Cell Death Discovery最新文献

{"title":"FGFR inhibition as a new therapeutic strategy to sensitize glioblastoma stem cells to tumor treating fields.","authors":"Pauline Deshors, Ziad Kheil, Laetitia Ligat, Valerie Gouazé-Andersson, Elizabeth Cohen-Jonathan Moyal","doi":"10.1038/s41420-025-02542-5","DOIUrl":"10.1038/s41420-025-02542-5","url":null,"abstract":"<p><p>Glioblastomas (GBM) are aggressive tumors, which systematically relapse despite standard treatment associating surgery, chemotherapy and radiation therapy. More recently, GBM therapy now includes another therapeutic modality option, Tumor Treating Fields (TTFields) given in combination with Temozolomide (TMZ) following standard treatment. However even with the adjunction of TTFields, GBM remains a lethal disease due to treatment resistance. One of the causes of resistance is the presence of cancer stem cells (GSC) known to be chemo and radioresistant and responsible for tumor regrowth. Studying mechanisms of resistance of GSC to TTFields is thus a major issue to address. Fibroblast Growth Factor Receptors (FGFR) play a major role in numerous processes essential for cancer development, and dysregulation of FGFR signaling has been observed in many cancer types, including GBM. We have previously shown that tyrosine kinase receptor Fibroblast Growth Factor Receptor 1 (FGFR1) controls GBM aggressiveness and GSC radioresistance and that its inhibition leads to radiosensitization through increasing mitotic cell death and microenvironment modulation. Because one of the main mechanisms of action of TTFields is mitotic disturbance and because TTFields act synergistically in vitro with irradiation (IR), we hypothesize that targeting FGFR could sensitize GSC to TTFields. Here we show that, like IR, TTFields significantly decrease GSC growth. Treatment of GSC with pemigatinib (Pem), a FGFR1-3 inhibitor, alters FGFR signalling pathway. We demonstrate that Pem, sensitizes GSC to TTFields by synergistically decreasing their survival and clonogenic ability. Finally, the adjunction of Pem to treatment combining IR and TTFields could sensitize GSC by inducing, in some GSC, a further decrease in the repair of IR-induced DNA damages. Altogether, these results highlight the potential benefits of inhibiting FGFR with the concomitant application of TTFields in the first-line standard GBM treatment to improve patient prognosis.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"265"},"PeriodicalIF":6.1,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12137614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224412","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}

{"title":"ERK1-mediated GLYCTK2 phosphorylation promotes fructolysis to sustain glioblastoma survival under glucose deprivation.","authors":"Yingping Li, Fenna Zhang, Fumin Hu, Rui Tong, Yueqi Wen, Guokai Fu, Xueli Bian","doi":"10.1038/s41420-025-02544-3","DOIUrl":"10.1038/s41420-025-02544-3","url":null,"abstract":"<p><p>Metabolic plasticity sustains glioblastoma (GBM) survival under nutrient stress, yet how fructolytic adaptation compensates for glucose deprivation remains unclear. Here, we identify glycerate kinase 2 (GLYCTK2) as a glucose-sensing metabolic checkpoint that maintains GBM cell viability through ERK1-mediated phosphorylation. Mechanistically, glucose deprivation-activated ERK1 phosphorylates GLYCTK2 at serine 220 directly, which prevents STUB1 (ubiquitin E3 ligase) binding, thereby abrogating the ubiquitination and degradation of GLYCTK2. Importantly, Functional studies demonstrated that fructose supplementation rescues glucose deprivation-induced death in wild-type GBM cells, but fails to protect GLYCTK2-depleted cells, establishing GLYCTK2 as the gatekeeper of fructolytic salvage pathways. These findings demonstrate an important mechanism by which GBM cells rewire glucose metabolism to fructose metabolism via phosphorylating and stabilizing GLYCTK2 to maintain GBM cell survival under glucose deprivation condition, underscoring the potential to target GLYCTK2 for the treatment of patients with GBM.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"266"},"PeriodicalIF":6.1,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12137673/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224411","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}

