International Journal of Biochemistry & Cell Biology最新文献

{"title":"Unveiling a novel signalling pathway involving NRF2 and PGAM5 in regulating the mitochondrial unfolded protein response in stressed cardiomyocytes","authors":"Rahme Nese Safakli ,&nbsp;Stephen Gray ,&nbsp;Nadia Bernardi ,&nbsp;Ioannis Smyrnias","doi":"10.1016/j.biocel.2024.106704","DOIUrl":"10.1016/j.biocel.2024.106704","url":null,"abstract":"<div><div>The mitochondrial unfolded protein response (UPRmt) is a conserved signalling pathway that initiates a specific transcriptional programme to maintain mitochondrial and cellular homeostasis under stress. Previous studies have demonstrated that UPRmt activation has protective effects in the pressure-overloaded human heart, suggesting that robust UPRmt stimulation could serve as an intervention strategy for cardiovascular diseases. However, the precise mechanisms of UPRmt regulation remain unclear. In this study, we present evidence that the NRF2 transcription factor is involved in UPRmt activation in cardiomyocytes during conditions of mitochondrial stress. Silencing NRF2 partially reduces UPRmt activation, highlighting its essential role in this pathway. However, constitutive activation of NRF2 via inhibition of its cytosolic regulator KEAP1 does not increase levels of UPRmt activation markers, suggesting an alternative regulatory mechanism independent of the canonical KEAP1-NRF2 axis. Further analysis revealed that NRF2 likely affects UPRmt activation through its interaction with PGAM5 at the mitochondrial membrane. Disruption of PGAM5 in cardiomyocytes subjected to mitochondrial stress reduces the interaction between PGAM5 and NRF2, enhancing nuclear translocation of NRF2 and significantly upregulating the UPRmt in an NRF2-dependent manner. This NRF2-regulated UPRmt amplification improves mitochondrial respiration, reflecting an enhanced capacity for cardiomyocytes to meet elevated energetic demands during mitochondrial stress. Our findings highlight the therapeutic potential of targeting the NRF2-PGAM5-KEAP1 signalling complex to amplify the UPRmt in cardiomyocytes for cardiovascular and other diseases associated with mitochondrial dysfunction. Future studies should aim to elucidate the mechanisms via which NRF2 enhances the protective effects of UPRmt, thereby contributing to more targeted therapeutic approaches.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"178 ","pages":"Article 106704"},"PeriodicalIF":3.4,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142752208","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":"Regulatory role of AMPK/Nrf2 signaling pathway in sevoflurane-enhanced intestinal protection against ischemia-reperfusion injury","authors":"Xiaohua Zeng ,&nbsp;Shan Jiang ,&nbsp;Yinghui Wu ,&nbsp;Liang Zhong ,&nbsp;Xin Liu","doi":"10.1016/j.biocel.2024.106702","DOIUrl":"10.1016/j.biocel.2024.106702","url":null,"abstract":"<div><div>Intestinal ischemia-reperfusion (I/R) injury is common in clinical settings and is associated with high mortality. Sevoflurane, a widely used anesthetic, has long recognized for its protective effects against intestinal I/R injury, though the underlying mechanisms remain largely uncharacterized. In this study, using both <em>in vivo</em> and <em>in vitro</em> models, we uncovered a novel role of sevoflurane in preventing ferroptotic cell death during intestinal I/R injury. Sevoflurane treatment activated transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) and upregulated its target genes involved in iron sequestration (FTL) and glutathione biosynthesis (SLC7A11 and GCLM). These changes reduced intracellular ferrous iron levels and alleviated iron-dependent oxidative stress and lipid peroxidation, a hallmark of ferroptosis. Importantly, through large-scale kinome screening, we revealed that sevoflurane-induced Nrf2 activation was mediated by AMP-activated protein kinase (AMPK). Sevoflurane treatment activated AMPK, which subsequently phosphorylated Nrf2 and prevented its degradation. Stabilized Nrf2 then entered nucleus, where it promoted the transcription of downstream targets. We concluded that sevoflurane exerts anti-ferroptoic function in intestinal I/R through the AMPK/Nrf2 signaling pathway. These results expand our knowledge about the pathogenesis of intestinal I/R injury, and provide novel insights for optimizing clinical treatments and developing novel therapeutic strategies.