JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献_第9页

Loss of FTH1 Induces Ferritinophagy-Mediated Ferroptosis in Anaemia of Myelodysplastic Syndromes 在骨髓增生异常综合征贫血中，FTH1缺失诱导铁蛋白吞噬介导的铁凋亡。

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-01-13 DOI: 10.1111/jcmm.70350

Liyan Yang, Mengying Zhang, Mengyuan Liu, Yating Yu, Yue Zhang, Jinyue Yang, Limin Xing, Zonghong Shao, Huaquan Wang

{"title":"Loss of FTH1 Induces Ferritinophagy-Mediated Ferroptosis in Anaemia of Myelodysplastic Syndromes","authors":"Liyan Yang, Mengying Zhang, Mengyuan Liu, Yating Yu, Yue Zhang, Jinyue Yang, Limin Xing, Zonghong Shao, Huaquan Wang","doi":"10.1111/jcmm.70350","DOIUrl":"10.1111/jcmm.70350","url":null,"abstract":"Single-cell sequencing of lineage negative (Lin-) cells from patients with myelodysplastic syndromes (MDS) revealed a reduction in ferritin heavy chain 1 (FTH1) levels, yet the significance of this decrease in FTH1 in the pathophysiology of MDS remains unclear. In this study, we evaluated the role of FTH1 in patients with MDS. The mRNA expression of FTH1 in GlycoA+ nucleated erythrocytes from MDS patients was significantly lower than that in control group. FTH1 was implicated in both ferritinophagy and ferroptosis in MDS patients, processes that are linked to the development of anaemia. To further validate our observations, we employed shRNA to knock down the FTH1 gene in K562 and SKM1 cells. This knockdown confirmed that the elevated ferroptosis levels observed after FTH1 depletion were indeed due to the induction of ferritinophagy. Hemin stimulation promoted the differentiation of K562 cells, while downregulation of FTH1 gene expression had an impact on erythroid differentiation and haemoglobin synthesis. Taken together, our results suggest that FTH1-mediated ferritinophagy may represent a novel therapeutic target for MDS.","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/PMC11726652/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970937","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}

引用次数: 0

RETRACTION: HSP27 Associates With Epithelial–Mesenchymal Transition, Stemness and Radioresistance of Salivary Adenoid Cystic Carcinoma 回撤：HSP27与唾液腺样囊性癌的上皮-间质转化、干性和放射耐药相关。

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-01-13 DOI: 10.1111/jcmm.70365

{"title":"RETRACTION: HSP27 Associates With Epithelial–Mesenchymal Transition, Stemness and Radioresistance of Salivary Adenoid Cystic Carcinoma","authors":"","doi":"10.1111/jcmm.70365","DOIUrl":"10.1111/jcmm.70365","url":null,"abstract":"RETRACTION: W. Chen, X. Ren, J. Wu, X. Gao, X. Cen, S. Wang, S. Sheng, Q. Chen, Y.-J. Tang, X.-H. Liang, and Y.-L. Tang, “HSP27 Associates with Epithelial–Mesenchymal Transition, Stemness and Radioresistance of Salivary Adenoid Cystic Carcinoma,” Journal of Cellular and Molecular Medicine 22, no. 4 (2018): 2283–2298, https://doi.org/10.1111/jcmm.13510.The above article, published online on 09 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 upon following an investigation into concerns raised by a third party, which revealed inappropriate image panel duplications within the article depicting different experimental conditions (Figure 1B Control and EV, Figure 2C Control and Neg, Figure 3A Control and EV, Figure 1F SACC-LM Control and CM+HSP27, and Figure 6B SACC-LM CM without IR and CM with IR panels). Additionally, irregularities were discovered regarding the appearance of the dissected tumors in Figure 5A and another instance of image duplication was identified between Figure 1F SACC-LM Control panel and another image published previously by an overlapping group of authors in a different scientific context. The explanation provided by the authors was unsatisfactory and the partial raw data shared could not address these concerns. Thus, the editors have lost confidence in the presented data and consider the conclusions of this manuscript substantially compromised. The authors disagree with the retraction wording.","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/PMC11727396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970950","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}

引用次数: 0

Osterix mRNA Enrichment in Small Extracellular Vesicles Derived From Osteogenically Induced ADSCs: A Promoter of Osteogenic Differentiation in BMSCs 骨诱导 ADSCs 的细胞外小泡中富含 Osterix mRNA：BMSCs 中的成骨分化促进因子。

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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-01-13 DOI: 10.1111/jcmm.70353