{"title":"Nesprin-2 contains BH3-like motifs that can promote cell death.","authors":"Hila Zohar, Amit Kessel, Liora Lindenboim, Dang Nguyen, Nir Ben-Tal, Gregg G Gundersen, Howard J Worman, David W Andrews, Reuven Stein","doi":"10.1038/s41420-025-02534-5","DOIUrl":"10.1038/s41420-025-02534-5","url":null,"abstract":"<p><p>BH3-only proteins are a subgroup of the pro-apoptotic Bcl-2 family proteins. They initiate apoptosis by interacting with the multidomain pro- and anti-apoptotic Bcl-2 family proteins. SYNE2 encodes multiple nesprin-2 (Nes2) isoforms of which the most abundant and the largest is the nuclear envelope protein nesprin-2 giant (Nes2G). Nes2G is a component of the nuclear envelope Linker of Nucleoskeleton and Cytoskeleton (LINC) complex that connects the nucleus and the cytoskeleton. Previously, we showed that Nes2 has pro-apoptotic activity. We now show that Nes2G can bind multidomain pro-apoptotic and anti-apoptotic Bcl-2 family proteins and contains two BH3-like motifs near its N- and C-termini. Molecular modeling predicts that these BH3-like motifs have amphipathic α-helix structures and can dock onto the canonical groove of Bax and anti-apoptotic proteins as well as the trigger site of Bax. A chimeric tBid with its BH3 domain replaced with the C-terminal Nes2 BH3-like domain binds to Bax in cells. Furthermore, Nes2 BH3-like motif-containing fragments from the N- and the C-termini bind both pro-apoptotic and anti-apoptotic Bcl-2 proteins and promote cytochrome c release (indicative of apoptosis). Our results suggest that Nes2 acts as a BH3-only protein that regulates apoptosis by binding to the multidomain Bcl-2 family proteins.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"263"},"PeriodicalIF":6.1,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215040","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}

{"title":"LEADR, a p63 target, dampens interferon signalling in bladder cancer.","authors":"Damiano Barnaba, Mariacristina Franzese Canonico, Manuela Helmer-Citterich, Paolo Gandellini, Gerry Melino, Artem Smirnov, Eleonora Candi","doi":"10.1038/s41420-025-02546-1","DOIUrl":"10.1038/s41420-025-02546-1","url":null,"abstract":"<p><p>Bladder cancer affects over half a million people worldwide each year. Recent advances in early detection allowed a successful management of non-aggressive cancers, yet the recurrence rate remains high. Aggressive muscle-invasive bladder tumours are life-threatening and challenging to cure. Therefore, understanding of key molecular pathways involved in cancer progression is critical for developing of new personalised targeted therapies. Recently, non-coding RNAs (ncRNAs) have emerged as key regulators orchestrating complex biological processes in cancer, yet their function is not fully understood. Here, we compare non-muscle invasive and muscle invasive cell lines and identify a ncRNA gene MIR205HG and its transcript LEADR among the top ncRNAs downregulated in muscle invasive urothelial tumours. We show that LEADR expression is epigenetically regulated by master transcription factor p63. LEADR is localised in the nuclei of non-muscle invasive bladder cancer cells where it dampens hyperactivation of interferon stimulated genes possibly increasing sensitivity of bladder cancer cells to interferon signalling. These findings uncover an anti-tumoral role of non-coding RNA LEADR in mediating immune response in bladder cancer.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"264"},"PeriodicalIF":6.1,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215039","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}

{"title":"RGS3 acts as a tumor promoter by facilitating the regulation of the TGF-β signaling pathway and promoting EMT in ovarian cancer.","authors":"Zizhao Wang, Huating Sun, Shunpeng Zhu, Fang Wang, Quan Li, Jinhua Zhou","doi":"10.1038/s41420-025-02536-3","DOIUrl":"10.1038/s41420-025-02536-3","url":null,"abstract":"<p><p>Ovarian cancer (OC) is one of the most common and lethal solid malignancies among women, with its incidence steadily rising. Despite substantial advancements in OC research, its pathogenesis remains largely elusive. Recent studies indicate that the regulator of G protein signaling 3 (RGS3) is implicated in tumorigenesis, however, its specific role in OC development has not been extensively investigated. Herein, this research elucidated that the overexpression of RGS3 in OC correlates with adverse clinical pathological features and tumor progression. Furthermore, we demonstrated that silencing RGS3 promotes apoptosis, effectively inhibiting tumor growth and metastasis. Additionally, our findings reveal that RGS3 enhances oncogenic activity by participating in the regulation of the transforming growth factor-beta (TGF-β) pathway and corresponding epithelial-mesenchymal transition (EMT). The in-depth mechanism lies in the RGS3 facilitating the phosphorylation of SMAD2/3 by directly interacting with AT-rich interactive domain-containing protein 3B (ARID3B), which ultimately drives OC cell proliferation and metastasis. Therefore, our results position RGS3 as a significant prognostic biomarker and tumor-promoting factor in OC, underscoring the pivotal role of the RGS3/TGF-β/EMT signaling pathway in the pathogenesis of this malignancy.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"262"},"PeriodicalIF":6.1,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12130528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207779","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}

