Apoptosis最新文献_第3页

GPR37 promotes colorectal cancer against ferroptosis by reprogramming lipid metabolism via p38-SCD1 axis GPR37 通过 p38-SCD1 轴重塑脂质代谢，促进结直肠癌对抗铁变态反应。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-09-21 DOI: 10.1007/s10495-024-02018-4

Jiamin Zhou, Xigan He, Weixing Dai, Qingguo Li, Zhen Xiang, Yixiu Wang, Ti Zhang, Weiqi Xu, Lu Wang, Anrong Mao

引用次数: 0

Is long-term administration of PLD-pegylated liposomal doxorubicin able to induce oral cancer? 长期服用PLD-pegylated多柔比星脂质体能否诱发口腔癌？

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-09-06 DOI: 10.1007/s10495-024-02017-5

Arjun Pandian, Azhagu Madhavan Sivalingam

引用次数: 0

PRELP inhibits colorectal cancer progression by suppressing epithelial-mesenchymal transition and angiogenesis via the inactivation of the FGF1/PI3K/AKT pathway. PRELP 通过抑制 FGF1/PI3K/AKT 通路，抑制上皮-间质转化和血管生成，从而抑制结直肠癌的进展。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-09-06 DOI: 10.1007/s10495-024-02015-7

Xiaoqing Li, Zhongxiang Jiang, Junfeng Li, Kun Yang, Jin He, Qianxi Deng, Shuman Xu, Zhihang Jiang, Fuqiang Liu, Zheng Jiang

{"title":"PRELP inhibits colorectal cancer progression by suppressing epithelial-mesenchymal transition and angiogenesis via the inactivation of the FGF1/PI3K/AKT pathway.","authors":"Xiaoqing Li, Zhongxiang Jiang, Junfeng Li, Kun Yang, Jin He, Qianxi Deng, Shuman Xu, Zhihang Jiang, Fuqiang Liu, Zheng Jiang","doi":"10.1007/s10495-024-02015-7","DOIUrl":"https://doi.org/10.1007/s10495-024-02015-7","url":null,"abstract":"<p><p>Proline/arginine-rich end and leucine-rich protein (PRELP) is identified as a small proteoglycan in the extracellular matrix that has been tightly associated with cell adhesion. At present, the role of PRELP in colorectal cancer (CRC) remains largely unknown. PRELP expression in human CRC tissue samples was analyzed by qRT-PCR and immunochemistry. CCK-8, colony formation, transwell, and tube formation assays were utilized to determine the influences of PRELP on the malignant phenotypes of CRC cells. Mouse xenograft and tumor metastasis models were constructed to further validate the function of PRELP. Furthermore, we investigated the efficacy of PRELP combined with bevacizumab treatment in a mouse xenograft model of CRC. Additionally, RNA-seq was performed to analyze the potential signaling pathways regulated by PRELP. Immunofluorescence staining and coimmunoprecipitation were conducted to confirm the interaction between PRELP and fibroblast growth factor 1 (FGF1). In this study, we found that PRELP exerted a tumor-suppressive effect on CRC. The expression level of PRELP was significantly reduced in CRC tissues and cell lines. Both in vivo and in vitro experiments confirmed that PRELP inhibited CRC cell proliferation, promoted apoptosis, and suppressed migration and invasion via a reduction in the epithelial-mesenchymal transition and attenuated angiogenesis, thereby dampening tumor progression. In addition, PRELP markedly potentiated the efficacy of bevacizumab in a mouse xenograft model. Mechanistically, PRELP bound to FGF1 and reduced the stability of the FGF1 protein, accompanied by an increase in its degradation, which subsequently inactivated the PI3K/AKT/mTOR pathway, thereby leading to reduction in tumor angiogenesis and metastasis. Our study for the first time unveiled the tumor-suppressive role of PRELP in CRC and provided a potential effective strategy for the treatment of CRC.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":" ","pages":""},"PeriodicalIF":6.1,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142144995","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

BH3-mimetics or DNA-damaging agents in combination with RG7388 overcome p53 mutation-induced resistance to MDM2 inhibition BH3模拟物或DNA损伤剂与RG7388联合使用，可克服p53突变诱导的对MDM2抑制的耐药性。

IF 6.1 2区生物学

Apoptosis Pub Date : 2024-09-02 DOI: 10.1007/s10495-024-02014-8

N. V. Pervushin, D. K. Nilov, S. V. Pushkarev, V. O. Shipunova, A. S. Badlaeva, M. A. Yapryntseva, D. V. Kopytova, B. Zhivotovsky, G. S. Kopeina

引用次数: 0

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