Zhaoquan Liang, Yuelin Wu, Junhao Bao, Qiang Xiao, Sidong Luo, Xinfang Liu, Yeyang Wang, Chao Xie, Li Zhang

{"title":"Osterix mRNA Enrichment in Small Extracellular Vesicles Derived From Osteogenically Induced ADSCs: A Promoter of Osteogenic Differentiation in BMSCs","authors":"Zhaoquan Liang, Yuelin Wu, Junhao Bao, Qiang Xiao, Sidong Luo, Xinfang Liu, Yeyang Wang, Chao Xie, Li Zhang","doi":"10.1111/jcmm.70353","DOIUrl":"10.1111/jcmm.70353","url":null,"abstract":"Osteogenic differentiation of bone marrow stem cells (BMSCs) is essential for bone tissue regeneration and repair. However, this process is often hindered by an unstable differentiation influenced by local microenvironmental factors. While small extracellular vesicles (sEVs) derived from osteogenically induced adipose mesenchymal stem cells (ADSCs) reportedly can promote osteogenic differentiation of BMSCs, the underlying molecular mechanisms remain incompletely understood. In this study, we investigated the mRNA expression profile of ADSC-sEVs+ and explored the role of specific mRNAs in the osteogenic differentiation of BMSCs. We first validated the osteogenic induction activity of ADSC-sEVs+ through both in vitro and in vivo experiments. Using reverse transcription polymerase chain reaction, we compared mRNA expression between ADSC-sEVs+ and ADSC-sEVs and further assessed the impact of specific mRNAs on the differentiation of BMSCs through a series of in vitro experiments. One of our key findings was that osterix mRNA was highly enriched in ADSC-sEVs+, which significantly enhanced alkaline phosphatase staining and upregulated downstream osteoblastic markers in BMSCs. Both overexpression and knockdown experiments confirmed that osterix mRNA is a critical signalling molecule that facilitates the differentiation of BMSCs into osteoblasts through ADSC-sEVs+. This finding expands our understanding of the molecular mechanisms underlying the osteogenic differentiation of BMSCs and offers a promising strategy for targeted osteoblastic differentiation in clinical applications.","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/PMC11727376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970938","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}

引用次数: 0

USP18 Promotes Cholesterol Efflux and Mitigates Atherosclerosis by Deubiquitinating ABCG1 USP18通过去泛素化ABCG1促进胆固醇外流并减轻动脉粥样硬化。

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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-01-13 DOI: 10.1111/jcmm.70320

Yang An, Chuxian Guo, Xiaoli Wang, Jiangjin Liu, Zhu Li, Jiuyang Ding, Qiaojun Zhang, Hongmei Zhou, Bing Xia, Jiawen Wang, Yanni Yu, Changwu Wan, Jie Wang, Jialin Dai

{"title":"USP18 Promotes Cholesterol Efflux and Mitigates Atherosclerosis by Deubiquitinating ABCG1","authors":"Yang An, Chuxian Guo, Xiaoli Wang, Jiangjin Liu, Zhu Li, Jiuyang Ding, Qiaojun Zhang, Hongmei Zhou, Bing Xia, Jiawen Wang, Yanni Yu, Changwu Wan, Jie Wang, Jialin Dai","doi":"10.1111/jcmm.70320","DOIUrl":"10.1111/jcmm.70320","url":null,"abstract":"Deubiquitinating enzymes (DUBs) are integral regulators of protein stability. Among these, Ubiquitin-specific protease 18 (USP18) has emerged as a potential therapeutic target for heart failure. However, its precise role in atherosclerosis remains to be comprehensively understood. This study endeavours to examine the impact of USP18 on atherosclerosis and elucidate its corresponding molecular mechanisms. Our studies indicate an elevated expression of USP18 in human coronary atherosclerotic plaques. Notably, the knockdown of USP18 significantly exacerbated lipid accumulation in macrophages. This knockdown effect impaired cholesterol efflux and influenced the downregulation of ATP-binding cassette transporter G1 (ABCG1) expression, achieved by altering the ubiquitination level of ABCG1. Comprehensive mechanistic studies unveiled that USP18 directly affiliates with ABCG1, reducing its ubiquitination and consequently bolstering ABCG1 stability within macrophages. Furthermore, in vivo studies elucidated that the knockdown of USP18 notably elevated atherosclerotic lesions and diminished ABCG1 levels in the plaques of Apoe−/− mice. In summary, our results suggested that USP18 plays a crucial role in managing the progression of atherosclerosis by strengthening the expression of ABCG1 protein through its deubiquitinating effect on ABCG1.","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/PMC11728483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142978499","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}

