Apoptosis最新文献_第7页

Deubiquitinating enzyme USP28 inhibitor AZ1 alone and in combination with cisplatin for the treatment of non-small cell lung cancer 去泛素化酶 USP28 抑制剂 AZ1 单独或与顺铂联合治疗非小细胞肺癌。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-09-02 DOI: 10.1007/s10495-024-02008-6

Yiqiong Song, Longhao Wang, Yuanyuan Zheng, Lanqi Jia, Chunwei Li, Ke Chao, Lifeng Li, Shilong Sun, Yujie Wei, Yahao Ge, Yaqi Yang, Lili Zhu, Yixing Zhang, Jie Zhao

{"title":"Deubiquitinating enzyme USP28 inhibitor AZ1 alone and in combination with cisplatin for the treatment of non-small cell lung cancer","authors":"Yiqiong Song, Longhao Wang, Yuanyuan Zheng, Lanqi Jia, Chunwei Li, Ke Chao, Lifeng Li, Shilong Sun, Yujie Wei, Yahao Ge, Yaqi Yang, Lili Zhu, Yixing Zhang, Jie Zhao","doi":"10.1007/s10495-024-02008-6","DOIUrl":"10.1007/s10495-024-02008-6","url":null,"abstract":"<div><p>Lung cancer is one of the most common malignant tumors. Despite decades of research, the treatment of lung cancer remains challenging. Non-small cell lung cancer (NSCLC) is the primary type of lung cancer and is a significant focus of research in lung cancer treatment. The deubiquitinase ubiquitin-specific protease 28 (USP28) plays a role in the progression of various tumors and serves as a potential therapeutic target. This study aims to determine the role of USP28 in the progression of NSCLC. We examined the impact of the USP28 inhibitor AZ1 on the cell cycle, apoptosis, DNA damage response, and cellular immunogenicity in non-small cell lung cancer. We observed that AZ1 and siUSP28 induce DNA damage, leading to the activation of Noxa-mediated mitochondrial apoptosis. The dsDNA and mtDNA released from DNA damage and mitochondrial apoptosis activate tumor cell immunogenicity through the cGAS-STING signaling pathway. Simultaneously, targeting USP28 promotes the degradation of c-MYC, resulting in cell cycle arrest and inhibition of DNA repair. This further promotes DNA damage-induced cell apoptosis mediated by the Noxa protein, thereby enhancing tumor cell immunogenicity mediated by dsDNA and mtDNA. Moreover, we found that the combination of AZ1 and cisplatin (DDP) can enhance therapeutic efficacy, thereby providing a new strategy to overcome cisplatin resistance in NSCLC. These findings suggest that targeting USP28 and combining it with cisplatin are feasible strategies for treating NSCLC.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 9-10","pages":"1793 - 1809"},"PeriodicalIF":6.1,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

5-Aminolevulinic acid-mediated photodynamic therapy in combination with kinase inhibitor lapatinib enhances glioblastoma cell death 5-氨基乙酰丙酸介导的光动力疗法与激酶抑制剂拉帕替尼联合使用可增强胶质母细胞瘤细胞的死亡。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-08-27 DOI: 10.1007/s10495-024-02012-w

