Cell Death and Differentiation最新文献

{"title":"Collaborative orchestration of BH3-only proteins governs Bak/Bax-dependent hepatocyte apoptosis under antiapoptotic protein-deficiency in mice","authors":"Shinnosuke Kudo, Hayato Hikita, Yoshinobu Saito, Kazuhiro Murai, Takahiro Kodama, Tomohide Tatsumi, Tetsuo Takehara","doi":"10.1038/s41418-025-01458-y","DOIUrl":"https://doi.org/10.1038/s41418-025-01458-y","url":null,"abstract":"<p>The fine-tuned balance between anti-apoptotic Bcl-2 family proteins, such as Bcl-xL and Mcl-1, and pro-apoptotic Bcl-2 family proteins, like Bak and Bax, is crucial for maintaining hepatocyte integrity. BH3-only proteins, including Bid, Bim, Puma, Noxa, Bad, Bmf, Bik and Hrk, serve as apoptosis initiators. They are activated by various stimuli, which leads to Bak/Bax activation. We previously reported that Bid and Bim contributed to hepatocyte apoptosis through Bak/Bax activation in the absence of anti-apoptotic proteins Bcl-xL and/or Mcl-1. However, the comprehensive involvement of all eight BH3-only proteins in Bak/Bax-dependent hepatocyte apoptosis remains unclear. Puma disruption suppressed hepatocyte apoptosis in hepatocyte-specific Bcl-xL or Mcl-1 knockout (Bcl-xL^ΔHep/ΔHep or Mcl-1^ΔHep/ΔHep) mice. Disruption of Bid and Bim partially prevented lethality in Mcl-1^ΔHep/+ Bcl-xL^ΔHep/ΔHep mice, although severe hepatocyte apoptosis persisted, which was suppressed by additional Puma disruption. However, hepatocyte apoptosis was still induced compared to that in Mcl-1^ΔHep/+ Bcl-xL^ΔHep/ΔHep Bax^ΔHep/ΔHep Bak^−/− mice. Triple disruption of Bid, Bim and Puma did not prevent induction of hepatocyte apoptosis in tamoxifen-induced Mcl-1^{iΔHep/iΔHep} Bcl-xL^{iΔHep/iΔHep} mice. Primary hepatocytes, isolated from Mcl-1^fl/fl Bcl-xL^fl/fl Bid^−/− Bim^−/− Puma^−/− mice and immortalized, underwent apoptosis with doxycycline-dependent Cre recombination. Among the remaining five BH3-only proteins, Bik and Hrk were not expressed in these cells, and Noxa knockdown, but not Bad or Bmf knockdown, reduced apoptosis. Noxa disruption alleviated hepatocyte apoptosis in Mcl-1^ΔHep/ΔHep mice and tamoxifen-induced Mcl-1^{iΔHep/iΔHep} Bcl-xL^{iΔHep/iΔHep} Bid^−/− Bim^−/− Puma^−/− mice, prolonging survival. Apoptosis persisted in immortalized primary hepatocytes isolated from Mcl-1^fl/fl Bcl-xL^fl/fl Bid^−/− Bim^−/− Puma^−/− Noxa^−/− mice where doxycycline-dependent Cre recombination was induced, but was completely suppressed by Bak/Bax knockdown, while Bad or Bmf knockdown had no effect. In conclusion, among the eight BH3-only proteins, Puma and Noxa, alongside Bid and Bim, contributed to Bak/Bax-dependent hepatocyte apoptosis, but not indispensably, in the absence of Mcl-1 and Bcl-xL.</p><figure></figure>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"65 5 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tripartite motif-containing protein 26 promotes colorectal cancer growth by inactivating p53","authors":"Zhihui Tan, Hyun Min Ko, Parnian Naji, Rong Zhu, Jieqiong Wang, Shibo Huang, Yiwei Zhang, Shelya X. Zeng, Hua Lu","doi":"10.1038/s41418-025-01463-1","DOIUrl":"https://doi.org/10.1038/s41418-025-01463-1","url":null,"abstract":"<p>Tripartite motif-containing protein 26 (TRIM26) is an E3 ubiquitin ligase that exhibits divergent roles in various cancer types (oncogenic and anti-oncogenic). This study investigates the interaction of TRIM26 with the tumor suppressor protein p53 in colorectal cancer (CRC) cells by performing a comprehensive set of biochemical, cell-based assays, and xenograft experiments. As a result, we found that overexpression of TRIM26 significantly enhances CRC cell proliferation and colony formation, while knockdown of TRIM26 suppresses these processes. Xenograft experiments further validated the tumor-promoting role of TRIM26 in CRC. Supporting this is that TRIM26 is highly expressed in human CRC tissues as revealed by our analysis of