引用次数: 0

Therapeutic Ultrasound Modulates Cell Proliferation and Proinflammatory Cytokine Levels in Osteoarthritic Chondrocytes 治疗性超声调节骨关节炎软骨细胞的细胞增殖和促炎细胞因子水平

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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-01-12 DOI: 10.1111/jcmm.70257

Ahmet Çagdas Yilmaz, Hasan Toktas, Sefa Celik, Serkan Sen

{"title":"Therapeutic Ultrasound Modulates Cell Proliferation and Proinflammatory Cytokine Levels in Osteoarthritic Chondrocytes","authors":"Ahmet Çagdas Yilmaz, Hasan Toktas, Sefa Celik, Serkan Sen","doi":"10.1111/jcmm.70257","DOIUrl":"10.1111/jcmm.70257","url":null,"abstract":"The development and progression of osteoarthritis (OA) are believed to involve inflammation. This study aimed to investigate the effects of applying therapeutic ultrasound (US) to human osteoarthritic chondrocytes in continuous and pulsed modes on cell proliferation and proinflammatory cytokine levels. Human osteoarthritic chondrocytes (HC-OA 402OA-05a) were proliferated in appropriate media and then seeded into culture plates. The plates were grouped and exposed to underwater continuous, pulsed and control US at 0.1 W/cm2 and 1 MHz for 10 min daily for 10 days. Cell viability/proliferation was assessed using the MTT assay, total protein was measured by ELISA and cytokine levels per protein were determined. Cells were photographed using microscopic analysis. Both continuous and pulsed US groups showed a significant increase in viability compared to the control group. No significant difference was found between the continuous and pulsed US groups for IL-1β, TNF-α and IL-6 levels. Both groups showed significant cytokine reduction compared to the control group. For IL-17 and IL-32 levels, both US groups had reduced cytokine levels compared to the control group, but the results were not significant. Underwater US at 0.1 W/cm2 and 1 MHz stimulated cell proliferation and reduced proinflammatory cytokine levels in osteoarthritic chondrocyte cell cultures. This study extensively focused on proinflammatory IL levels, and the meaningful results may inspire future in vivo/in vitro studies. While adapting in vitro data to in vivo conditions poses challenges, our results could guide future in vivo studies and clinical applications.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11725177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970924","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}

引用次数: 0

Comparative Analysis of Acquired Resistance to Bortezomib in Prostate Cancer Cells Using Proteomic and Bioinformatic Tools 利用蛋白质组学和生物信息学工具比较分析前列腺癌细胞对硼替佐米的获得性耐药性

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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-01-12 DOI: 10.1111/jcmm.70254

Semih Seker, Betul Sahin, Azmi Yerlikaya

{"title":"Comparative Analysis of Acquired Resistance to Bortezomib in Prostate Cancer Cells Using Proteomic and Bioinformatic Tools","authors":"Semih Seker, Betul Sahin, Azmi Yerlikaya","doi":"10.1111/jcmm.70254","DOIUrl":"10.1111/jcmm.70254","url":null,"abstract":"Chemotherapy is a potent tool against cancer, but drug resistance remains a major obstacle. To combat this, understanding the molecular mechanisms behind resistance in cancer cells and the protein expression changes driving these mechanisms is crucial. Targeting the Ubiquitin-Proteasome System (UPS) has proven effective in treating multiple myeloma and shows promise for solid tumours. Despite initial success with the proteasome inhibitor bortezomib, acquired resistance soon after treatment poses a significant challenge to its efficacy. In this study, we explored proteins potentially involved in acquired resistance to bortezomib using label-free nLC–MS/MS proteomic analysis. The investigation revealed 299 proteins with notable differences in expression levels in the bortezomib-resistant PC3 prostate cancer cell line. Using bioinformatics tools, we illustrated the top 10 gene ontology (GO) processes [e.g., translational initiation (p = 5.964E-10), CRD-mediated mRNA stabilisation (p = 1.636E-5), and hydrogen ion transmembrane transport (p = 6.46E-5)] and the top 20 KEGG [e.g., metabolic pathways (p = 7.601E-13), biosynthesis of amino acids (p = 3.834E-12), and chemical carcinogenesis—reactive oxygen species (p = 1.891E-4)] and REACTOME [e.g., metabolism (p = 4.182E-21), translation (p = 9.484E-18), and Nonsense-Mediated Decay (NMD) (p = 1.829E-8)] pathways in the PC3-resistant cells. We further refined our results by comparing them with globally validated TCGA datasets. We correlated the 299 proteins identified through proteomic analysis with tumour aggressiveness and resistance by comparing them with the TCGA nodal metastasis N0 vs. N1 datasets using the UALCAN portal and identified 37 proteins consistent with our results. We believe that a combination of bortezomib with chemotherapeutics targeting these proteins could be effective in overcoming the resistance developed against bortezomib.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11725179/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970933","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}