Sharayu Chandratre, Daniel Merenich, Kenneth Myers, Bin Chen

{"title":"5-Aminolevulinic acid-mediated photodynamic therapy in combination with kinase inhibitor lapatinib enhances glioblastoma cell death","authors":"Sharayu Chandratre, Daniel Merenich, Kenneth Myers, Bin Chen","doi":"10.1007/s10495-024-02012-w","DOIUrl":"10.1007/s10495-024-02012-w","url":null,"abstract":"<div><p>5-Aminolevulinic acid (ALA) is an intraoperative imaging agent approved for protoporphyrin IX (PpIX) fluorescence-guided resection of glioblastoma (GBM). It is currently under clinical evaluation for photodynamic therapy (PDT) after the completion of GBM surgery. We previously showed that lapatinib, a clinical kinase inhibitor of epidermal growth factor receptor 1 & 2 (EGFR and HER2), enhanced PpIX fluorescence in a panel of GBM cell lines by blocking ABCG2 (ATP-binding cassette super-family G member 2)-mediated PpIX efflux, which suggests its potential for improving ALA for GBM surgery and PDT. Here we show that lapatinib enhanced PDT-induced cytotoxicity by promoting GBM cell death with the induction of apoptosis followed by necrosis. While the induction of tumor cell apoptosis was massive and rapid in the H4 cell line with no detectable Bcl-2 and a low level of Bcl-xL, it was delayed and much less in extent in A172, U-87 and U-118 cell lines with higher levels of pro-survival Bcl-2 family proteins. Lapatinib treatment alone neither reduced GBM cell viability nor had any significant effect on EGFR downstream signaling. Its enhancement of ALA–PDT was largely due to the increase of intracellular PpIX particularly in the mitochondria, resulting in the activation of mitochondria-mediated apoptosis in H4 cells. Our present study demonstrates that lapatinib inhibits ABCG2-mediated PpIX efflux and sensitizes GBM cells to ALA–PDT by inducing tumor cell death.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 11-12","pages":"1978 - 1987"},"PeriodicalIF":6.1,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142071804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Heme oxygenase-1 binds gasdermin D to inhibit airway epithelium pyroptosis in allergic asthma 血红素加氧酶-1 可与气敏素 D 结合，抑制过敏性哮喘患者气道上皮细胞的脓毒症。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-08-27 DOI: 10.1007/s10495-024-02016-6

Jiajia Lv, Min Wu, Zhenwei Xia

引用次数: 0

Kynurenic acid protects against ischemia/reperfusion injury by modulating apoptosis in cardiomyocytes 犬尿酸通过调节心肌细胞凋亡防止缺血再灌注损伤

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-08-17 DOI: 10.1007/s10495-024-02004-w

Renáta Gáspár, Dóra Nógrádi-Halmi, Virág Demján, Petra Diószegi, Nóra Igaz, Anna Vincze, Márton Pipicz, Mónika Kiricsi, László Vécsei, Tamás Csont

{"title":"Kynurenic acid protects against ischemia/reperfusion injury by modulating apoptosis in cardiomyocytes","authors":"Renáta Gáspár, Dóra Nógrádi-Halmi, Virág Demján, Petra Diószegi, Nóra Igaz, Anna Vincze, Márton Pipicz, Mónika Kiricsi, László Vécsei, Tamás Csont","doi":"10.1007/s10495-024-02004-w","DOIUrl":"10.1007/s10495-024-02004-w","url":null,"abstract":"<div><p>Acute myocardial infarction, often associated with ischemia/reperfusion injury (I/R), is a leading cause of death worldwide. Although the endogenous tryptophan metabolite kynurenic acid (KYNA) has been shown to exert protection against I/R injury, its mechanism of action at the cellular and molecular level is not well understood yet. Therefore, we examined the potential involvement of antiapoptotic mechanisms, as well as N-methyl-D-aspartate (NMDA) receptor modulation in the protective effect of KYNA in cardiac cells exposed to simulated I/R (SI/R). KYNA was shown to attenuate cell death induced by SI/R dose-dependently in H9c2 cells or primary rat cardiomyocytes. Analysis of morphological and molecular markers of apoptosis (i.e., membrane blebbing, apoptotic nuclear morphology, DNA double-strand breaks, activation of caspases) revealed considerably increased apoptotic activity in cardiac cells undergoing SI/R. The investigated apoptotic markers were substantially improved by treatment with the cytoprotective dose of KYNA. Although cardiac cells were shown to express NMDA receptors, another NMDA antagonist structurally different from KYNA was unable to protect against SI/R-induced cell death. Our findings provide evidence that the protective effect of KYNA against SI/R-induced cardiac cell injury involves antiapoptotic mechanisms, that seem to evoke independently of NMDA receptor signaling.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 9-10","pages":"1483 - 1498"},"PeriodicalIF":6.1,"publicationDate":"2024-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141995120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

CD24 flags anastasis in melanoma cells. CD24 是黑色素瘤细胞吻合的标志。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-08-13 DOI: 10.1007/s10495-024-01990-1

Martina H Vasileva, Anette Bennemann, Karolin Zachmann, Michael P Schön, Jorge Frank, Vijay Kumar Ulaganathan