the TCGA database. Biochemically, TRIM26 directly bound to the C-terminus of p53 and facilitated its ubiquitination, resulting in proteolytic degradation and attenuated p53 activity independently of MDM2. Also, TRIM26 increased the MDM2-mediated ubiquitination of p53 by binding to MDM2’s C-terminus. This study uncovers the oncogenic potential of TRIM26 in CRC by inhibiting p53 function. Through its ubiquitin ligase activity, TRIM26 destabilizes p53, consequently promoting CRC cell proliferation and tumor growth. These findings shed light on the complex involvement of TRIM26 in cancer and identify this ubiquitin ligase as a potential therapeutic target for future development of CRC treatment.</p><figure></figure>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"18 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143477659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP38 functions as an oncoprotein by downregulating the p53 pathway through deubiquitination and stabilization of MDM2","authors":"Shanyu Zhao, Xiaoli Liu, Rongkui Luo, Zitao Jian, Chen Xu, Yingyong Hou, Xiuping Liu, Pingzhao Zhang","doi":"10.1038/s41418-025-01462-2","DOIUrl":"https://doi.org/10.1038/s41418-025-01462-2","url":null,"abstract":"<p>Dysregulation of the MDM2-p53 pathway is a commonly observed phenomenon in cancer, where overexpression or amplification of MDM2 leads to increased degradation of p53. This results in reduced levels of p53, leading to the loss of its tumor-suppressive functions. The study focused on investigating the role of Ubiquitin-specific protease 38 (USP38) in cancer and its interaction with the MDM2-p53 axis. We revealed that USP38 positively correlates with MDM2 and negatively correlates with p53 expression. Mechanistically, USP38 directly binds to MDM2, functioning as a deubiquitinating enzyme (DUB) to stabilize MDM2 and suppress p53 expression. Knockout of USP38 hindered cancer cell proliferation, migration, and invasion, and enhanced apoptosis. Moreover, USP38 deficiency increased sensitivity to chemotherapy drugs and promoted ferroptosis in gastric and breast cancer cell lines. Importantly, these effects were found to be dependent on p53, as the downregulation of p53 reversed the phenotypic changes induced by USP38 knockout. These findings shed light on the oncogenic role of USP38 by modulating the MDM2-p53 axis, providing valuable insights into the molecular mechanisms of USP38 in cancer and potential therapeutic strategies for gastric and breast cancer.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"65 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143470743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CSTF2-impeded innate αβ T cell infiltration and activation exacerbate immune evasion of pancreatic cancer","authors":"Xiaowei He, Ji Liu, Yifan Zhou, Sihan Zhao, Ziming Chen, Zilan Xu, Chunling Xue, Lingxing Zeng, Shuang Liu, Shaoqiu Liu, Ruihong Bai, Shaojia Wu, Lisha Zhuang, Mei Li, Hongzhe Zhao, Quanbo Zhou, Dongxin Lin, Jian Zheng, Xudong Huang, Jialiang Zhang","doi":"10.1038/s41418-025-01464-0","DOIUrl":"https://doi.org/10.1038/s41418-025-01464-0","url":null,"abstract":"<p>Alternative cleavage and polyadenylation (APA) have gained increasing attention in cancer biology, yet its role in modulating anti-tumor immune response remains largely unexplored. Here, we identify the cleavage stimulation factor 2 (<i>CSTF2</i>), an APA-related gene, as a pivotal suppressor of anti-tumor immunity in pancreatic ductal adenocarcinoma (PDAC). <i>CSTF2</i> promotes tumor development by inhibiting the infiltration and cytotoxic immune cell recruitment function of TCRαβ⁺CD4⁻CD8⁻NK1.1⁻ innate αβ T (iαβT) cells. Mechanistically, CSTF2 diminishes CXCL10 expression by promoting PolyA polymerase alpha (PAPα) binding to the 3’ untranslated regions of <i>CXCL10</i> RNA, resulting in shortened PolyA tails and compromised RNA stability. Furthermore, we identify Forsythoside B, a selective inhibitor targeting the RNA recognition motif of CSTF2, can effectively activate anti-tumor immunity and overcome resistance to immune checkpoint blockade (ICB) therapy. Collectively, our findings unveil CSTF2 as a promising therapeutic target for sensitizing PDAC to ICB therapy.