引用次数: 0

Renal Tubular Epithelial Cell–Derived hsa_circ_0008925 From Urine Is Related to Chronic Renal Fibrosis 尿液中肾小管上皮细胞衍生的 hsa_circ_0008925 与慢性肾纤维化有关。

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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-01-12 DOI: 10.1111/jcmm.70335

Yuanhui Shi, Yuye Chen, Zihao Xiao, Yajie Wang, Cong Fu, Yuhan Cao

{"title":"Renal Tubular Epithelial Cell–Derived hsa_circ_0008925 From Urine Is Related to Chronic Renal Fibrosis","authors":"Yuanhui Shi, Yuye Chen, Zihao Xiao, Yajie Wang, Cong Fu, Yuhan Cao","doi":"10.1111/jcmm.70335","DOIUrl":"10.1111/jcmm.70335","url":null,"abstract":"Renal fibrosis (RF) is a crucial pathological factor in the progression of chronic kidney disease (CKD) to end-stage renal failure, and accurate and noninvasive assays to monitor the progression of renal fibrosis are needed. Circular RNAs (circRNAs) are noncoding RNAs that can be used as diagnostic biomarkers and therapeutic targets for human diseases. In this study, we analysed the expression of hsa_circ_0008925 in human urinary renal tubular cells and investigated its role in renal fibrosis. Urinary samples were collected from CKD patients with varying degrees of renal fibrosis; renal tubular epithelial cells were isolated from the urinary samples using magnetic bead sorting. In patients with moderate–severe renal fibrosis, the expression of hsa_circ_0008925 in urinary renal tubular epithelial cells was elevated compared to that in patients with no renal fibrosis to mild renal fibrosis. Spearman correlation analysis indicated that the hsa_circ_0008925 expression was positively correlated with serum creatinine (Scr, rs = 0.424, p = 0.031). The expression of hsa_circ_0008925 was elevated in TGF-β1-treated HK-2 cells in vitro. Silencing of hsa_circ_0008925 using siRNA inhibited TGF-β1-induced fibrosis in HK2 cells. RNA pull-down and mass spectrometric analyses indicated that serine/arginine-rich splicing factor 6 (SRSF6) is the downstream of hsa_circ_0008925. Silencing mmu_circ_0002215 and inhibiting SRSF6 alleviated renal fibrosis in a UUO model in vivo. Inhibiting hsa_circ_0008925/SRSF6 alleviated renal fibrosis in vitro and in vivo. These findings suggest that targeting the hsa_circ_0008925/SRSF6 pathway could hold promise as a potential therapeutic strategy for treating renal fibrosis.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11725181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142970940","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}

引用次数: 0

FT538, iPSC-derived NK cells, enhance AML cell killing when combined with chemotherapy FT538， ipsc衍生的NK细胞，在联合化疗时增强AML细胞杀伤。

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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-01-11 DOI: 10.1111/jcmm.70169

Amanda Eckstrom, Anudishi Tyagi, Sajid Mahmood, Lilly Wong, Bahram Valamehr, Adishwar Rao, Akriti Agrawal, Maryam Siddiqui, V. Lokesh Battula

{"title":"FT538, iPSC-derived NK cells, enhance AML cell killing when combined with chemotherapy","authors":"Amanda Eckstrom, Anudishi Tyagi, Sajid Mahmood, Lilly Wong, Bahram Valamehr, Adishwar Rao, Akriti Agrawal, Maryam Siddiqui, V. Lokesh Battula","doi":"10.1111/jcmm.70169","DOIUrl":"10.1111/jcmm.70169","url":null,"abstract":"Induced pluripotent stem cell (iPSC)–derived natural killer (NK) cells offer an opportunity for a standardized, off-the-shelf treatment with the potential to treat a wider population of acute myeloid leukaemia (AML) patients than the current standard of care. FT538 iPSC-NKs express a high-affinity, noncleavable CD16 to maximize antibody dependent cellular cytotoxicity, a CD38 knockout to improve metabolic fitness, and an IL-15/IL-15 receptor fusion preventing the need for cytokine administration, the main source of adverse effects in NK cell–based therapies. Here, we sought to evaluate the potential of FT538 iPSC-NKs as a therapy for AML through their effect on AML cell lines and primary AML cells. We observed that FT538 iPSC-NKs induce effector-to-target cell ratio dependent apoptosis in cell lines and primary AML cells, including cells from high-risk patients. Flow cytometric analysis revealed that FT538 iPSC-NKs induce AML cell death when combined with the AML therapies: cytarabine, venetoclax and gilteritinib. Moreover, cytarabine did not affect FT538 iPSC-NK viability, suggesting that iPSC-derived NK therapies and chemotherapy may be a promising treatment combination. This study provides the basis for further study of iPSC-derived NK cell therapies as a treatment option for high-risk AML patients, particularly those with disease resistant to standard therapies.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142964964","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}

