Cell Biology International最新文献

{"title":"Predictive action of oncomiR in suppressing TP53 signaling pathway in hypoxia-conditioned colon cancer cell line HCT-116","authors":"R. Susanti,&nbsp;Muchamad Dafip,&nbsp;Dewi Mustikaningtyas,&nbsp;Agung Putra","doi":"10.1002/cbin.12243","DOIUrl":"10.1002/cbin.12243","url":null,"abstract":"<p>Hypoxia-induced heterogeneity in colorectal cancer (CRC) significantly impacts patient survival by promoting chemoresistance. These conditions alter the regulation of miRNAs, key regulators of crucial processes like proliferation, apoptosis, and invasion, leading to tumor progression. Despite their promising potential as diagnostic and therapeutic targets, the underlying mechanisms by which miRNAs influence hypoxia-mediated tumorigenesis remain largely unexplored. This study aims to elucidate the action of miRNAs in HCT-116 colorectal cancer stem cells (CSCs) under hypoxia, providing valuable insights into their role in tumor adaptation and progression. MiRNA expression was determined using Nanostring nCounter, and bioinformatic analysis was performed to explain the molecular pathway. A total of 50 miRNAs were obtained with an average count of ≥ 20 reads for comparative expression analysis. The results showed that hypoxia-affected 36 oncomiRs were increased in HCT-116, and 14 suppressor-miRs were increased in MSCs. The increase in miRNA expression occurred consistently from normoxia to hypoxia and significantly differed between mesenchymal stem cells (MSCs) and HCT-116. Furthermore, miR-16-5p and miR-29a-3p were dominant in regulating the p53 signaling pathway, which is thought to be related to the escape mechanism against hypoxia and maintaining cell proliferation. More research with a genome-transcriptome axis approach is needed to fully understand miRNAs’ role in adapting CRC cells and MSCs to hypoxia. Further research could focus on developing specific biomarkers for diagnosis. In addition, anti-miR can be developed as a therapy to prevent cancer proliferation or inhibit the adaptation of cancer cells to hypoxia.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 12","pages":"1891-1905"},"PeriodicalIF":3.3,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142267126","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}

{"title":"Breast cancer cell derived exosomes reduces glycolysis of activated CD8 + T cells in a AKT-mTOR dependent manner","authors":"Abhishek Choudhury,&nbsp;Soumya Chatterjee,&nbsp;Shauryabrota Dalui,&nbsp;Pronabesh Ghosh,&nbsp;Altamas Hossain Daptary,&nbsp;Golam Kibria Mollah,&nbsp;Arindam Bhattacharyya","doi":"10.1002/cbin.12241","DOIUrl":"10.1002/cbin.12241","url":null,"abstract":"<p>Cytotoxic CD8⁺ T cells plays a pivotal role in the adaptive immune system to protect the organism against infections and cancer. During activation and response, T cells undergo a metabolic reprogramming that involves various metabolic pathways, with a predominant reliance on glycolysis to meet their increased energy demands and enhanced effector response. Recently, extracellular vesicles (EVs) known as exosomes have been recognized as crucial signaling mediators in regulating the tumor microenvironment (TME). Recent reports indicates that exosomes may transfer biologically functional molecules to the recipient cells, thereby facilitate cancer progression, angiogenesis, metastasis, drug resistance, and immunosuppression by reprogramming the metabolism of cancer cells. This study sought to enlighten possible involvement of cancer-derived exosomes in CD8 + T cell glucose metabolism and discover a regulated signalome as a mechanism of action. We observed reduction in glucose metabolism due to downregulation of AKT/mTOR signalome in activated CD8 + T cells after cancer derived exosome exposure. In-vivo murine breast tumor studies showed better tumor control and antitumor CD8 + T cell glycolysis and effector response after abrogation of exosome release from breast cancer cells. Summarizing, the present study establishes an immune evasion mechanism of breast cancer cell secreted exosomes that will act as a foundation for future precision cancer therapeutics.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 1","pages":"45-54"},"PeriodicalIF":3.3,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142269640","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}

