Cell Biology International最新文献_第9页

Induced expression of AMOT reverses adriamycin resistance in breast cancer cells 诱导表达 AMOT 可逆转乳腺癌细胞对阿霉素的耐药性。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-17 DOI: 10.1002/cbin.12198

Haige Zhang, Yingyi Wang, Ya Gao, Mingming Du, Erhu Pan, Mingliang Sun, Xiaozhi Zhang

{"title":"Induced expression of AMOT reverses adriamycin resistance in breast cancer cells","authors":"Haige Zhang, Yingyi Wang, Ya Gao, Mingming Du, Erhu Pan, Mingliang Sun, Xiaozhi Zhang","doi":"10.1002/cbin.12198","DOIUrl":"10.1002/cbin.12198","url":null,"abstract":"Adriamycin (ADR) is widely used against breast cancer, but subsequent resistance always occurs. YAP, a downstream protein of angiomotin (AMOT), importantly contributes to ADR resistance, whereas the mechanism is largely unknown. MCF-7 cells and MDA-MB-231 cells were used to establish ADR-resistant cell. Then, mRNA and protein expressions of AMOT and YAP expressions were determined. After AMOT transfection alone or in combination with YAP, the sensitivity of the cells to ADR were evaluated in vitro by examining cell proliferation, apoptosis, and cell cycle, as well as in vivo by examining tumor growth. Additionally, the expressions of proteins in YAP pathway were determined in AMOT-overexpressing cells. In the ADR-resistant cells, the expression of AMOT was decreased while YAP was increased, respectively, and the nucleus localization of YAP was increased at the same time. After AMOT overexpression, these were inhibited, whereas the cell sensitivity to ADR was enhanced. However, the AMOT-induced changes were significantly suppressed by YAP knockdown. The consistent results in vivo showed that AMOT enhanced the inhibition of ADR on tumor growth, and inhibited YAP signaling, evidenced by decreased levels of YAP, CycD1, and p-ERK. Our data revealed that decreased AMOT contributed to ADR resistance in breast cancer cells, which was importantly negatively mediated YAP. These observations provide a potential therapy against breast cancer with ADR resistance.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 9","pages":"1301-1312"},"PeriodicalIF":3.3,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141632803","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}

引用次数: 0

The migrasome as a developmental learning paradigm in cell biology 迁移体是细胞生物学中的发展学习范例。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-15 DOI: 10.1002/cbin.12220

Yujiao Wang, Zirui Wang, Haoran Cui, Leiliang Zhang

{"title":"The migrasome as a developmental learning paradigm in cell biology","authors":"Yujiao Wang, Zirui Wang, Haoran Cui, Leiliang Zhang","doi":"10.1002/cbin.12220","DOIUrl":"10.1002/cbin.12220","url":null,"abstract":"Migrasome is a newly discovered organelle composed of small vesicular structures enclosed in membrane structures. Since its discovery in 2014, migrasome has attracted increasing attention in cell biology due to its critical role in multiple disease processes. Its pivotal role in various disease processes, including cell migration, intercellular communication, removal of damaged mitochondria, embryogenesis localization, immune cell chemotaxis, and virus transmission, underscores its significance in biological systems. With research on migrasome steadily increasing, it becomes a unique resource for undergraduate cell biology education. For deeper understanding of migrasome, we applied a bibliometric approach. Here we conducted a comprehensive analysis of migrasome research by retrieving relevant literature from databases such as Web of Science, Scopus, and PubMed using the keywords “migrasome” or “migrasomes.” Employing CiteSpace software and Prism, we analyzed annual publication trends, identified core authors and institutions, assessed national contributions, examined keywords, and scrutinized highly cited literature related to migrasome research. This study presents a comprehensive overview of migrasome research, elucidating its literature characteristics, key contributors, research hotspots, and emerging trends. By shedding light on the current status and future trajectories of migrasome research, we aim to provide valuable insights for teachers in cell biology education. We propose for the integration of migrasome research into undergraduate curricula to enhance the understanding of cell biology among premedical, medical, and biomedical students, thereby fostering a deeper appreciation for the intricate mechanisms governing cellular behavior and disease processes.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 9","pages":"1254-1265"},"PeriodicalIF":3.3,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619407","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}

