JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献

{"title":"Anticancer Effects of MAPK6 siRNA-Loaded PLGA Nanoparticles in the Treatment of Breast Cancer","authors":"Ceyhun Toruntay,&nbsp;Fatma Sayan Poyraz,&nbsp;Seda Susgun,&nbsp;Emrah Yucesan,&nbsp;Banu Mansuroglu","doi":"10.1111/jcmm.70309","DOIUrl":"10.1111/jcmm.70309","url":null,"abstract":"<p>siRNA-loaded nanoparticles open new perspectives for cancer treatment. <i>MAPK6</i> is upregulated in breast cancer and is involved in cell growth, differentiation and cell cycle regulation. Herein, we aimed to investigate the anticancer effects of <i>MAPK6</i> knockdown by using MAPK6 siRNA-loaded PLGA nanoparticles (siMAPK6-PLGA-NPs) in MCF-7 breast cancer cells. After the synthesis and characterisation of nanoparticles, treatment concentrations were determined with cytotoxicity assay. Subsequently, <i>MAPK6</i> knockdown and anticancer effects of siMAPK6-PLGA-NPs were evaluated by in vitro assays. siMAPK6-PLGA-NPs have been determined to suppress <i>MAPK6</i> expression efficiently. In vitro studies revealed that siMAPK6-PLGA-NPs significantly reduced the migration, proliferation and colony-forming ability and enhanced the apoptosis in MCF-7 cells. Taken together, siMAPK6-PLGA-NPs exhibited robust and promising anticancer effects against MCF-7 cells. Our findings demonstrated that siRNA-loaded PLGA nanoparticles have great potential for breast cancer treatment and <i>MAPK6</i> gene may be the therapeutic target in breast cancer.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 2","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11740982/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006028","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":"Hypoxia Combined With Interleukin-17 Regulates Hypoxia-Inducible Factor-1α/Endothelial Nitric Oxide Synthase Expression in Pulmonary Artery Endothelial Cells","authors":"Shuai Sun,&nbsp;Jianjun Mao,&nbsp;Yuan Ding,&nbsp;Lin Liu,&nbsp;Juanni Gong,&nbsp;Suqiao Yang,&nbsp;Jifeng Li,&nbsp;Tuguang Kuang,&nbsp;Ran Miao,&nbsp;Yuanhua Yang","doi":"10.1111/jcmm.70289","DOIUrl":"10.1111/jcmm.70289","url":null,"abstract":"<p>The pathogenesis of chronic thromboembolic pulmonary hypertension may be multifactorial and requires further studies. We explored alterations in pulmonary artery endothelial cells under the hypoxic and elevated interleukin-17 conditions that are commonly present in patients with chronic thromboembolic pulmonary hypertension. We measured the serum interleukin-17 levels in 10 chronic thromboembolic pulmonary hypertension patients and 10 healthy control persons. The expressions and localisations of hypoxia-inducible factor-1α and endothelial nitric oxide synthase were detected in tissues. The levels of hypoxia-inducible factor-1α, endothelial nitric oxide synthase, nitric oxide, and reactive oxygen species in cultured pulmonary artery endothelial cells were examined under hypoxia and/or interleukin-17 treatment. The serum interleukin-17 level was increased in chronic thromboembolic pulmonary hypertension patients. Hypoxia-inducible factor-1α was increased, and endothelial nitric oxide synthase was decreased in chronic thromboembolic pulmonary hypertension pulmonary vascular tissue. After receiving the hypoxia combined with interleukin-17 treatment, pulmonary artery endothelial cells showed increased levels of hypoxia-inducible factor-1α and phospho-endothelial nitric oxide synthase (Thr495) (<i>p</i> = 0.001 and 0.063, respectively) and a decreased level of endothelial nitric oxide synthase (<i>p</i> &lt; 0.001). In addition, the nitric oxide level was significantly decreased (<i>p</i> = 0.001), whereas the reactive oxygen species level was insignificantly increased in pulmonary artery endothelial cells. Chronic thromboembolic pulmonary hypertension patients might experience increased inflammation and hypoxia due to dysregulation of the hypoxia-inducible factor-1α/endothelial nitric synthase pathway in pulmonary artery endothelial cells under inflammation and hypoxia, contributing to the pathogenesis of chronic thromboembolic pulmonary hypertension.