{"title":"The m6A modification of ACSL4 mRNA sensitized esophageal squamous cell carcinoma to irradiation via accelerating ferroptosis","authors":"Yingying Jin,&nbsp;Shupei Pan,&nbsp;Mincong Wang,&nbsp;Shan Huang,&nbsp;Yue Ke,&nbsp;Dan Li,&nbsp;Hen Luo,&nbsp;Zhanfeng Kou,&nbsp;Dongwen Shi,&nbsp;Weihua Kou,&nbsp;Hongxiao Fu,&nbsp;Jiyuan Pan","doi":"10.1002/cbin.12245","DOIUrl":"10.1002/cbin.12245","url":null,"abstract":"<p>Radioresistance is a major obstacle for the therapy of esophageal squamous cell carcinoma (ESCC) and lead to a poor prognosis. Ferroptosis is supposed to be responsible for radioresistance. However, the ferroptosis-induced radioresistance in ESCC and its related regulatory mechanisms are not yet fully understood. In this study, human ESCC cell line and the corresponding radioresistance cells were irradiated with 6 megavolts (MV) X-ray. It was showed that irradiation led to less ferroptosis in radioresistant ESCC cells as compared to the parental cells, as depicted by transmission electron microscopy, intracellular Fe²⁺ iron contents, lipid peroxidation, and expression of COX2. The increase of ASCL4 expression levels in radioresistant cells after radiotherapy was smaller than that in the parental cells. ACSL4 overexpression significantly enhanced ferroptosis. The fold increase in ACSL4 m⁶A modification in the radioresistant cells was significantly smaller than that in the parental cells as detected by methylated RNA immunoprecipitation with qRT-PCR. METTL14 overexpression accelerated ferroptosis induced by irradiation via upregulating m⁶A modification of ACSL4 mRNA. In conclusions, ferroptosis ablation was responsible for the radioresistant of ESCC. The METTL14-mediated m⁶A modification of ACSL4 mRNA sensitized ESCC to irradiation via accelerating ferroptosis. This study sheds new light on our understanding of radioresistant in ESCC, and provides potential strategies for ESCC radiotherapy.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 12","pages":"1877-1890"},"PeriodicalIF":3.3,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142267125","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}

{"title":"Ectonucleotidase activity driven by acid ectophosphatase in luminal A MCF-7 breast cancer cells","authors":"Marco Antonio Lacerda-Abreu,&nbsp;Bruna dos Santos Mendonça,&nbsp;Gabriela Nestal de Moraes,&nbsp;José Roberto Meyer-Fernandes","doi":"10.1002/cbin.12237","DOIUrl":"10.1002/cbin.12237","url":null,"abstract":"<p>Ectophosphatases catalyse the hydrolysis of phosphorylated molecules, such as phospho-amino acids, in the extracellular environment. Nevertheless, the hydrolysis of nucleotides in the extracellular environment is typically catalysed by ectonucleotidases. Studies have shown that acid ectophosphatase, or transmembrane-prostatic acid phosphatase (TM-PAP), a membrane-bound splice variant of prostatic acid phosphatase, has ecto-5′-nucleotidase activity. Furthermore, it was demonstrated that ectophosphatase cannot hydrolyse ATP, ADP, or AMP in triple-negative breast cancer cells. In contrast to previous findings in MDA-MB-231 cells, the ectophosphatase studied in the present work displayed a remarkable capacity to hydrolyse AMP in luminal A breast cancer cells (MCF-7). We showed that AMP dose-dependently inhibited <i>p</i>-nitrophenylphosphate (<i>p</i>-NPP) hydrolysis. The <i>p</i>-NPP and AMP hydrolysis showed similar biochemical behaviours, such as increased hydrolysis under acidic conditions and comparable inhibition by NiCl₂, ammonium molybdate, and sodium orthovanadate. In addition, this ectophosphatase with ectonucleotidase activity was essential for the release of adenosine and inorganic phosphate from phosphorylated molecules available in the extracellular microenvironment. This is the first study to show that prostatic acid phosphatase on the membrane surface of breast cancer cells (MCF-7) is correlated with cell adhesion and migration.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 11","pages":"1637-1648"},"PeriodicalIF":3.3,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142267127","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}

{"title":"Establishment and characterization of fibroblast lines from the northern tiger cat (Leopardus tigrinus, Schreber, 1775) during extended passage and cryopreservation","authors":"João Vitor da Silva Viana,&nbsp;Lhara Ricarliany Medeiros de Oliveira,&nbsp;Luanna Lorenna Vieira Rodrigues,&nbsp;Yara Letícia Frutuoso e Silva,&nbsp;Ana Lívia Rocha Rodrigues,&nbsp;Alexandre Rodrigues Silva,&nbsp;Patrícia Vasconcelos Alves,&nbsp;Herlon Victor Rodrigues Silva,&nbsp;Alexsandra Fernandes Pereira","doi":"10.1002/cbin.12244","DOIUrl":"10.1002/cbin.12244","url":null,"abstract":"<p>The establishment of fibroblast lines enables several applications from the formation of biobanks for the conservation of biodiversity to the use of these cells in physiological and toxicological assays. Considered a species vulnerable to extinction, the characterization of fibroblastic lines of northern tiger cat would contribute to its conservation. Therefore, we established and characterized fibroblasts derived from northern tiger cat during extended passage (third, seventh, and eleventh passages) and cryopreservation with regard to the morphology, viability, apoptotic classification, metabolism, proliferative activity, and oxidative stress by reactive oxygen species (ROS) levels and mitochondrial membrane potential (ΔΨm). Initially, we identified four dermal fibroblast lines by morphology, immunophenotyping, and karyotyping assays. <i>In vitro</i> culture after the third, seventh, and eleventh passages did not affect the viability, apoptotic classification, and ROS levels. Nevertheless, cells at seventh and eleventh passages featured a reduction in metabolism and an alteration in ΔΨm when compared to third passage cells. Additionally, cells at eleventh passage showed changes in the proliferative activity and morphology when compared to other passages. Regarding cryopreservation, no effect was observed on cryopreserved cells for morphology, viability, apoptotic classification, metabolism, and proliferative activity. Nevertheless, cryopreserved cells had alteration for ROS levels and ΔΨm. In summary, fibroblasts from northern tiger cat were affected by extended passage (seventh and eleventh passages) and cryopreservation. Adjustments to the in vitro culture and cryopreservation are necessary to reduce cellular oxidative stress caused by in vitro conditions.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"49 1","pages":"33-44"},"PeriodicalIF":3.3,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142267350","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}