{"title":"Combined inhibition by PRMT5 and MAT2A demonstrates a strong synthetic lethality in MTAP homozygous-deficient glioma models.","authors":"Zuoyu Jiang, Xuetao Li, Zongyu Xiao, Wenjuan Gan, Xuewen Zhang, Yang Zhang, Weichao Wang, Qinzhi E, Yu Huang, Qikun Shi, Yi Tang, Jiaming Du, Hanmiao Dong, Jian Li, Yulun Huang","doi":"10.1038/s41420-025-02545-2","DOIUrl":"10.1038/s41420-025-02545-2","url":null,"abstract":"<p><p>The intra- and intertumoral heterogeneity of gliomas present major challenges to effective chemotherapy. This study explored the combined effects of PRMT5 and MAT2A inhibitors on glioma progression. The expression of drug targets was determined in cell models using western blotting and immunofluorescence assay. CCK-8, colony-formation, EdU fluorescence, and flow cytometry cell cycle assays were conducted to assess the effect of the drugs on cell proliferation. Additionally, TUNEL fluorescence assay, flow cytometry apoptosis assay, western blotting, and comet assay were used to evaluate drug-induced apoptosis and DNA damage. Immunohistochemistry was used to validate the effect of the drugs in a 3D glioma organoid model. Patient-derived orthotopic xenograft models were used for in vivo efficacy evaluations. Lastly, transcriptome sequencing was used to elucidate the mechanism of action of the drugs, which was confirmed using western blotting. In phenotypic experiments, PRMT5 inhibitors reduced SDMA levels, inhibited cell proliferation, and promoted apoptosis in glioma models. The combination of PRMT5 inhibitors with MAT2A inhibitors enhanced synthetic lethality, leading to more potent antitumor effects. In vivo studies demonstrated that the drug combination significantly inhibited tumor growth and prolonged survival time. Our study proved the combination of PRMT5 and MAT2A inhibitors may induce synthetic lethality by downregulating the PI3K-AKT pathway, indicating the potential of this approach in treating gliomas.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"261"},"PeriodicalIF":6.1,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126582/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191564","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}

{"title":"Melanoma innervation, noradrenaline and cancer progression in zebrafish xenograft model.","authors":"Francesca Lorenzini, Johanna Marines, Julien Le Friec, Nam Do Khoa, Maria Angela Nieto, Berta Sanchez-Laorden, Maria Caterina Mione, Laura Fontenille, Karima Kissa","doi":"10.1038/s41420-025-02523-8","DOIUrl":"10.1038/s41420-025-02523-8","url":null,"abstract":"<p><p>The tumor microenvironment, including the peripheral nervous system, plays a key role in regulating tumor biology, from initiation to cancer progression. Here, by modeling aggressive melanoma in larval zebrafish xenografts, we shed light on the dynamics of tumor innervation in the tumor microenvironment (TME). Axonogenesis and dendritogenesis were detected in the neurons surrounding the melanoma niche and neurogenesis was observed in the nearby population of the enteric nervous system. We also demonstrate the crucial role of noradrenaline in promoting melanoma progression with the dissemination and invasion of cancer cells to distant tissues. This zebrafish model will allow to uncover neural markers associated with melanoma progression to help in the design of innovative anti-neurogenic therapies targeting specifically the neuronal signals that regulate melanoma progression.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"260"},"PeriodicalIF":6.1,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191576","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}