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106702"},"PeriodicalIF":3.4,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711848","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":"Antitumor effect of bromo-naphthoquinone associated with tannic acid in triple negative breast cancer cells","authors":"Emanuelle Pangoni de Carvalho ,&nbsp;Adriano de Souza Pessoa ,&nbsp;Flávia Godoy Iano ,&nbsp;Laura Ribeiro ,&nbsp;Bianca Leme ,&nbsp;Luis Francisco Borges ,&nbsp;Mariana Liessa Rovis Sanches ,&nbsp;Valdecir Farias Ximenes ,&nbsp;Rodrigo Cardoso de Oliveira","doi":"10.1016/j.biocel.2024.106697","DOIUrl":"10.1016/j.biocel.2024.106697","url":null,"abstract":"<div><div>Triple-negative breast cancer (TNBC) is an aggressive type of tumor that tends to recur in women. It is characterized by the absence of hormonal receptors, making it challenging to diagnosis and treatment. In this study, we investigated the anti-tumor effects of a pro-oxidant naphthoquinone derivative called bromo-naphthoquinone (BrNQ) isolated and combined with the antioxidant tannic acid (TA) in order to improve treatment. We used tumor cell lines MDA-MB-231 and HCC-70, as well as normal breast cells, HB4a, as control. Initially, viability assays conducted within 72 hours showed that the combination of compounds had a synergistic and notable cytotoxic effect on the tumor cells. The increased cytotoxicity appeared to be linked to changes in the cellular redox status, as indicated by a significant rise in reactive oxygen species (ROS) and though alterations in the level of thiol. The treatment also induced apoptosis, inhibited proliferation, and reduced migration, particularly in the MDA-MB-231 cell line. Furthermore, relevant changes were detected in the expression of Bcl-2, BAX, FAS, and BIRC-5, while no significant alteration in the expression of NOXs was observed. In conclusion, our findings suggested that the combination of BrNQ and TA though the ability to change redox status in tumor cells could act as a potential adjuvant treatment modality for improve prognosis in TNBC.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106697"},"PeriodicalIF":3.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142683277","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":"Use of Myriocin as co-adjuvant in glaucoma surgery: An in vitro study","authors":"Linda Montavoci ,&nbsp;Dario Romano ,&nbsp;Leonardo Colombo ,&nbsp;Aida Zulueta ,&nbsp;Michele Dei Cas ,&nbsp;Mariangela Scavone ,&nbsp;Delfina Tosi ,&nbsp;Clara Bernardelli ,&nbsp;Alessandro Autelitano ,&nbsp;Marco Trinchera ,&nbsp;Luca Rossetti ,&nbsp;Anna Caretti","doi":"10.1016/j.biocel.2024.106699","DOIUrl":"10.1016/j.biocel.2024.106699","url":null,"abstract":"<div><div>Mitomycin C as well as other antiproliferative drugs are off-label agents widely used to prevent the failure of glaucoma surgery due to activation of Tenon’s fibroblasts and the ensuing excessive subconjunctival scarring. Though efficacious, these treatments are associated with some severe long-term complications, so it is crucial to investigate less cytotoxic compounds as adjuvant therapy in glaucoma surgery. The aim of this study was to evaluate the effect and potential cytotoxicity of Myriocin, a natural sphingolipid synthesis inhibitor, on TGF-β1-induced myofibroblasts transformation of human dermal fibroblasts. We found that myriocin significantly attenuated the transcript levels of αSMA, CTGF, and MMP9 which are involved in the fibrosis process. Mitomycin C poorly affects the same pro-fibrotic markers while reducing fibroblasts motility as much as myriocin. At similar doses, five minutes of mitomycin C treatment consistently affects human dermal fibroblast viability and proliferation compared to prolonged myriocin application, strengthening already published data on the good tolerability of this natural compound. Our results draw attention to the use of myriocin as an adjuvant in glaucoma surgery due to the effectiveness in reducing fibroblasts to myofibroblasts transformation and the low cytotoxicity.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106699"},"PeriodicalIF":3.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142689403","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":"Transcriptomic and in silico analysis of BLACE (B-cell acute lymphoblastic leukemia expressed), a new non-coding RNA, as a diagnostic biomarker in B-cell ALL","authors":"Saadiya Zia ,&nbsp;Nazia Rehman ,&nbsp;Saima Ejaz ,&nbsp;Muhammad Shahid ,&nbsp;Muhammad Ali ,&nbsp;Ramla Shahid","doi":"10.1016/j.biocel.2024.106698","DOIUrl":"10.1016/j.biocel.2024.106698","url":null,"abstract":"<div><div>ALL (acute lymphoblastic leukemia) is a type of hematological malignancy that involves developmental and differentiation arrest at the lymphoblast stage. BLACE, a gene specifically expressed in B-cell acute lymphoblastic leukemia shows little or no expression in mature B-lymphocytes. The current pilot study involves transcriptional analysis of BLACE in B-cell ALL patients. Expression of BLACE was high in both pediatric and adult ALL patients. Promoter analysis of the BLACE gene showed the presence of CAAT and TATA box promoters and G-rich sequences with a potential to form G-quadruplexes. Due to identification of TAL1 transcription factor binding sites within the BLACE promoter region, expression of TAL1 gene was measured and found to correlate with the BLACE expression. The presence of an overlapping G-rich sequence and TAL1 binding site at −1291 bps within BLACE promoter indicated a new target site for controlling BLACE expression. The docking studies performed between BLACE-TAL1 protein showed a binding score of −208.68 kcal/mol and identified 21 BLACE nucleotide - TAL1 residues interacting at the docking interface. Together, our findings suggested that BLACE gene specifically expressed in B-cell ALL could serve as a new therapeutic target. Further investigations are required to get a comprehensive understanding of the BLACE gene mechanism.