{"title":"Lactate-mitochondrial crosstalk: A new direction in the treatment of sepsis-induced acute kidney injury","authors":"Zhixiong Wu,&nbsp;Wei Qing Liu,&nbsp;Liang Tang,&nbsp;Qiong Yuan,&nbsp;Yaling Li,&nbsp;Hongyu Hu,&nbsp;Xin Luo,&nbsp;Fan Ouyang","doi":"10.1002/cbin.12240","DOIUrl":"10.1002/cbin.12240","url":null,"abstract":"<p>Independent risk factors for sepsis-associated acute kidney injury (S-AKI) patients include elevated lactate levels, but the specific mechanism remains unclear. Recently, An et al. discovered that excessive acetylation and inactivation of PDHA1 lead to overproduction of lactate, resulting in mitochondrial fragmentation, ATP depletion, excessive mtROS production, and mitochondrial apoptosis, thereby exacerbating AKI in sepsis. Therefore, understanding the pathophysiological processes of mitochondrial function and lactate generation in SAKI is essential and can aid in the development of novel therapeutic strategies. This review elucidates the pathological mechanisms of mitochondrial autophagy and dynamics in AKI. We also discuss the sources of lactate in SAKI and some consequences of lactonization, which may provide new strategies for improving renal injury and delaying the progression of these diseases.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 11","pages":"1621-1624"},"PeriodicalIF":3.3,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142177692","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}

{"title":"Lysosomes accumulate at the perinuclear region of muscle cells during chick myogenesis","authors":"Kayo Moreira Bagri,&nbsp;Miria Gomes Pereira,&nbsp;Kamila Souto Leichtweis,&nbsp;Jose G. Abreu,&nbsp;Manoel Luis Costa,&nbsp;Claudia Mermelstein","doi":"10.1002/cbin.12238","DOIUrl":"10.1002/cbin.12238","url":null,"abstract":"<p>Lysosomes are involved in a myriad of cellular functions, such as degradation of macromolecules, endocytosis and exocytosis, modulation of several signaling pathways, and regulation of cell metabolism. To fulfill these diverse functions, lysosomes can undergo several dynamic changes in their content, size, pH, and location within cells. Here, we studied some of these parameters during embryonic chick skeletal muscle cells. We used an anti-lysosome-associated membrane protein 2 (LAMP2) antibody to specifically determine the intracellular localization of lysosomes in these cells. Our data shows that lysosomes are highly enriched in the perinuclear region of chick embryonic muscle cells. We also showed that the wingless signaling pathway (Wnt)/β-catenin signaling pathway can modulate the location of LAMP2 in chick myogenic cells. Our results highlight the role of lysosomes during muscle differentiation and particularly the presence of a subcellular population of lysosomes that are concentrated in the perinuclear region of muscle cells.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 11","pages":"1625-1636"},"PeriodicalIF":3.3,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142177693","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}

{"title":"Deciphering the cellular landscape and potential targets of nasopharyngeal and oral cancers using single-cell RNA sequencing","authors":"Yanfei Zhang,&nbsp;Xiaoyu Qin,&nbsp;Weihua Lou,&nbsp;Liang Wang,&nbsp;Wuhao Lu,&nbsp;Changhui Gao,&nbsp;Shousen Hu","doi":"10.1002/cbin.12236","DOIUrl":"10.1002/cbin.12236","url":null,"abstract":"<p>Cellular heterogeneity in nasopharyngeal cancer (NPC) and oral cancer remains unclear. In the current study, using single-cell RNA sequencing techniques, we investigated the cellular landscape in NPC and oral cancers. We identified a diverse range of cell types within the tumor microenvironment (TME) and variations in cell infiltration between NPC and oral cancer. In oral cancer, we observed a predominant infiltration of epithelial cells, fibroblasts, and endothelial cells (ECs), while T cells were the main infiltrating cell population in NPCs. We further classified these infiltrating cells into subclusters. Additionally, we observed complex interactions among cells that led to distinct trajectories. In particular, a unique epithelial subcluster with high expression of major histocompatibility complex class II (MHC-II) molecules was correlated with a favorable outcome and infiltration of CD4⁺ T cells. In addition, MHC-II⁺ epithelial cells inhibited mouse tumor growth and promoted T-cell infiltration. Consequently, our findings provide a deep understanding of the TME showing a significant prognostic value and therapeutic potential.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 12","pages":"1849-1861"},"PeriodicalIF":3.3,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104774","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}