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 2","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11740980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006122","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":"In-Depth Examination of TPBG as a New Predictive Indicator for Gastric Cancer","authors":"Lianlei Yang,&nbsp;Chunyan Weng,&nbsp;Yaping Zhang,&nbsp;Yu Zhao,&nbsp;Kexin Chen,&nbsp;Guodong Li,&nbsp;Xueqing Zhong,&nbsp;Chenghai He","doi":"10.1111/jcmm.70354","DOIUrl":"10.1111/jcmm.70354","url":null,"abstract":"<p>Trophoblast glycoprotein (TPBG) plays a significant part in the growth of specific cancers, yet its connection to gastric cancer (GC) remains uncertain. This research seeks to analyse the fluctuation in TPBG levels in GC and evaluate how TPBG expression relates to the prognosis of GC patients. TPBG expression in GC and normal gastric tissues was investigated in The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) database, further extracting the immunohistochemistry images from HPA database and validating by Western blot. The connection between TPBG and GC patients' survival rates was investigated by Kaplan–Meier and COX regression analysis. Genes related to TPBG were enriched using GO and KEGG data. In vitro and in vivo tumour models were utilised to evaluate the function of TPBG in GC. Western blot analysis was performed to detect the expression of PI3K/AKT signalling pathway proteins following TPBG knockdown. Immune infiltration was analysed using the CIBERSOFT and ssGSEA methods. The association between TPBG and immune cells that infiltrate tumours was evaluated through the utilisation of GSVA. TPBG expression increased in several tumour tissues (including GC) more than in adjacent noncancerous tissues. Elevated TPBG level predicted worse outcomes, such as poorer overall survival, pathological stage, and therapy response in GC. Enrichment analysis primarily focused on biological processes like the organisation of external encapsulating structures, extracellular structure, and collagen metabolism. Biological experiments further demonstrated that TPBG knockdown successfully inhibits the progression, migration, and invasion of GC cells. Western blot analysis revealed that TPBG knockdown inhibits the PI3K/AKT signalling pathway. Furthermore, TPBG is associated with the infiltration of immune cells in GC, which correlates with the expression of macrophage cells. There is a positive relationship between TPBG and malignant behaviour of GC tissues and cells, suggesting that TPBG can be useful for diagnosing and prognosing GC.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 2","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11740983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006125","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":"Cellular Senescence Genes as Cutting-Edge Signatures for Abdominal Aortic Aneurysm Diagnosis: Potential for Innovative Therapeutic Interventions","authors":"Shuli Zhang,&nbsp;Jiayin Li,&nbsp;Ruichen Wang,&nbsp;Xiaojie Zhao,&nbsp;Zhu Mei,&nbsp;Xiaozeng Wang","doi":"10.1111/jcmm.70323","DOIUrl":"10.1111/jcmm.70323","url":null,"abstract":"<p>Abdominal aortic aneurysm (AAA) is the most prevalent dilated arterial aneurysm that poses a significant threat to older adults, but the molecular mechanisms linking senescence to AAA progression remain poorly understood. This study aims to identify cellular senescence-related genes (SRGs) implicated in AAA development and assess their potential as therapeutic targets. Four hundred and twenty-nine differentially expressed genes (DEGs) were identified from the GSE57691 training set, and 867 SRGs were obtained. Through the intersection of DEGs with SRGs, 19 differentially expressed senescence-related genes (DESRGs) were uncovered. Functional enrichment analysis was performed to explore their biological roles in AAA. To identify hub genes, we applied machine learning algorithms, including LASSO, SVM-RFE and random forest. These hub genes were then validated in two independent datasets. In the initial validation