{"title":"Contrasting pathophysiological mechanisms of OPA1 mutations in autosomal dominant optic atrophy.","authors":"Shi-Qi Yao, Jia-Jian Liang, Hui Zhou, Shaoying Tan, Yingjie Cao, Chong-Bo Chen, Ciyan Xu, Ruixi Wang, Tai-Ping Li, Fang-Fang Zhao, Yun Wang, Han-Jie He, Dan Zhang, Meng Wang, Lifang Liu, Patrick Yu-Wai-Man, Shihui Wei, Ling-Ping Cen","doi":"10.1038/s41420-025-02442-8","DOIUrl":"10.1038/s41420-025-02442-8","url":null,"abstract":"<p><p>Autosomal dominant optic atrophy (ADOA) caused by mutations in the nuclear-encoded OPA1 gene result in the preferential loss of retinal ganglion cells (RGCs) and progressive optic nerve degeneration. The severity of ADOA can be highly variable. This study compared the pathophysiological consequences of the c.1034 G > A OPA1 missense mutation and the c.1305+2delGT OPA1 deletion. There was a significant correlation between the severity of visual loss and the extent of macular RGC loss as determined by optical coherence tomography imaging. In cells transfected with the c.1034 G > A mutant, the percentage of fragmented mitochondria was greater than 60% with cytochrome c (cyt c) overflow, and significantly elevated levels of reactive oxygen species (ROS) and apoptosis. In contrast, the c.1305+2delGT mutant caused mitochondrial fragmentation in ~ 20% of HeLa cells, resulting in less cyt c overflow and apoptosis. The extent of mitochondrial network fragmentation and apoptosis increased with decreasing WT OPA1 mRNA expression levels. The c.1034 G > A OPA1 missense mutation is likely to induce a dominant-negative effect compared with haploinsufficiency with the c.1305+2delGT OPA1 deletion. These contrasting pathophysiological mechanisms could influence disease severity in ADOA through their differential consequences on mitochondrial structure and function. The small drug molecule Paromomycin was able to rescue the mitochondrial fragmentation induced by the c.1034 G > A mutation, providing proof-of-concept for further therapeutic validation in ADOA.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"259"},"PeriodicalIF":6.1,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186656","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}

{"title":"Unveiling the nexus between environmental exposures and testicular damages: revelations from autophagy and oxidative stress imbalance.","authors":"Xiuwen Kong, Xinda Wang, Qiushi Xia, Qingqing Hu, Wenqian Yu, Qiuru Huang, Jiaxin Li, Chenyu Wang, Ziwen Lin, Yiheng Liu, Yujuan Qi, Xiaofang Tan, Bo Zheng, Jun Yu","doi":"10.1038/s41420-025-02543-4","DOIUrl":"10.1038/s41420-025-02543-4","url":null,"abstract":"<p><p>Recent evidence consolidates the deleterious impact of environmental exposure on testicular damage. Environmental exposures can instigate testicular toxicity, causing damage to the Sertoli-Sertoli cell-mediated blood-testis barrier (BTB) integrity, alterations in hormone levels orchestrated by aberrant Leydig cells, and disruption of spermatogenesis. Despite diverse study designs and methodologies, a consensus is emerging on how environmental factors induce oxidative stress by elevating ROS levels, affecting autophagy through pathways such as the ROS-mediated mTOR signaling pathway, ultimately culminating in testicular damage. This review synthesizes existing literature on how environmental exposures, including metals, air pollutants, industrial contaminants, and pesticides, disturb testicular homeostasis via autophagy-mediated oxidative stress, highlighting recent significant advancements. It also explores interventions like antioxidant support and autophagy regulation to alleviate testicular damage. These findings underscore the importance of elucidating the mechanisms of autophagy influenced by environmental exposures in disrupting the equilibrium of oxidative stress, identifying potential drug targets, and establishing a groundwork for enhancing future treatments and clinical management of testicular injuries.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"258"},"PeriodicalIF":6.1,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12122914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180785","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}

{"title":"Artemisinin derivatives differently affect cell death of lung cancer subtypes by regulating GPX4 in patient-derived tissue cultures.","authors":"Johanna Mölleken, Angelique Kragl, Astrid Monecke, Isabella Metelmann, Sebastian Krämer, Sonja Kallendrusch","doi":"10.1038/s41420-025-02537-2","DOIUrl":"10.1038/s41420-025-02537-2","url":null,"abstract":"<p><p>Resistant tumor cell populations are common after cytostatic drugs treatment. To overcome resistance mechanisms artemisinin derivatives, known for its complementary use during cancer treatement and ferroptosis induction, were investigated both as single agents and in combination with cisplatin (3 µM) in a complex organotypic tissue model of non-small cell lung cancer (NSCLC) patient samples. All substances-artemisinin (ART, 100 µM), artemether (ATM, 50 µM), artesunate (ATS, 20 µM), and dihydroartemisinin (DHA, 10 µM)-showed beneficial effects in most of the investigated patient-derived tissue cultures (PDTC). Tumor proliferation was reduced by DHA and ATS in both, standalone treatment and in combination with cisplatin, surpassing the efficacy of single cisplatin supplementation. In combination with cisplatin tumor apoptosis increased in most of lung squamous cell carcinoma (LUSC) PDTC, but not in lung adenocarcinoma (LUAD). The enzyme GPX4, inhibiting ferroptosis was up-regulated in LUAD but not in LUSC. Taken together, in the complex PDTC model system, LUSC displayed a higher sensitivity to ART derivatives, due to the lack of GPX4-mediated resistance to ferroptosis.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"256"},"PeriodicalIF":6.1,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12119945/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144172876","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}