引用次数: 0

RETRACTION: Circular RNA circFBXO11 Modulates Hepatocellular Carcinoma Progress and Oxaliplatin Resistance Through miR-605/FOXO3/ABCB1 Axis 撤回：环状RNA circFBXO11通过miR-605/FOXO3/ABCB1轴调节肝细胞癌进展和奥沙利铂耐药性。

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JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-01-11 DOI: 10.1111/jcmm.70355

{"title":"RETRACTION: Circular RNA circFBXO11 Modulates Hepatocellular Carcinoma Progress and Oxaliplatin Resistance Through miR-605/FOXO3/ABCB1 Axis","authors":"","doi":"10.1111/jcmm.70355","DOIUrl":"10.1111/jcmm.70355","url":null,"abstract":"RETRACTION: J. Li, X. Qin, R. Wu, L. Wan, L. Zhang, and R. Liu, “Circular RNA circFBXO11 Modulates Hepatocellular Carcinoma Progress and Oxaliplatin Resistance Through miR-605/FOXO3/ABCB1 Axis,” Journal of Cellular and Molecular Medicine 24, no. 9 (2020): 5152–5161, https://doi.org/10.1111/jcmm.15162.The above article, published online on 28 March 2020 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 upon following an investigation into concerns raised by a third party, which revealed implausible similarities between Figure 2G NC of this study and another article published earlier in the same year by a different group of authors in a different scientific context, suggesting that the images were likely obtained from the same flow-cytometry data set. The explanation and the partial raw data shared by the authors were deemed insufficient to address these concerns. Thus, the editors have lost confidence in the presented data and consider the conclusions of this manuscript substantially compromised.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11724332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142965131","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}

引用次数: 0

METTL3-Mediated m6A Modification of ISG15 mRNA Regulates Doxorubicin-Induced Endothelial Cell Apoptosis mettl3介导的m6A修饰ISG15 mRNA调控阿霉素诱导的内皮细胞凋亡

IF 5.3

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-01-09 DOI: 10.1111/jcmm.70339

Dongdong Jian, Han Li, Chenqiu Wang, Fang Li, Runhua Li, Shouyi Jin, Jia Shen, Jiamian Chen, Wanjun Zhang, Ling Pan, Wengong Wang, Hao Tang, Liguo Jian, Datun Qi

{"title":"METTL3-Mediated m6A Modification of ISG15 mRNA Regulates Doxorubicin-Induced Endothelial Cell Apoptosis","authors":"Dongdong Jian, Han Li, Chenqiu Wang, Fang Li, Runhua Li, Shouyi Jin, Jia Shen, Jiamian Chen, Wanjun Zhang, Ling Pan, Wengong Wang, Hao Tang, Liguo Jian, Datun Qi","doi":"10.1111/jcmm.70339","DOIUrl":"10.1111/jcmm.70339","url":null,"abstract":"N6-adenosine methylation (m6A) of RNA is involved in the regulation of various diseases. However, its role in chemotherapy-related vascular endothelial injury has not yet been elucidated. We found that methyltransferase-like 3 (METTL3) expression was significantly reduced during doxorubicin (DOX)-induced apoptosis of vascular endothelial cells both in vivo and in vitro, and that silencing of METTL3 further intensified this process. Combined transcriptome and proteome sequencing analyses revealed that the expression levels of interferon-stimulated gene 15 (ISG15) mRNA and protein significantly increased after METTL3 silencing. Methylated RNA immunoprecipitation (meRIP)-quantitative polymerase chain reaction (qPCR) and mRNA stability assays confirmed that METTL3 regulates the expression of ISG15 by methylating the 1,014,147 site on ISG15 RNA, thereby decreasing ISG15 mRNA levels. Silencing ISG15 significantly suppressed DOX-induced endothelial cell apoptosis and dysfunction caused by METTL3 silencing. In summary, our study revealed that METTL3-mediated methylation of ISG15 mRNA is involved in DOX-induced endothelial cell apoptosis and explored potential therapeutic targets for alleviating chemotherapy-associated vascular injury.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11717669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142949428","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}

引用次数: 0