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106698"},"PeriodicalIF":3.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142689402","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":"MLN4924 Suppresses head and neck squamous cell carcinoma progression by inactivating the mTOR signaling pathway via the NEDD8/CUL4/TSC2 axis","authors":"Youfang Jiang ,&nbsp;Fei Le ,&nbsp;Shuangling Huang ,&nbsp;Xuezhong Chen ,&nbsp;Ziqing Deng","doi":"10.1016/j.biocel.2024.106696","DOIUrl":"10.1016/j.biocel.2024.106696","url":null,"abstract":"<div><div>Head and neck squamous cell carcinoma (HNSCC) is an aggressive cancer with a five-year survival rate below 50 %. Standard treatments for HNSCC include surgery, radiotherapy, chemotherapy, and targeted therapies, but they still have significant limitations. Neddylation, a post-translational modification involving the attachment of NEDD8 (neural precursor cells expressed developmentally down-regulated 8) to proteins, is frequently dysregulated in HNSCC, thereby promoting tumor growth. MLN4924, also known as Pevonedistat, is a Neddylation inhibitor that has shown promise in suppressing HNSCC cell proliferation and invasion, establishing it as a potential therapeutic option. However, its precise molecular mechanism remains unclear. This study aims to investigate the mechanism of MLN4924 in HNSCC. This study examined the effects of MLN4924 on HNSCC and its associated molecular pathways. Bioinformatic analysis indicated that NEDD8, a critical component of the Neddylation pathway, is linked to poor prognosis and the mTOR (mammalian target of rapamycin) signaling pathway in HNSCC. MLN4924 significantly suppressed cell migration, invasion, and the epithelial-mesenchymal transition (EMT) pathway, and downregulated NEDD8 expression. Mechanistic studies demonstrated that MLN4924 inhibited the binding of NEDD8 to cullin4 (CUL4) and prevented the Neddylation of tuberous sclerosis complex 2 (TSC2), leading to the inactivation of the mTOR pathway. These findings were confirmed <em>in vivo</em>, where MLN4924 effectively inhibited tumor growth. Overall, MLN4924 disrupted Neddylation pathway and stabilized TSC2, thereby inactivating the mTOR pathway. The study provided a theoretical basis for the clinical potential of MLN4924 in improving treatment outcomes for HNSCC patients, offering a novel strategy for addressing this challenging disease.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106696"},"PeriodicalIF":3.4,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142683280","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":"Human pluripotent stem cell-derived models of the hippocampus","authors":"Haruka Nishimura ,&nbsp;Yun Li","doi":"10.1016/j.biocel.2024.106695","DOIUrl":"10.1016/j.biocel.2024.106695","url":null,"abstract":"<div><div>The hippocampus is a crucial structure of the brain, recognised for its roles in the formation of memory, and our ability to navigate the world. Despite its importance, clear understanding of how the human hippocampus develops and its contribution to disease is limited due to the inaccessible nature of the human brain. In this regard, the advent of human pluripotent stem cell (hPSC) technologies has enabled the study of human biology in an unprecedented manner, through the ability to model development and disease as both 2D monolayers and 3D organoids. In this review, we explore the existing efforts to derive the hippocampal lineage from hPSCs and evaluate the various aspects of the <em>in vivo</em> hippocampus that are replicated <em>in vitro.</em> In addition, we highlight key diseases that have been modelled using hPSC-derived cultures and offer our perspective on future directions for this emerging field.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106695"},"PeriodicalIF":3.4,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142669573","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":"Prolonged glutamine starvation reactivates mTOR to inhibit autophagy and initiate autophagic lysosome reformation to maintain cell viability","authors":"Amruta Singh ,&nbsp;Kewal Kumar Mahapatra ,&nbsp;Prakash Priyadarshi Praharaj ,&nbsp;Srimanta Patra ,&nbsp;Soumya Ranjan Mishra ,&nbsp;Sankargouda Patil ,&nbsp;Sujit Kumar Bhutia","doi":"10.1016/j.biocel.2024.106694","DOIUrl":"10.1016/j.biocel.2024.106694","url":null,"abstract":"<div><div>Autophagy, a cellular recycling mechanism, utilizes lysosomes for cellular degradation. Prolonged autophagy reduces the pool of functional lysosomes in the cell. However, lysosomal homeostasis is maintained through