cohort, significant differences in the expression levels of BTG2, ETS1, ID1 and ITPR3 were observed between the AAA and control groups. Receiver operating characteristic (ROC) analysis demonstrated a robust diagnostic performance. Further validation across different AAA stages (small, large and ruptured AAA) identified ETS1 and ITPR3 as potential diagnostic genes. Subsequently, the diagnostic relevance of ETS1 and ITPR3 was further validated in human serum samples and mouse models of AAA. In addition, single-cell RNA sequencing suggests that senescent endothelial cells play a pivotal role in AAA progression, we further confirmed the correlation between ETS1 and ITPR3 and senescent endothelial cells by WB, IF and RT-qPCR. In conclusion, our study reveals the pivotal role of cellular senescence in AAA progression and identifies ETS1 and ITPR3 as promising diagnostic biomarkers.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 2","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11740988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006062","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":"miR-143-3p/TET1 Axis Regulates GPC1 Through DNA Methylation and Impairs the Malignant Biological Behaviour of HCC via the Hippo Signalling Pathway","authors":"Yan Liu,&nbsp;Di Du,&nbsp;Xue Gu,&nbsp;Qing He,&nbsp;Bin Xiong","doi":"10.1111/jcmm.70282","DOIUrl":"10.1111/jcmm.70282","url":null,"abstract":"<p>Hepatocellular carcinoma (HCC) is a malignant tumour that poses a serious threat to human health and places a heavy burden on individuals and society. However, the role of GPC1 in the malignant progression of HCC is unknown. In this study, we analysed the expression of GPC1 in HCC, and its association with poor patient prognosis. The effects of GPC1 on the proliferation, invasion and migration of HCC were analysed through cellular functional experiments in vitro and in vivo. Mechanistically, DNA methylation of GPC1 was analysed by DNA extraction, methylation-specific PCR and bisulfite Sanger sequencing (BSP), and the target genes TET1 and miRNA regulating DNA methylation of GPC1 were found through the bioinformatics database. The results revealed that GPC1 was highly expressed in HCC, and its high expression was significantly associated with poor prognosis of HCC patients. Inhibiting the expression of GPC1 can inhibit the proliferation, invasion and migration of HCC cells. GPC1 was hypomethylated in HCC, and its methylation level was regulated by TET1. miR-143-3p can significantly regulated the expression of TET1 and affect the methylation level and protein expression of GPC1. Furthermore, GPC1 also affects the malignant biological behaviour of HCC by regulating the expression of Hippo signalling pathway. In summary, miR-143-3p regulates the expression of TET1, affects the expression of GPC1 through DNA methylation and regulates the malignant progression of HCC via Hippo signalling pathway.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 2","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11740985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006127","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":"Antagonisation of Prokineticin Receptor-2 Attenuates Preeclampsia Symptoms","authors":"Frédéric Sergent,&nbsp;Daniel Vaiman,&nbsp;Tiphaine Raia-Barjat,&nbsp;Hadi Younes,&nbsp;Christel Marquette,&nbsp;Morgane Desseux,&nbsp;Roland Abi Nahed,&nbsp;Trinh-Le-Vi Kieu,&nbsp;Nguyen Viet Dung,&nbsp;Mathilde Keck,&nbsp;Pascale Hoffmann,&nbsp;Padma Murthi,&nbsp;Mohamed Benharouga,&nbsp;Nadia Alfaidy","doi":"10.1111/jcmm.70346","DOIUrl":"10.1111/jcmm.70346","url":null,"abstract":"<p>Preeclampsia (PE) is the most threatening pathology of human pregnancy. Placenta from PE patients releases harmful factors that contribute to the exacerbation of the disease. Among these factors is the prokineticin1 (PROK1) and its receptor, PROKR2 that we identified as a mediators of PE. Here we tested the effects of PKRA, an antagonist of PROKR2, on the attenuation of PE symptoms. We used the genetic PE mouse model, STOX1 that overexpresses <i>Stox1</i> gene