</p><figure></figure>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"65 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatic factor MANF drives hepatocytes reprogramming by detaining cytosolic CK19 in intrahepatic cholangiocarcinoma","authors":"Qiong Mei, Yu Zhang, Hong Li, Wei Ma, Wenkai Huang, Zhengsheng Wu, Yongli Huang, Yanyan Liang, Chuansheng Wei, Jinfeng Wang, Yuefeng Ruan, Lin Yang, Yan Huang, Yujun Shen, Jun Liu, Lijie Feng, Yuxian Shen","doi":"10.1038/s41418-025-01460-4","DOIUrl":"https://doi.org/10.1038/s41418-025-01460-4","url":null,"abstract":"<p>Intrahepatic cholangiocarcinoma (ICC) is characterized by poor prognosis and limited treatment. Hepatocytes have been considered as one of the origins of ICC, however, the underlying mechanisms remain unclear. Here, we found mesencephalic astrocyte-derived neurotrophic factor (MANF), a hepatoprotective factor, was exceptionally upregulated in human ICC tissues and experimental mouse ICC models induced by sleeping beauty transposon (SBT) or thioacetamide (TAA) challenge. We identified MANF as a biomarker for distinguishing the primary liver cancer and verified the oncogenic role of MANF in ICC using cell lines overexpressing/knocked down MANF and mice specifically knocked in/out MANF in hepatocytes. Lineage tracing revealed that MANF promoted mature hepatocyte transformation into ICC cells. Mechanistically, MANF interacted with CK19 at Ser35 to suppress CK19 membrane recruitment. Cytosolic CK19 bound to AR domain of Notch2 intracellular domain (NICD2) to stabilize NICD2 protein level and trigger Notch signaling, which contributed to hepatocyte transformation to ICC cells. We uncover a novel profile of MANF and the original mechanism, which shed light on ICC diagnosis and intervention.</p><figure></figure>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"6 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143443320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The LINC01315-encoded small protein YAPer-ORF competes with PRP4k to hijack YAP signaling to aberrantly promote cell growth","authors":"Zhu Xie, Chao Li, Rui Huang, Bo Wu, Qian Huang, Zhe Zhang, Tongjin Zhao, Lingqian Wu, Chengtao Li, Jianfeng Shen, Hongyan Wang","doi":"10.1038/s41418-025-01449-z","DOIUrl":"https://doi.org/10.1038/s41418-025-01449-z","url":null,"abstract":"<p>The dysregulation of YAP activity is implicated in abnormal organ size and the pathogenesis of diverse diseases, including cancer. However, the functional regulation of YAP activity by lncRNA-encoded peptides remains elusive. In this study, we report the identification of a small protein (93 aa) encoded by the lncRNA LINC01315. This small protein, termed YAPer-ORF, preferentially interacted with GNAQ/11 mutants to augment YAP activity. Mechanistically, YAPer-ORF was located in the nucleus and competed with YAP to bind the nuclear kinase PRP4K to hinder YAP phosphorylation. This decreased phosphorylation of YAP by YAPer-ORF promoted YAP retention in the nucleus and facilitated the expression of downstream target genes such as <i>CCND1</i>. In both cancerous and noncancerous models, YAPer-ORF prominently drove cell proliferation in a CCND1-dependent manner. Notably, cardiac-specific genetic knock-in of the human YAPer-ORF in mice significantly increased heart size through increased cardiomyocyte proliferation, underscoring the role of YAPer-ORF in cell proliferation. Moreover, treatment with an anti-YAPer-ORF neutralizing antibody effectively suppressed uveal melanoma growth, highlighting the therapeutic potential of targeting YAPer-ORF. These findings collectively establish YAPer-ORF as a critical regulator of YAP activity, further highlighting the disruption of YAPer-ORF activity as a potential therapeutic strategy against YAP-driven human cancers and developmental diseases.