引用次数: 0

Microproteins/micropeptides dysregulation contributes to cancer progression and development: A mechanistic review 微蛋白/微肽失调导致癌症进展和发展：机理综述。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-15 DOI: 10.1002/cbin.12219

Paul Rodrigues, Harun Bangali, Eyhab Ali, M. K. Sharma, Bekhzod Abdullaev, Adnan Taan Alkhafaji, Maha Medha Deorari, Rahman S. Zabibah, Ali Haslany

{"title":"Microproteins/micropeptides dysregulation contributes to cancer progression and development: A mechanistic review","authors":"Paul Rodrigues, Harun Bangali, Eyhab Ali, M. K. Sharma, Bekhzod Abdullaev, Adnan Taan Alkhafaji, Maha Medha Deorari, Rahman S. Zabibah, Ali Haslany","doi":"10.1002/cbin.12219","DOIUrl":"10.1002/cbin.12219","url":null,"abstract":"Microproteins, known as micropeptides, are small protein molecules encoded by short open reading frames. These recently identified molecules have been proven to be an essential part of the human proteome that participates in multiple processes, such as DNA repair, mitochondrial respiration, and regulating different signaling pathways. A growing body of studies has evidenced that microproteins exhibit dysregulated expression levels in various malignancies and contribute to tumor progression. It has been reported that microproteins interact with many proteins, such as enzymes (e.g., adenosine triphosphate synthase) and signal transducers (e.g., c-Jun), and regulate malignant cell metabolism, proliferation, and metastasis. Moreover, microproteins have been found to play a significant role in multidrug resistance in vitro and in vivo by their activity in DNA repair pathways. Considering that, this review intended to summarize the roles of microproteins in different aspects of tumorigenesis with diagnostic and therapeutic perspectives.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 10","pages":"1395-1405"},"PeriodicalIF":3.3,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141619406","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}

引用次数: 0

Integrated analysis of differentially m6A modified and expressed lncRNAs for biomarker identification in coronary artery disease 综合分析不同 m6A 修饰和表达的 lncRNA，用于冠状动脉疾病的生物标记物鉴定。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-14 DOI: 10.1002/cbin.12224

Rongli Jiang, Qiaowei Jia, Chengcheng Li, Xiongkang Gan, Yaqing Zhou, Yang Pan, Yahong Fu, Xiumei Chen, Lanyu Liang, Enzhi Jia

{"title":"Integrated analysis of differentially m6A modified and expressed lncRNAs for biomarker identification in coronary artery disease","authors":"Rongli Jiang, Qiaowei Jia, Chengcheng Li, Xiongkang Gan, Yaqing Zhou, Yang Pan, Yahong Fu, Xiumei Chen, Lanyu Liang, Enzhi Jia","doi":"10.1002/cbin.12224","DOIUrl":"10.1002/cbin.12224","url":null,"abstract":"N6-methyladenosine (m6A) is the most prevalent internal RNA modification in mammals. However, limited research has been conducted on the role of m6A in coronary artery disease (CAD). We conducted methylated RNA immunoprecipitation sequencing and RNA sequencing to obtain a genome-wide profile of m6A-modified long noncoding RNAs (lncRNAs) in human coronary artery smooth muscle cells either exposed to oxidized low-density lipoprotein treatment or not, and the characteristics of the expression profiles were explored using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses. The predictive effects of seven selected lncRNAs on CAD were evaluated in peripheral blood mononuclear cells (PBMCs). The differentially m6A-modified and expressed lncRNAs related genes were predominantly enriched in small GTPase-mediated signal transduction, ErbB signaling, and Rap1 signaling. Additionally, the expression levels of uc003pes.1, ENST00000422847, and NR_110155 were significantly associated with CAD, with uc003pes.1 identified as an independent risk factor and NR_110155 as an independent protective factor for CAD. NR_110155 and uc003pes.1 in PBMCs have the potential to serve as biomarkers for predicting CAD.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 11","pages":"1664-1679"},"PeriodicalIF":3.3,"publicationDate":"2024-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.12224","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141615976","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}