in a heterozygosis manner in the placenta. This model allowed exploiting two genotypes of the offspring, those that overexpress the <i>Stox1</i> gene, and the WT that grow in a PE environment (STE). We characterised the effect PKRA (1 μM) on the attenuation of PE symptoms and compared its effects on STOX1 and STE placentas. We also used <i>STOX1</i> overexpressing trophoblast cells to decipher the PROK1-underlying mechanism. We demonstrated that (i) antagonisation of PROKR2 attenuated PE-mediated hypertension and proteinuria, (ii) STE placentas and foetuses exhibited better outcomes in response to PKRA, (iii) the secretome of STOX1-trophoblasts impacted the integrity of the fetal vasculature that was attenuated by PKRA treatment. This study demonstrates the direct involvement of the PROK1 in PE and identifies PKRA as a promising therapy for PE.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 2","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006027","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":"Deciphering the Anti-Diabetic Potential of Gymnema Sylvestre Using Integrated Computer-Aided Drug Design and Network Pharmacology","authors":"Amal Mayyas,&nbsp;Ali Al-Samydai,&nbsp;Amjad Ibrahim Oraibi,&nbsp;Nawres Debbabi,&nbsp;Sara S. Hassan,&nbsp;Hany Aqeel Al-Hussainy,&nbsp;Ahmad Mohammad Salamatullah,&nbsp;Musaab Dauelbait,&nbsp;Mohammed Bourhia,&nbsp;Khalid S. Almaary","doi":"10.1111/jcmm.70349","DOIUrl":"10.1111/jcmm.70349","url":null,"abstract":"<p>This study explores novel therapeutic avenues for diabetes, a global health concern marked by elevated blood glucose levels. We investigated the anti-diabetic potential of <i>Gymnema Sylvestre's</i> bioactive compounds, including Gymnemic acid I, Stigmasterol, Deacylgymnemic acid, Beta-Amyrin acetate, Longispinogenin, Gymnemic acid II, Gymnemic acid, Gymnemic acid X, Gymnemaside VI, Phytic acid and Gymnemic acid X. Employing network pharmacology, molecular docking and molecular dynamics (MD), we elucidated the potential mechanism of action. SwissTargetPrediction identified targets for bioactive constituents, while DisGeNET provided diabetes-related targets. A GeneVenn diagram revealed 397 common potential targets for diabetes management. The protein–protein interaction network, constructed via the STRING database, underwent topological analysis in Cytoscape, identifying AKT1, SRC, TNF, PPARG and IL1B as top targets. Gene ontology analysis using FunRich identified crucial roles of screened targets in integrin family cell surface interactions and glypican pathways for diabetes management. Molecular interactions and binding affinities with the top target, AKT1, were assessed, with Gymnemic acid I displaying the least binding energy (−9.813) with H- and non-H-bond interactions. Molecular dynamics simulations provided insights into the distinct behaviours of Gymnemic acid I within the protein complex. In conclusion, our study elucidates the potential anti-diabetic mechanism of Gymnemic acid I, underscoring the need for further in vitro, in vivo and clinical studies to validate our findings.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142983590","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":"Hydrogen-Rich Saline Combined With Vacuum Sealing Drainage Promotes Wound Healing by Altering Biotin Metabolism","authors":"Xinwen Kuang,&nbsp;Zhengyun Liang,&nbsp;Yijun Xia,&nbsp;Mengjie Shan,&nbsp;Yan Hao,&nbsp;Hao Liu,&nbsp;Zhi Wang,&nbsp;Qianjun He,&nbsp;Chao Xia,&nbsp;Cheng Feng,&nbsp;Guojing Chang,&nbsp;Youbin Wang","doi":"10.1111/jcmm.70292","DOIUrl":"10.1111/jcmm.70292","url":null,"abstract":"<p>Impaired wound healing affects the life quality of patients and causes a substantial financial burden. Hydrogen-rich medium is reported to have antioxidant and anti-inflammatory effects. However, the role of hydrogen-rich saline (HRS) in cutaneous wound healing remains largely unexplored, especially by metabolomics. Thus, untargeted metabolomics profiling was analysed to study the effects and mechanism of HRS combined with vacuum sealing drainage (VSD) in a rabbit full-thickness wound