the regeneration of functional lysosomes during the terminal stage of autophagy, i.e. Autophagic lysosome reformation (ALR). Through confocal microscopy during glutamine starvation, we unravel the regeneration of tubules from autolysosomes by undertaking significant membrane remodeling, which majorly depends on mTOR reactivation, RAB7 dissociation, phosphatidyl inositol 3 phosphate (PI3P) dependent-dynamin 2 and clathrin recruitment. In glutamine-starved cells, we found mTOR is the central modulator in regulating ALR initiation, and its pharmacological inhibition with rapamycin leads to a decrease in lysosomal tubulation. Moreover, RAB7 and Clathrin are essential for tubule elongation and it showed that siRNA targeting RAB7 and Clathrin restricts tubule initiation under glutamine starvation. In this setting, we examined the physiological relevance of ALR during prolonged glutamine deprivation and found that genetic and pharmacological inhibition of critical proteins involved in ALR promotes cell death in oral cancer cells, establishing ALR is essential for maintaining cell survival during stress.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106694"},"PeriodicalIF":3.4,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142640192","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":"Regulation of autophagy by Rab27B in colorectal cancer","authors":"Sahida Afroz ,&nbsp;Ranjan Preet ,&nbsp;Vikalp Vishwakarma ,&nbsp;Andrew E. Evans ,&nbsp;Alexa N. Magstadt ,&nbsp;Dan A. Dixon","doi":"10.1016/j.biocel.2024.106693","DOIUrl":"10.1016/j.biocel.2024.106693","url":null,"abstract":"<div><div>Autophagy is a cellular recycling process that is associated with tumor growth, anti-tumor immune responses, and therapy resistance in colorectal cancer (CRC). In this report, we identify the small GTPase Rab27B to control the autophagy process in CRC. Depletion of Rab27B showed an abnormal accumulation of autophagy vesicles and increased autophagy markers in CRC cells, indicating autophagy dysregulation. Image analysis indicated that autophagy flux is blocked at the autophagosome/lysosome fusion step when Rab27B is lost. While Rab27B deficient cells are proficient at growth under 2D <em>in vitro</em> conditions, cell growth was significantly impacted in both <em>in vitro</em> 3D growth and <em>in vivo</em> tumorigenesis studies. Together, these results demonstrate a new role of Rab27B in the autophagy trafficking process in CRC and identify Rab27B as a potential therapeutic target for CRC.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106693"},"PeriodicalIF":3.4,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142631038","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":"TFAP2C/FLT3 axis reduces ferroptosis in breast cancer cells by inhibiting mitochondrial autophagy","authors":"Jiayue Shen ,&nbsp;Yali He ,&nbsp;Bingchuan Zhou ,&nbsp;Huabo Qin ,&nbsp;Shuai Zhang ,&nbsp;Zixiang Huang ,&nbsp;Xiangcheng Zhang","doi":"10.1016/j.biocel.2024.106691","DOIUrl":"10.1016/j.biocel.2024.106691","url":null,"abstract":"<div><h3>Background</h3><div>FMS-like tyrosine kinase 3 (FLT3), a key target protein for treating acute myeloid leukemia, has recently been found to be closely related to ferroptosis in breast cancer (BC). However, the mechanism by which FLT3 regulates ferroptosis in BC remains unknown. Whether this regulatory relationship can be exploited for BC treatment needs further exploration.</div></div><div><h3>Methods</h3><div>This study combined analysis from The Cancer Genome Atlas database with immunohistochemistry/quantitative reverse transcription-PCR/Western blot experiments to verify the expression of FLT3 in BC. FLT3 knockdown/overexpression plasmids were used in conjunction with mitochondrial autophagy inducers to treat BC cells, analyzing the effects of FLT3 on autophagy and ferroptosis. Key transcription factors for FLT3 were determined through predictions from the KnockTF database and dual luciferase/chromatin immunoprecipitation experiments, further analyzing the impact of this regulatory axis on autophagy and ferroptosis in BC cells.</div></div><div><h3>Results</h3><div>FLT3 was significantly overexpressed in BC tissues and cells. Overexpression of FLT3 could inhibit autophagy and ferroptosis in BC cells, a regulation that was restored upon the addition of mitochondrial autophagy inducers. Additionally, transcription factor AP-2 gamma (TFAP2C) could mediate the transcriptional activation of FLT3, further inhibiting ferroptosis induced by mitochondrial autophagy.</div></div><div><h3>Conclusion</h3><div>The TFAP2C/FLT3 axis reduced ferroptosis in BC cells by inhibiting mitochondrial autophagy. These research findings elucidated the mechanism by which FLT3 regulated ferroptosis in BC and provided potential targets for BC treatment.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106691"},"PeriodicalIF":3.4,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142631041","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}