引用次数: 0

tRNA-derived fragment tRF-30 propels diabetes-induced retinal microvascular complications by regulating STAT3 signaling tRNA衍生片段tRF-30通过调节STAT3信号传导推动糖尿病诱发的视网膜微血管并发症。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-12 DOI: 10.1002/cbin.12210

Dongqing Yuan, Yingnan Xu, Lian Xue, Weiwei Zhang, Liuwei Gu, Qinghuai Liu

{"title":"tRNA-derived fragment tRF-30 propels diabetes-induced retinal microvascular complications by regulating STAT3 signaling","authors":"Dongqing Yuan, Yingnan Xu, Lian Xue, Weiwei Zhang, Liuwei Gu, Qinghuai Liu","doi":"10.1002/cbin.12210","DOIUrl":"10.1002/cbin.12210","url":null,"abstract":"Transfer RNA-derived fragments (tRFs) represent a novel class of non-coding RNA transcripts that possess specific biological functions. However, the involvement of tRFs in retinal microvascular diseases remains poorly understood. In this study, we aimed to reveal whether modulation of tRF-30 expression could attenuate pathological retinal neovascular diseases. Our findings demonstrate a significant upregulation of tRF-30 expression levels in both in vivo models of diabetic retinopathy (DR) and in vitro endothelial sprouting models. Conversely, inhibition of tRF-30 expression suppressed the formation of abnormal neovascularization in the retina in vivo, while reducing the proliferation and migration activity of retinal vascular endothelial cells in vitro. We also found that tRF-30 modulates retinal neovascularization through the tRF-30/TRIB3/signal transducer and activated transcription 3 signaling pathway. Furthermore, we validated a significant upregulation of tRF-30 expression levels in the vitreous humor of DR patients, with high levels of both validity and specificity in diagnostic testing. Collectively, our findings highlight a pro-angiogenic role for tRF-30 in DR. Intervening in the tRF-30 signaling pathway may represent a promising prevention and treatment strategy for retinal angiogenesis.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 10","pages":"1548-1558"},"PeriodicalIF":3.3,"publicationDate":"2024-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141598734","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}

引用次数: 0

Chrysin attenuates epithelial prostatic hyperplasia in the ventral prostate of spontaneously hypertensive rats 蛹虫草素能减轻自发性高血压大鼠腹侧前列腺的上皮性前列腺增生。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-11 DOI: 10.1002/cbin.12218

Nathany R. L. dos Santos, Gessica C. de Sousa, Phâmella N. Lima, Bárbara C. M. Medeiros, Luana A. Manso, Cinthia R. B. Silva, Carla C. R. da Silveira, Paulo C. Ghedini, Hericles M. Campos, Matheus S. Costa, Isadora G. Fernandes, Elizabeth P. Mendes, Sebastião R. Taboga, Carlos H. de Castro, Fernanda C. A. dos Santos, Manoel F. Biancardi