{"title":"CD24 flags anastasis in melanoma cells.","authors":"Martina H Vasileva, Anette Bennemann, Karolin Zachmann, Michael P Schön, Jorge Frank, Vijay Kumar Ulaganathan","doi":"10.1007/s10495-024-01990-1","DOIUrl":"https://doi.org/10.1007/s10495-024-01990-1","url":null,"abstract":"<p><p>Anastasis is a phenomenon observed in cancer cells, where cells that have initiated apoptosis are able to recover and survive. This molecular event is increasingly recognized as a potential contributor to cancer metastasis, facilitating the survival and migration of tumor cells. Nevertheless, the identification of a specific surface marker for detecting cancer cells in anastasis remained elusive. Here we report our observation that the cell surface expression of CD24 is preferentially enriched in a non-adherent FSC<sup>low</sup>SSC<sup>high</sup> melanoma subpopulation, which is generally considered a non-viable population in cultivated melanoma cell lines. More than 90% of non-adherent FSC<sup>low</sup>SSC<sup>high</sup>CD24<sup>+ve</sup> metastatic melanoma cells exhibited bonafide features of apoptosis on the cell surface and in the nucleus, marking apoptotic or seemingly apoptotic subpopulations of the in vitro cultivated metastatic melanoma cell lines. Unexpectedly, however, the CD24<sup>+ve</sup> subpopulation, despite being apoptotic, showed evidence of metabolic activity and exhibited proliferative capacities, including anchorage-independent growth, when inoculated in soft agarose growth medium. These findings indicate that apoptotic FSC<sup>low</sup>SSC<sup>high</sup>CD24<sup>+ve</sup> melanoma subpopulations are capable of reversing the progression of apoptosis. We report CD24 as the first novel cell surface marker for anastasis in melanoma cells.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141970468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Disulfidptosis-related long non-coding RNA signature predicts the prognosis, tumor microenvironment, immunotherapy, and antitumor drug options in colon adenocarcinoma 二硫化相关长非编码 RNA 特征可预测结肠腺癌的预后、肿瘤微环境、免疫疗法和抗肿瘤药物选择。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-08-08 DOI: 10.1007/s10495-024-02011-x

Kang Wang, Jing Yu, Qihuan Xu, Yuanhong Peng, Haibin Li, Yan Lu, Manzhao Ouyang

{"title":"Disulfidptosis-related long non-coding RNA signature predicts the prognosis, tumor microenvironment, immunotherapy, and antitumor drug options in colon adenocarcinoma","authors":"Kang Wang, Jing Yu, Qihuan Xu, Yuanhong Peng, Haibin Li, Yan Lu, Manzhao Ouyang","doi":"10.1007/s10495-024-02011-x","DOIUrl":"10.1007/s10495-024-02011-x","url":null,"abstract":"<div><p>This study aims to investigate the role and prognostic significance of long non-coding RNAs (lncRNAs) associated with disulfidptosis in colon adenocarcinoma (COAD). The TCGA database’s clinical data and transcriptome profiles were employed. Analysis of previous studies identified 10 disulfidptosis-related genes (DRGs). We used these genes to construct a signature that could independently and accurately predict the prognosis of patients with COAD. The Kaplan-Meier (K-M) curve analysis showed that the lower-risk group had a better prognosis. With the help of multivariate Cox regression analysis, the risk score produced from the patient’s signature might independently predict the outcomes. Utilizing a nomogram, the receiver operating characteristic (ROC) curve, and principal component analysis (PCA), the signature’s predictive ability was also confirmed. It’s interesting to note that immunotherapy, especially PD-1 immune checkpoint suppression, was more likely to benefit low-risk patients. The IC50 levels for certain anticancer agents were lower in the high-risk group. Finally, qRT-PCR analyses in colon cancer cell lines revealed elevated levels of lncRNAs CASC9, ZEB1-AS1, ATP2A1-AS1, SNHG7, AL683813.1, and AP003555.1, and reduced levels of FAM160A1-DT and AC112220.2, compared to normal cell lines. This signature offers insights into prognosis, tumor microenvironment, and options for immunotherapy and antitumor drugs in patients with COAD.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 11-12","pages":"2074 - 2090"},"PeriodicalIF":6.1,"publicationDate":"2024-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141900754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