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"10 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143435019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct developmental outcomes in DNA repair-deficient FANCC c.67delG mutant and FANCC−/− Mice","authors":"Swarna Beesetti, Cliff Guy, Shyam Sirasanagandla, Mao Yang, Rhea Jr Sumpter, Heather Sheppard, Stephane Pelletier, Marcin W. Wlodarski, Douglas R. Green","doi":"10.1038/s41418-025-01461-3","DOIUrl":"https://doi.org/10.1038/s41418-025-01461-3","url":null,"abstract":"<p>Fanconi Anemia (FA) is an autosomal recessive disorder characterized by diverse clinical manifestations such as aplastic anemia, cancer predisposition, and developmental defects including hypogonadism, microcephaly, organ dysfunction, infertility, hyperpigmentation, microphthalmia, and skeletal defects. In addition to the well-described defects in DNA repair, mitochondrial dysfunction due to defects in mitochondrial autophagy (mitophagy) is also associated with FA, although its contribution to FA phenotypes is unknown. This study focused on the FANCC gene, which, alongside other FA genes, is integral to DNA repair and mitochondrial quality control. In the present study, we created a FANCC mutant mouse model, based on a human mutation (FANCC c.67delG) that is defective in DNA repair but proficient in mitophagy. We found that the FANCC c.67delG mutant mouse model recapitulates some phenotypes observed in FA patients, such as cellular hypersensitivity to DNA cross-linking agents and hematopoietic defects. In contrast, FA phenotypes such as microphthalmia, hypogonadism, and infertility, present in FANCC-deficient mice, were absent in the FANCC c.67delG mice, suggesting that the N-terminal 55 amino acids of FANCC are dispensable for these developmental processes. Furthermore, the FANCC c.67delG mutation preserved mitophagy, and unlike the FANCC null mutation, did not lead to the accumulation of damaged mitochondria in cells or tissues. This study highlights the multifaceted nature of the FANCC protein, with distinct domains responsible for DNA repair and mitophagy. Our results suggest that developmental defects in FA may not solely stem from DNA repair deficiencies but could also involve other functions, such as mitochondrial quality control.</p>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"64 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"STING directly interacts with PAR to promote apoptosis upon acute ionizing radiation-mediated DNA damage","authors":"Yirong Sun, Saba R. Aliyari, Kislay Parvatiyar, Lulan Wang, Anjie Zhen, Wei Sun, Xiaobo Han, Adele Zhang, Ethan Kato, Helen Shi, Elena De Schutter, William H. McBride, Samuel W. French, Genhong Cheng","doi":"10.1038/s41418-025-01457-z","DOIUrl":"https://doi.org/10.1038/s41418-025-01457-z","url":null,"abstract":"<p>Acute ionizing radiation (IR) causes severe DNA damage, leading to cell cycle arrest, cell death, and activation of the innate immune system. The role and signaling pathway of stimulator of interferon genes (STING) in IR-induced tissue damage and cell death are not well understood. This study revealed that STING is crucial for promoting apoptosis in response to DNA damage caused by acute IR both in vitro and in vivo. STING binds to poly (ADP‒ribose) (PAR) produced by activated poly (ADP‒ribose) polymerase-1 (PARP1) upon IR. Compared with that in WT cells, apoptosis was suppressed in <i>Sting</i>^{<i>gt-/gt-</i>} cells. Excessive PAR production by PARP1 due to DNA damage enhances STING phosphorylation, and inhibiting PARP1 reduces cell apoptosis after IR. In vivo, IR-induced crypt cell death was significantly lower in <i>Sting</i>^{<i>gt-/gt-</i>} mice or with low-dose PARP1 inhibitor, PJ34, resulting in substantial resistance to abdominal irradiation. STING deficiency or inhibition of PARP1 function can reduce the expression of the proapoptotic gene PUMA, decrease the localization of Bax on the mitochondrial membrane, and thus reduce cell apoptosis. Our findings highlight crucial roles for STING and PAR in the IR-mediated induction of apoptosis, which may have therapeutic implications for controlling radiation-induced apoptosis or acute radiation symptoms.