{"title":"Chrysin attenuates epithelial prostatic hyperplasia in the ventral prostate of spontaneously hypertensive rats","authors":"Nathany R. L. dos Santos, Gessica C. de Sousa, Phâmella N. Lima, Bárbara C. M. Medeiros, Luana A. Manso, Cinthia R. B. Silva, Carla C. R. da Silveira, Paulo C. Ghedini, Hericles M. Campos, Matheus S. Costa, Isadora G. Fernandes, Elizabeth P. Mendes, Sebastião R. Taboga, Carlos H. de Castro, Fernanda C. A. dos Santos, Manoel F. Biancardi","doi":"10.1002/cbin.12218","DOIUrl":"10.1002/cbin.12218","url":null,"abstract":"The aim of this study was to evaluate the effects of chrysin on the ventral prostate of spontaneously hypertensive rats (SHR). Ten-week-old male Wistar and SHR rats received 100 mg/kg/day of chrysin (TW and TSHR) or 200 µL/day of the dilution vehicle (CW and CSHR) for 70 days. After the treatment, the animals were euthanized and the prostates were dissected out, fixed, and processed for further morphological, immunohistochemical, and biochemical analyses. Blood was collected for serological analysis. Chrysin did not interfere with the blood pressure. Morphologically, the epithelial height increased in TW and decreased in TSHR. Stereology showed an increase in the epithelial and stromal relative frequency, and a decrease in the lumen of TW, whereas the epithelium in TSHR was reduced. Normal alveoli decreased, and hyperplastic alveoli had an increment in TW, whereas in TSHR normal alveoli increased and intense hyperplasia decreased. The secretion area was reduced in TW. Immunohistochemical analysis showed a smaller number of PCNA-positive cells in TW. Finally, the biochemical analysis showed a reduction in malondialdehyde, carbonylated proteins, superoxide dismutase, and catalase in TW and TSHR. We concluded that the chrysin effect is dependent on the context in which this flavonoid is employed. In normal conditions, the anabolic potential of the chrysin was favored, disrupting the morphology of the prostate. However, when used in animals predisposed to develop hyperplasia, this flavonoid attenuates the hyperplastic status, improving the morphology of the gland.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 10","pages":"1533-1547"},"PeriodicalIF":3.3,"publicationDate":"2024-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141589665","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}

引用次数: 0

Progranulin mitigates intestinal injury in a murine model of necrotizing enterocolitis by suppressing M1 macrophage polarization 在小鼠坏死性小肠结肠炎模型中，Progranulin 通过抑制 M1 巨噬细胞极化减轻肠道损伤。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-08 DOI: 10.1002/cbin.12209

Dandan Mo, Youjun Qiu, Bing Tian, Xinli Liu, Yujie Chen, Guotao Zou, Chunbao Guo, Chun Deng

{"title":"Progranulin mitigates intestinal injury in a murine model of necrotizing enterocolitis by suppressing M1 macrophage polarization","authors":"Dandan Mo, Youjun Qiu, Bing Tian, Xinli Liu, Yujie Chen, Guotao Zou, Chunbao Guo, Chun Deng","doi":"10.1002/cbin.12209","DOIUrl":"10.1002/cbin.12209","url":null,"abstract":"Neonatal necrotizing enterocolitis (NEC) is a critical digestive disorder frequently affecting premature infants. Characterized by intestinal inflammation caused by activated M1 macrophages, modulation of macrophage polarization is considered a promising therapeutic strategy for NEC. It has been demonstrated that the growth factor-like protein progranulin (PGRN), which plays roles in a number of physiological and pathological processes, can influence macrophage polarization and exhibit anti-inflammatory characteristics in a number of illnesses. However, its role in NEC is yet to be investigated. Our research showed that the levels of PGRN were markedly elevated in both human and animal models of NEC. PGRN deletion in mice worsens NEC by encouraging M1 polarization of macrophages and escalating intestinal damage and inflammation. Intravenous administration of recombinant PGRN to NEC mice showed significant survival benefits and protective effects, likely due to PGRN's ability to inhibit M1 polarization and reduce the release of pro-inflammatory factors. Our findings shed new light on PGRN's biological role in NEC and demonstrate its potential as a therapeutic target for the disease.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 10","pages":"1520-1532"},"PeriodicalIF":3.3,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554263","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}

引用次数: 0

Correction to “Stem cells technology as a platform for generating reproductive system organoids and treatment of infertility-related diseases” 更正 "干细胞技术作为生成生殖系统器官组织和治疗不孕不育相关疾病的平台"。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-04 DOI: 10.1002/cbin.12217

引用次数: 0

Transcriptome-wide profiling for melanocytes derived from newborn and adult human epidermis with enhanced proliferation 从新生儿和成人表皮中提取的黑素细胞的全转录组图谱，其增殖能力增强。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-03 DOI: 10.1002/cbin.12214