model. Our results indicated that the combination treatment of HRS and VSD could accelerate wound healing. In vitro experiments further confirmed its effects on HaCaT keratinocytes. We found that 45 metabolites were significantly changed between the VSD + HRS group and the VSD + saline-treated group. Pathway enrichment analysis indicated that biotin metabolism was the potential target pathway. The biochemical interpretation analysis demonstrated that combining HRS and VSD might enhance mitochondrial function, ATP synthesis, and GSH homeostasis by altering biotin metabolism. The detection of representative indicators of oxidative stress supported the critical metabolic pathway analysis as well. In summary, VSD combined with HRS might provide a new strategy to enhance wound healing.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11728484/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142978495","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":"Enhancing Molecular Network-Based Cancer Driver Gene Prediction Using Machine Learning Approaches: Current Challenges and Opportunities","authors":"Hao Zhang,&nbsp;Chaohuan Lin,&nbsp;Ying'ao Chen,&nbsp;Xianrui Shen,&nbsp;Ruizhe Wang,&nbsp;Yiqi Chen,&nbsp;Jie Lyu","doi":"10.1111/jcmm.70351","DOIUrl":"10.1111/jcmm.70351","url":null,"abstract":"<p>Cancer is a complex disease driven by mutations in the genes that play critical roles in cellular processes. The identification of cancer driver genes is crucial for understanding tumorigenesis, developing targeted therapies and identifying rational drug targets. Experimental identification and validation of cancer driver genes are time-consuming and costly. Studies have demonstrated that interactions among genes are associated with similar phenotypes. Therefore, identifying cancer driver genes using molecular network-based approaches is necessary. Molecular network-based random walk-based approaches, which integrate mutation data with protein–protein interaction networks, have been widely employed in predicting cancer driver genes and demonstrated robust predictive potential. However, recent advancements in deep learning, particularly graph-based models, have provided novel opportunities for enhancing the prediction of cancer driver genes. This review aimed to comprehensively explore how machine learning methodologies, particularly network propagation, graph neural networks, autoencoders, graph embeddings, and attention mechanisms, improve the scalability and interpretability of molecular network-based cancer gene prediction.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970935","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: Alpha B-Crystallin Promotes the Invasion and Metastasis of Gastric Cancer via NF-κB-Induced Epithelial-Mesenchymal Transition","authors":"","doi":"10.1111/jcmm.70369","DOIUrl":"10.1111/jcmm.70369","url":null,"abstract":"<p>RETRACTION: D. Chen, G. Cao, C. Qiao, G. Liu, H. Zhou, and Q. Liu, “Alpha B-Crystallin Promotes the Invasion and Metastasis of Gastric Cancer via NF-κB-Induced Epithelial-Mesenchymal Transition,” <i>Journal of Cellular and Molecular Medicine</i> 22, no. 6 (2018): 3215–3222, https://doi.org/10.1111/jcmm.13602.</p><p>The above article, published online on 22 March 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Stefan N. Constantinescu; the Foundation for Cellular and Molecular Medicine; and John Wiley &amp; Sons Ltd. The retraction has been agreed due to concerns raised by third parties. The article presents experiments in an unverifiable/unknown cell line, MGC823. Furthermore, additional flaws and inconsistencies between results presented and experimental methods described were found. Accordingly, the article is retracted as its conclusions are considered invalid by the editors. The authors did not respond to our requests for clarification regarding the identified issues and have been informed of the decision of retraction.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11727248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970946","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}