</p><figure><p>STING responds to acute ionizing radiation-mediated DNA damage by directly binding to poly (ADP-ribose) (PAR) produced by activated poly (ADP-ribose) polymerase-1 (PARP1), and mainly induces cell apoptosis through Puma-Bax interaction. STING deficiency or reduced production of PAR protected mice against Acute Radiation Syndrome.</p></figure>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"7 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143401328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EZH2 suppresses IR-induced ferroptosis by forming a co-repressor complex with HIF-1α to inhibit ACSL4: Targeting EZH2 enhances radiosensitivity in KDM6A-deficient esophageal squamous carcinoma","authors":"Guizhen Pan, Yeye Xia, Mengyu Hao, Jiahao Guan, Qianqian Zhu, Tianqi Zha, Lei Sheng, Zhenfeng Zhao, Huaguang Pan, Weiyang Fang, Xiaoyong Xu, Xiangcun Chen, Shuguang Zhou, Zhuting Tong","doi":"10.1038/s41418-025-01451-5","DOIUrl":"https://doi.org/10.1038/s41418-025-01451-5","url":null,"abstract":"<p>The mutation status of the lysine demethylase 6 A (KDM6A), a gene antagonist to Enhancer of zeste homolog 2 (EZH2), is closely related to the therapeutic efficacy of EZH2 inhibitors in several malignancies. However, the mutational landscape of KDM6A and the therapeutic targetability of EZH2 inhibitors in esophageal squamous carcinoma (ESCC) remain unreported. Here, we found that approximately 9.18% (9/98) of our study ESCC tissues had KDM6A mutations of which 7 cases resulted in a complete loss of expression and consequent loss of demethylase function. We found that KDM6A-deficient ESCC cells exhibited increased sensitivity to EZH2 inhibitor, and the radiosensitizing activity of EZH2 inhibitor was evident in KDM6A-dficient ESCC cells. Further transcriptome analysis revealed that ferroptosis is implicated in the radiosensitizing effect exerted by EZH2 inhibition on KDM6A-deficient ESCC cells. The following Chromatin Immunoprecipitation (ChIP), co-immunoprecipitation, and luciferase reporter assays demonstrated that in KDM6A-deficient ESCC cells, (1) Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4) is the target gene for EZH2 to regulate ferroptosis; (2) The IR-induced hypoxia inducible factor 1 subunit alpha (HIF-1α) is a predominant mediator of EZH2 to repress ACSL4; (3) the HRE7-8 regions of the ACSL4 promoter are required for the repressive function of EZH2 on ACSL4; (4) EZH2 regulates ACSL4 by forming a co-repressive complex with HIF-1α. Our study provides preclinical evidence supporting that EZH2 inhibitors may confer therapeutic benefit in KDM6A-deficient ESCC patients.</p><figure></figure>","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":"11 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143367249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: SENP3 inhibition suppresses hepatocellular carcinoma progression and improves the efficacy of anti-PD-1 immunotherapy.","authors":"Peng Wang, Jiannan Qiu, Yuan Fang, Songmao Li, Kua Liu, Yin Cao, Guang Zhang, Zhongxia Wang, Xiaosong Gu, Junhua Wu, Chunping Jiang","doi":"10.1038/s41418-025-01455-1","DOIUrl":"10.1038/s41418-025-01455-1","url":null,"abstract":"","PeriodicalId":9731,"journal":{"name":"Cell Death and Differentiation","volume":" ","pages":""},"PeriodicalIF":13.7,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143363917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}