TNF-α and RPLP0 drive the apoptosis of endothelial cells and increase susceptibility to high-altitude pulmonary edema TNF-α 和 RPLP0 驱动内皮细胞凋亡，增加高海拔肺水肿的易感性。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-08-07 DOI: 10.1007/s10495-024-02005-9

Yi-Ling Ge, Pei-Jie Li, Ying-Rui Bu, Bin Zhang, Jin Xu, Si-Yuan He, Qing-Lin Cao, Yun-Gang Bai, Jin Ma, Lin Zhang, Jie Zhou, Man-Jiang Xie

{"title":"TNF-α and RPLP0 drive the apoptosis of endothelial cells and increase susceptibility to high-altitude pulmonary edema","authors":"Yi-Ling Ge, Pei-Jie Li, Ying-Rui Bu, Bin Zhang, Jin Xu, Si-Yuan He, Qing-Lin Cao, Yun-Gang Bai, Jin Ma, Lin Zhang, Jie Zhou, Man-Jiang Xie","doi":"10.1007/s10495-024-02005-9","DOIUrl":"10.1007/s10495-024-02005-9","url":null,"abstract":"<div><p>High-altitude pulmonary edema (HAPE) is a fatal threat for sojourners who ascend rapidly without sufficient acclimatization. Acclimatized sojourners and adapted natives are both insensitive to HAPE but have different physiological traits and molecular bases. In this study, based on GSE52209, the gene expression profiles of HAPE patients were compared with those of acclimatized sojourners and adapted natives, with the common and divergent differentially expressed genes (DEGs) and their hub genes identified, respectively. Bioinformatic methodologies for functional enrichment analysis, immune infiltration, diagnostic model construction, competing endogenous RNA (ceRNA) analysis and drug prediction were performed to detect potential biological functions and molecular mechanisms. Next, an array of in vivo experiments in a HAPE rat model and in vitro experiments in HUVECs were conducted to verify the results of the bioinformatic analysis. The enriched pathways of DEGs and immune landscapes for HAPE were significantly different between sojourners and natives, and the common DEGs were enriched mainly in the pathways of development and immunity. Nomograms revealed that the upregulation of TNF-α and downregulation of RPLP0 exhibited high diagnostic efficiency for HAPE in both sojourners and natives, which was further validated in the HAPE rat model. The addition of TNF-α and RPLP0 knockdown activated apoptosis signaling in endothelial cells (ECs) and enhanced endothelial permeability. In conclusion, TNF-α and RPLP0 are shared biomarkers and molecular bases for HAPE susceptibility during the acclimatization/adaptation/maladaptation processes in sojourners and natives, inspiring new ideas for predicting and treating HAPE.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 9-10","pages":"1600 - 1618"},"PeriodicalIF":6.1,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141896610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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: Targeting PNPO to suppress tumor growth via inhibiting autophagic flux and to reverse paclitaxel resistance in ovarian cancer 更正：以 PNPO 为靶点，通过抑制自噬通量抑制肿瘤生长，并逆转卵巢癌对紫杉醇的耐药性。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-08-04 DOI: 10.1007/s10495-024-01998-7

Xin Li, Wencai Guan, Huiqiang Liu, Jia Yuan, Fanchen Wang, Bin Guan, Junyu Chen, Qi Lu, Lingyun Zhang, Guoxiong Xu

引用次数: 0

Comprehensive pancancer analysis reveals that LPCAT1 is a novel predictive biomarker for prognosis and immunotherapy response 胰腺癌综合分析表明，LPCAT1 是预测预后和免疫疗法反应的新型生物标志物。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-08-04 DOI: 10.1007/s10495-024-02010-y

