated in hypoxic HL-1 cells and AMI mice, while silencing of NEAT1 alleviated lipid peroxidation and myocardial ferroptosis both <em>in vitro</em> and <em>in vivo</em>. Mechanistically, NEAT1 directly sponged miR-450b-5p and negatively regulated its expression. In addition, miR-450b-5p directly targeted Acyl-CoA synthase long-chain family member 4 (ACSL4). Notably, inhibition of miR-450b-5p reversed the role of NEAT1 in AMI mice. Collectively, these findings newly illustrated that NEAT1 acts as a competitive endogenous RNA (ceRNA) of miR-450–5p in AMI. Especially, silencing of NEAT1 effectively ameliorated myocardium ischemia by suppression of ferroptosis <em>via</em> miR-450–5p/ACSL4 pathway, which providing a brand-new therapeutic strategy for myocardial ischemia injury.</p></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"442 2","pages":"Article 114217"},"PeriodicalIF":3.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014482724003082/pdfft?md5=894052ae35499039ef9f9aadf207a6e2&pid=1-s2.0-S0014482724003082-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL5 enhances the mRNA stability of TPRKB through m6A modification to facilitate the aggressive phenotypes of hepatocellular carcinoma cell","authors":"Ming Luo ,&nbsp;Xiong Luo ,&nbsp;Jichun Sun ,&nbsp;Xiang Ao ,&nbsp;Haoyan Han ,&nbsp;Xin Yang","doi":"10.1016/j.yexcr.2024.114219","DOIUrl":"10.1016/j.yexcr.2024.114219","url":null,"abstract":"<div><p>N6-methyladenosine (m⁶A) modification plays an important role in RNA molecular functions, therefore affecting the initiation and development of hepatocellular carcinoma (HCC). Herein, multiple datasets were applied to conduct a comprehensive analysis of DEGs within HCC and the analysis revealed significant dysregulation of numerous genes. Functional and signaling pathway enrichment analyses were performed. Further, TP53RK binding protein (TPRKB) emerged as a significant factor, exhibiting high expression level within HCC tissue samples and cells which could predict HCC patients’ poor OS. Knockdown investigations of TPRKB <em>in vitro</em> demonstrated the effect of TPRKB knockdown on attenuating the aggressiveness of HCC cells by suppressing the viability, colony formation, invasive ability, and migratory ability, inducing cell cycle arrest, and facilitating the apoptosis of HCC cells. Investigations <em>in vivo</em> revealed that TPRKB knockdown significantly suppressed tumor growth in mice model. Additionally, the study identified methyltransferase 5, N6-adenosine (METTL5) as a potential regulator of TPRKB expression via m⁶A modification, positively regulating TPRKB expression by enhancing TPRKB mRNA stability. The dynamic effects of METTL5 and TPRKB upon the phenotypes of HCC cells further confirmed that TPRKB overexpression partially abolished the anti-cancer effects of METTL5 knockdown upon the aggressiveness of HCC cells. Conclusively, our findings uncover that TPRKB, significantly overexpressed in HCC, exerts a critical effect on promoting tumor aggressiveness, and its expression shows to be positively regulated by METTL5 via m⁶A methylation. These insights deepen the understanding of HCC pathogenesis and open new avenues for targeted therapies, highlighting that METTL5-TPRKB axis is an underlying new therapeutic target in HCC management.</p></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"442 1","pages":"Article 114219"},"PeriodicalIF":3.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AGR2 facilitates teratoma progression by regulating glycolysis via the AnXA2/EGFR axis","authors":"Yahong Zhang ,&nbsp;Jing Zhang","doi":"10.1016/j.yexcr.2024.114228","DOIUrl":"10.1016/j.yexcr.2024.114228","url":null,"abstract":"<div><p>Anterior gradient-2 (AGR2) is highly expressed in several tumors and plays an important role in tumor development. However, the biological function of AGR2 in teratomas has not yet been thoroughly studied. In this study, AGR2 was found to be upregulated in teratoma tissues and in human testicular teratoma cell lines by Western blotting and qRT-PCR assays. A DNA Methylation-Specific PCR assay demonstrated that AGR2 upregulation resulted from hypomethylated AGR2 in teratoma cells. NCC-IT and NT2-D1 cells were transfected with pcDNA-AGR2 or sh-AGR2 to obtain AGR2-overexpressed or -silenced cells, and cell proliferation, invasion and glycolysis were determined using CCK-8, 5-ethynyl-2′-deoxyuridine (EdU), Transwell assays, and commercial kits. The results revealed that overexpression of AGR2 promoted teratoma cell proliferation and invasion and elevated glycolysis levels evidencing by the increase in lactate secretion, glucose consumption, ATP levels and the expression of glycolysis-related proteins, while knockdown of AGR2 showed the opposite results. The interactions between AGR2 and annexin A2 (AnXA2), as well as between AnXA2 and epidermal growth factor receptor (EGFR) were verified by co-immunoprecipitation assay. Mechanistic studies revealed that AGR2 interacts with AnXA2 and increases the level of AnXA2 to recruit more AnXA2 to EGFR, there by promoting EGFR expression. A series of rescue experiments showed that knockdown of AnXA2 or EGFR weakened the promotional effects of AGR2 overexpression on the proliferation, invasion, and glycolysis of teratoma cells. Finally, tumorigenicity assays were performed using NT2-D1 cells stably transfected with either LV-NC-shRNA or LV-shAGR2. The results showed that AGR2 knockdown significantly inhibited teratoma tumor growth <em>in vivo</em>. In conclusion, our data suggested that AGR2 facilitates glycolysis in teratomas through promoting EGFR expression by interacting with AnXA2, thereby promoting teratoma cells proliferation and invasion.</p></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"442 1","pages":"Article 114228"},"PeriodicalIF":3.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142092570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “High expression of enhancer RNA MARC1 or its activation by DHT is associated with the malignant behavior in bladder cancer” [Exp. Cell Res. Volume 370, Issue 2, 15 September 2018, Pages 303-311]","authors":"Yuhan Liu ,&nbsp;Mengting Ding ,&nbsp;Xinhui Liao ,&nbsp;Qunjun Gao ,&nbsp;Anbang He ,&nbsp;Baoer Liu ,&nbsp;Kun Hu ,&nbsp;Haibiao Xie ,&nbsp;Qun Zhou ,&nbsp;Hengji Zhan ,&nbsp;Yuchen Liu ,&nbsp;Weiren Huang ,&nbsp;Hongbing Mei","doi":"10.1016/j.yexcr.2024.114223","DOIUrl":"10.1016/j.yexcr.2024.114223","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"442 1","pages":"Article 114223"},"PeriodicalIF":3.3,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0014482724003148/pdfft?md5=12aa5fb6d3feacf98b1bc4a1275b8223&pid=1-s2.0-S0014482724003148-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142097745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}