{"title":"Prediction of clinical prognosis and drug sensitivity in hepatocellular carcinoma through the combination of multiple cell death pathways","authors":"QingKun Chen,&nbsp;ChenGuang Zhang,&nbsp;Tao Meng,&nbsp;Ke Yang,&nbsp;QiLi Hu,&nbsp;Zhong Tong,&nbsp;XiaoGang Wang","doi":"10.1002/cbin.12235","DOIUrl":"10.1002/cbin.12235","url":null,"abstract":"<p>Hepatocellular carcinoma (HCC) is the sixth most common malignant tumor, highlighting a significant need for reliable predictive models to assess clinical prognosis, disease progression, and drug sensitivity. Recent studies have highlighted the critical role of various programmed cell death pathways, including apoptosis, necroptosis, pyroptosis, ferroptosis, cuproptosis, entotic cell death, NETotic cell death, parthanatos, lysosome-dependent cell death, autophagy-dependent cell death, alkaliptosis, oxeiptosis, and disulfidptosis, in tumor development. Therefore, by investigating these pathways, we aimed to develop a predictive model for HCC prognosis and drug sensitivity. We analyzed transcriptome, single-cell transcriptome, genomic, and clinical information using data from the TCGA-LIHC, GSE14520, GSE45436, and GSE166635 datasets. Machine learning algorithms were used to establish a cell death index (CDI) with seven gene signatures, which was validated across three independent datasets, showing that high CDI correlates with poorer prognosis. Unsupervised clustering revealed three molecular subtypes of HCC with distinct biological processes. Furthermore, a nomogram integrating CDI and clinical information demonstrated good predictive performance. CDI was associated with immune checkpoint genes and tumor microenvironment components using single-cell transcriptome analysis. Drug sensitivity analysis indicated that patients with high CDI may be resistant to oxaliplatin and cisplatin but sensitive to axitinib and sorafenib. In summary, our model offers a precise prediction of clinical outcomes and drug sensitivity for patients with HCC, providing valuable insights for personalized treatment strategies.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 12","pages":"1816-1835"},"PeriodicalIF":3.3,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.12235","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142079385","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}

{"title":"OTUD6B promotes cholangiocarcinoma growth by regulating STAT3 phosphorylation through deubiquitination of PTK2","authors":"Guoqiang Xing,&nbsp;Hekai Chen,&nbsp;Zhiyue Guo,&nbsp;Yu Cui,&nbsp;Yongyuan Li,&nbsp;Jianwei Shen","doi":"10.1002/cbin.12234","DOIUrl":"10.1002/cbin.12234","url":null,"abstract":"<p>Cholangiocarcinoma (CCA) is a hepatobiliary carcinoma with uncontrolled cell proliferation, poor prognosis, and high mortality. The ovarian tumor structural domain (OTU) containing protein 6B (OTUD6B) belongs to the OTU deubiquitin family and is vital in tumor development. However, its expression and biological function in CCA remain unknown. The expression of OTUD6B in CCA was analyzed using TIMER2.0, UALCAN, and GEO databases. MTT, clonal formation assay, immunofluorescence staining, immunohistochemistry staining, and flow cytometry examined the regulation of OTUD6B on cell proliferation, cycle, and apoptosis. The effects of OTUD6B on tumor volume and weight were assessed using the xenograft tumor model. The activities of PTK2 and STAT3 were detected by western blot and CO-IP. The biological database identified that OTUD6B was upregulated in CCA. In CCA cells, OTUD6B knockdown reduced CCA cell proliferation and promoted apoptosis. Cell cycle analysis indicated that the cycle stopped at the G0/G1 phase after OTU6B downregulation. Furthermore, OTUD6B knockdown resulted in a decrease in tumor volume and weight in xenograft tumor models. Mechanistically, OTUD6B is involved in the deubiquitination of PTK2. PTK2 further affected the phosphorylation of STAT3 thereby regulating the CCA process. Our study demonstrates that OTUD6B knockdown participates in the ubiquitination of PTK2 and phosphorylation of STAT3 to alleviate the process of CCA. These results suggest that OTUD6B may be a potential new strategy for CCA treatment.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"48 11","pages":"1766-1778"},"PeriodicalIF":3.3,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142079384","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}