Hongyu Gao, Jinfeng Zhu, Tong Wu, Qian Long, Xinyu Guan, Qitong Chen, Wenjun Yi

{"title":"Comprehensive pancancer analysis reveals that LPCAT1 is a novel predictive biomarker for prognosis and immunotherapy response","authors":"Hongyu Gao, Jinfeng Zhu, Tong Wu, Qian Long, Xinyu Guan, Qitong Chen, Wenjun Yi","doi":"10.1007/s10495-024-02010-y","DOIUrl":"10.1007/s10495-024-02010-y","url":null,"abstract":"<div><p>Lysophosphatidylcholine acyltransferase 1 (LPCAT1) is a crucial enzyme involved in phospholipid metabolism and is essential for maintaining the structure and functionality of biofilms. However, a comprehensive examination of the role of LPCAT1 across various cancer types is lacking. Multiple public databases have been utilized to examine LPCAT1 expression, genetic alterations, methylation, prognosis, biological function, and its relationship with antitumor immunity in different cancer types. The function of LPCAT1 in glioma, breast cancer and liver cancer cells was further verified using in vitro experiments. Our research indicated that LPCAT1 is upregulated in various cancers and is accompanied by a wide range of amplification mutations. Higher LPCAT1 expression was associated with poorer prognosis across multiple cancers. Further in vitro experiments demonstrated that interfering with LPCAT1 expression increased apoptosis in glioma, breast cancer and liver cancer cells and concurrently suppressed their proliferation and migration. Functional enrichment analysis revealed that LPCAT1-associated genes were primarily enriched in immune and cancer progression pathways, such as the JAK/STAT, MYC, and EMT, etc. Moreover, LPCAT1 expression was closely associated with immune cell infiltration and immune checkpoint-related gene expression. Interestingly, LPCAT1 expression levels were generally higher in patients in the immunotherapy response group. The combination of LPCAT1 and PDL1 serves as an effective predictor of immunotherapy response. In conclusion, LPCAT1 is involved in immune regulation and tumor progression and holds promise as a biomarker for predicting patient outcomes and immunotherapy efficacy.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 11-12","pages":"2128 - 2146"},"PeriodicalIF":6.1,"publicationDate":"2024-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

SEH1L siliencing induces ferroptosis and suppresses hepatocellular carcinoma progression via ATF3/HMOX1/GPX4 axis SEH1L siliencing通过ATF3/HMOX1/GPX4轴诱导铁变态反应并抑制肝细胞癌的进展。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-08-02 DOI: 10.1007/s10495-024-02009-5

Ziyang Feng, Ke Cao, Haojia Sun, Xuewen Liu

{"title":"SEH1L siliencing induces ferroptosis and suppresses hepatocellular carcinoma progression via ATF3/HMOX1/GPX4 axis","authors":"Ziyang Feng, Ke Cao, Haojia Sun, Xuewen Liu","doi":"10.1007/s10495-024-02009-5","DOIUrl":"10.1007/s10495-024-02009-5","url":null,"abstract":"<div><p>SEH1 like nucleoporin (SEH1L) is an important component of nuclear pore complex (NPC), which is crucial in the regulation of cell division. However, the interrelation between SEH1L expression and tumor progression is less studied. In this research, we performed a systematic bioinformatic analysis about SEH1L using TCGA, Timer 2.0, Cbioportal, UCLAN and CellMiner™ databases in pan-cancer. Besides, we further validated the bioinformatic results through in vitro and in vivo experiments in HCC, including transcriptome sequencing, real-time quantitative PCR (RT-qPCR), western blotting (WB), immunohistochemistry (IHC), cell proliferation assays, clone formation, EdU, transwell, flow cytometry and subcutaneous tumor model. Our results suggested that SEH1L was significantly up-regulated and related to poor prognosis in most cancers, and may serve as a potential biomarker. SEH1L could promote HCC progression in vitro and in vivo. Besides, the next generation sequencing suggested that 684 genes was significantly up-regulated and 678 genes was down-regulated after the knock down of SEH1L. SEH1L siliencing could activate ATF3/HMOX1/GPX4 axis, decrease mitochondrial membrane potential and GSH, but increase ROS and MDA, and these effects could be reversed by the knock down of ATF3. This study indicated that SEH1L siliencing could induce ferroptosis and suppresses hepatocellular carcinoma (HCC) progression via ATF3/HMOX1/GPX4 axis.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"29 9-10","pages":"1723 - 1737"},"PeriodicalIF":6.1,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11416379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141878249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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