Cell Biology International最新文献_第6页

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

JRK binds satellite III DNA and is necessary for the heat shock response JRK 与卫星 III DNA 结合，是热休克反应所必需的。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-07-01 DOI: 10.1002/cbin.12216

Rosalie Waldron, Maria de los Angeles Becerra Rodriguez, John M. Williams, Zhenfei Ning, Abrar Ahmed, Andrew Lindsay, Tom Moore

{"title":"JRK binds satellite III DNA and is necessary for the heat shock response","authors":"Rosalie Waldron, Maria de los Angeles Becerra Rodriguez, John M. Williams, Zhenfei Ning, Abrar Ahmed, Andrew Lindsay, Tom Moore","doi":"10.1002/cbin.12216","DOIUrl":"10.1002/cbin.12216","url":null,"abstract":"JRK is a DNA-binding protein of the pogo superfamily of transposons, which includes the well-known centromere binding protein B (CENP-B). Jrk null mice exhibit epilepsy, and growth and reproductive disorders, consistent with its relatively high expression in the brain and reproductive tissues. Human JRK DNA variants and gene expression levels are implicated in cancers and neuropsychiatric disorders. JRK protein modulates β-catenin–TCF activity but little is known of its cellular functions. Based on its homology to CENP-B, we determined whether JRK binds centromeric or other satellite DNAs. We show that human JRK binds satellite III DNA, which is abundant at the chromosome 9q12 juxtacentromeric region and on Yq12, both sites of nuclear stress body assembly. Human JRK-GFP overexpressed in HeLa cells strongly localises to 9q12. Using an anti-JRK antiserum we show that endogenous JRK co-localises with a subset of centromeres in non-stressed cells, and with heat shock factor 1 following heat shock. Knockdown of JRK in HeLa cells proportionately reduces heat shock protein gene expression in heat-shocked cells. A role for JRK in regulating the heat shock response is consistent with the mouse Jrk null phenotype and suggests that human JRK may act as a modifier of diseases with a cellular stress component.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 8","pages":"1212-1222"},"PeriodicalIF":3.3,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.12216","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141466423","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

Correction to “potential role of heat shock proteins in neural differentiation of murine embryonal carcinoma stem cells (P19)” 更正 "热休克蛋白在小鼠胚胎癌干细胞（P19）神经分化中的潜在作用"。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-06-30 DOI: 10.1002/cbin.12193

{"title":"Correction to “potential role of heat shock proteins in neural differentiation of murine embryonal carcinoma stem cells (P19)”","authors":"","doi":"10.1002/cbin.12193","DOIUrl":"10.1002/cbin.12193","url":null,"abstract":"Afzal E, Ebrahimi M, Najafi SM, Daryadel A, Baharvand H. Potential role of heat shock proteins in neural differentiation of murine embryonal carcinoma stem cells (P19). Cell Biol Int. 2011 Jul;35(7):713-20. doi: 10.1042/CBI20100457.We regret to acknowledge a non-intentional human error related to data placement/handling during the preparation of the representative images of Figures 2d and 4. We, therefore, corrected them. A replacement to figures is included below:In Figure 4, the left column is the control group as demonstrated in Figure 2 (first row). At that time, we did this to compare the results and help the readers to have a better understanding of the story. It could be deleted without any changes in results and conclusion.These image displacement by no means change our conclusions, since the aim was to show the expression of HSC70 in non-heat treated (first row) with the heat treated (second row). As mentioned in the paper the expression of HSC70 did not change pre- and post-heated.The authors would like to apologize for any inconvenience caused.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 8","pages":"1223-1224"},"PeriodicalIF":3.3,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.12193","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141466422","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

TCF12 induces ferroptosis by suppressing OTUB1-mediated SLC7A11 deubiquitination to promote cisplatin sensitivity in oral squamous cell carcinoma TCF12通过抑制OTUB1介导的SLC7A11去泛素化诱导铁变态反应，从而促进口腔鳞状细胞癌对顺铂的敏感性。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2024-06-30 DOI: 10.1002/cbin.12211

Yanchun Liu, Qin Bai, Nan Pang, Jun Xue

{"title":"TCF12 induces ferroptosis by suppressing OTUB1-mediated SLC7A11 deubiquitination to promote cisplatin sensitivity in oral squamous cell carcinoma","authors":"Yanchun Liu, Qin Bai, Nan Pang, Jun Xue","doi":"10.1002/cbin.12211","DOIUrl":"10.1002/cbin.12211","url":null,"abstract":"Chemotherapy resistance is a major obstacle to effective cancer treatment, and promotion of ferroptosis can suppress cisplatin resistance in tumor cells. TCF12 plays a suppressive role in oral squamous cell carcinoma (OSCC), but whether it participates in the regulation of cisplatin resistance by modulating ferroptosis remains unclear. Here, we found that TCF12 expression was decreased in OSCC cells compared with normal oral cells, and it was reduced in cisplatin (DDP)-resistant OSCC cells compared with parental cells. Moreover, overexpression of TCF12 sensitized DDP-resistant cells to DDP by promoting ferroptosis. Intriguingly, silencing TCF12 reversed the promotion effect of the ferroptosis activator RSL3 on ferroptosis and DDP sensitivity, and overexpressing TCF12 antagonized the effect of the ferroptosis inhibitor liproxstatin-1 on ferroptosis and DDP resistance. Mechanically, TCF12 promoted ubiquitination of SLC7A11 and decreased SLC7A11 protein stability through transcriptional repression of OTUB1, thereby facilitating ferroptosis. Consistently, SLC7A11 overexpression neutralized the promotion effect of TCF12 on ferroptosis and DDP sensitivity. Additionally, upregulation of TCF12 hindered the growth of mouse OSCC xenografts and enhanced the DDP sensitivity of xenografts by inducing ferroptosis. In conclusion, TCF12 enhanced DDP sensitivity in OSCC cells by promoting ferroptosis, which was achieved through modulating SLC7A11 expression via transcriptional regulation of OTUB1.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 11","pages":"1649-1663"},"PeriodicalIF":3.3,"publicationDate":"2024-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141466426","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