Ai Orimoto, Sayo Kashiwagi, Ayaka Funakoshi, Takashi Shimizu, Tsuyoshi Ishii, Tohru Kiyono, Tomokazu Fukuda

{"title":"Transcriptome-wide profiling for melanocytes derived from newborn and adult human epidermis with enhanced proliferation","authors":"Ai Orimoto, Sayo Kashiwagi, Ayaka Funakoshi, Takashi Shimizu, Tsuyoshi Ishii, Tohru Kiyono, Tomokazu Fukuda","doi":"10.1002/cbin.12214","DOIUrl":"10.1002/cbin.12214","url":null,"abstract":"The senescence-associated protein p16INK4A acts as a limiter element in cell-cycle progression. The loss of p16INK4A function is causally related to cellular immortalization. The increase in p16INK4A levels with advancing age was demonstrated in melanocytes. However, the characteristic difference between young and senescent melanocytes affecting immortalization of melanocytes remains unclear. In this study, we generated 10 different cell lines in total from newborn (NB) and adult (AD) primary normal human epidermal melanocytes (NHEM) using four different methods, transduction of CDK4R24C and cyclin D1 (K4D), K4D with TERT (K4DT), SV40 T-antigen (SV40T), and HPV16 E6 and E7 (E6/E7) and performed whole transcriptome sequencing analysis (RNA-Seq) to elucidate the differences of genome-wide expression profiles among cell lines. The analysis data revealed distinct differences in expression pattern between cell lines from NB and AD although no distinct biological differences were detected in analyses such as comparison of cell morphology, evaluation of cell proliferation, and cell cycle profiles. This study may provide useful in vitro models to benefit the understanding of skin-related diseases.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 10","pages":"1573-1587"},"PeriodicalIF":3.3,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141497253","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}

引用次数: 0

Golgi protein ACBD3 downregulation sensitizes cells to ferroptosis 下调高尔基体蛋白 ACBD3 可使细胞对铁变态反应敏感。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-02 DOI: 10.1002/cbin.12213

Ying Qian, Shanchuan Ma, Rong Qiu, Zhiyang Sun, Wei Liu, Fan Wu, Sin Man Lam, Zhengguo Xia, Kezhen Wang, Linshen Fang, Guanghou Shui, Xinwang Cao

{"title":"Golgi protein ACBD3 downregulation sensitizes cells to ferroptosis","authors":"Ying Qian, Shanchuan Ma, Rong Qiu, Zhiyang Sun, Wei Liu, Fan Wu, Sin Man Lam, Zhengguo Xia, Kezhen Wang, Linshen Fang, Guanghou Shui, Xinwang Cao","doi":"10.1002/cbin.12213","DOIUrl":"10.1002/cbin.12213","url":null,"abstract":"Ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, is emerging as a promising target in cancer therapy. It is regulated by a network of molecules and pathways that modulate lipid metabolism, iron homeostasis and redox balance, and related processes. However, there are still numerous regulatory molecules intricately involved in ferroptosis that remain to be identified. Here, we indicated that suppression of Golgi protein acyl-coenzyme A binding domain A containing 3 (ACBD3) increased the sensitivity of Henrieta Lacks and PANC1 cells to ferroptosis. ACBD3 knockdown increases labile iron levels by promoting ferritinophagy. This increase in free iron, coupled with reduced levels of glutathione peroxidase 4 due to ACBD3 knockdown, leads to the accumulation of reactive oxygen species and lipid peroxides. Moreover, ACBD3 knockdown also results in elevated levels of polyunsaturated fatty acid-containing glycerophospholipids through mechanisms that remain to be elucidated. Furthermore, inhibition of ferrtinophagy in ACBD3 downregulated cells by knocking down the nuclear receptor co-activator 4 or Bafilomycin A1 treatment impeded ferroptosis. Collectively, our findings highlight the pivotal role of ACBD3 in governing cellular resistance to ferroptosis and suggest that pharmacological manipulation of ACBD3 levels is a promising strategy for cancer therapy.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 10","pages":"1559-1572"},"PeriodicalIF":3.3,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141476032","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}

引用次数: 0