Molecular and Cellular Biochemistry最新文献

{"title":"Liquid biopsy in breast cancer: clinical implications of ctDNA and CTCs in diagnosis, treatment and monitoring.","authors":"Muhammad Umer Khan, Arooj Khawar, Muhammad Ikram Ullah, Muhammad Adnan Shan, Luca Falzone, Massimo Libra, Graziana Spoto, Javad Sharifi-Rad, Daniela Calina","doi":"10.1007/s11010-025-05343-7","DOIUrl":"https://doi.org/10.1007/s11010-025-05343-7","url":null,"abstract":"<p><p>One of the leading causes of cancer-related death in women is breast cancer (BC). BC is a heterogeneous tumor. Although tissue biopsy is the gold standard for the diagnosis of BC, often tissue specimens are not informative enough about the tumor heterogeneity. The concept of \"Liquid Biopsy\" has recently emerged as a powerful clinical tool capable of better identifying mutations associated with the presence of primary or metastatic tumors. This article focuses on the clinical applications of circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA) in breast cancer progression, relapse, diagnosis, and treatment response. The most important molecules analyzed in Liquid Biopsy are cfDNA, ctDNA, and CTCs. All these factors may be considered as non-invasive biomarkers for the early diagnosis of BC or to predict the progression and prognosis of patients, including BC recurrence and patients' treatment response. However, the clinical utility of ctDNA analysis and CTCs requires further investigation through better-designed studies to ensure their precision and diagnostic performance. In conclusion, liquid biopsy and ctDNA analysis demonstrate the potential to transform breast cancer management, with applications in screening, monitoring tumor progression, or response to treatment.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528918","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}

{"title":"A review: oxidative stress in skeletal muscle and the non-coding RNAs behind it.","authors":"Dongdong Bo, Jiameng Shen, Yilin Bai, Jing Li, Yuanyuan Wang, Ziqi Li, Zerui You, Anran Gai, Qing Zhang, Yueyu Bai","doi":"10.1007/s11010-025-05339-3","DOIUrl":"https://doi.org/10.1007/s11010-025-05339-3","url":null,"abstract":"<p><p>Oxidative damage, primarily caused by reactive oxygen species (ROS), leads to the oxidation of cellular components, particularly in skeletal muscles. ROS accumulation in muscle fibers results in the oxidation of proteins, lipids, and nucleic acids, affecting the stability of muscle structure and function. Signaling pathways, including NF-κB, MAPK, Nrf2-ARE, PI3K-AKT, and p53 pathways, are intimately associated with oxidative stress. Understanding the impact of oxidative stress on skeletal muscles and the regulatory mechanisms of ncRNA on skeletal muscle oxidative stress is crucial for preventing muscle damage caused by oxidative stress. Oxidative stress mechanisms in skeletal muscles are intricate, and involve many regulatory factors and signaling pathways. NcRNAs play critical regulatory roles in these responses, but their specific functions and mechanisms require further research. Future research should explore in depth the interactions between ncRNAs and other molecules, providing new theoretical foundations and practical guidance for the prevention of muscle oxidative stress. This review summarizes current understanding of molecular mechanisms driving oxidative stress in skeletal muscle, with emphasis on regulatory networks mediated by ncRNAs. Future investigations should focus on multi-omics integration of ncRNA crosstalk with redox signaling pathways, potentially informing preventive strategies against muscle dysfunction in metabolic and aging-related conditions.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528915","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}

{"title":"Neprilysin regulates the progression of glioblastoma: an in-vitro study using siRNA mediated gene silencing and HDAC1 mediated upregulation of neprilysin in U87 MG cells.","authors":"Adarsh Gopinathan, Runali Sankhe, Raghavendra Upadhya, K Sreedhara Ranganath Pai, Anoop Kishore","doi":"10.1007/s11010-025-05341-9","DOIUrl":"https://doi.org/10.1007/s11010-025-05341-9","url":null,"abstract":"<p><p>Neprilysin (NEP) is a neutral endopeptidase that has gained attention due to its ability to cleave diverse peptides such as fibroblast growth factor-2 (FGF-2), insulin-like growth factors (IGFs), substance P, amyloid-β, thymopentin etc. NEP plays an important role in the functioning of the central nervous system, cardiovascular system, and in pathologies such as Alzheimer's disease, hypertension, and various cancers. In breast, ovarian, prostate, and lung cancers, reduced NEP levels are associated with cancer progression. In Glioblastoma (GBM), the level of NEP is downregulated. This study aims to understand the role and expression pattern of NEP in GBM. A web-based tool, UALCAN, was utilized to understand the expression pattern of NEP in GBM, followed by patient survival analysis using the Cancer Genome Atlas (TCGA) data. Further, in-vitro scratch assays were performed on U87 MG cells to understand the effect of NEP silencing, as well as its upregulation using certain HDAC1 inhibitors identified through in-silico studies (melphalan, tasimelteon and panobinostat), to study the cancer progression. The UALCAN web tool revealed that NEP levels are downregulated in GBM. Additionally, the in-vitro scratch assay demonstrated that silencing of NEP augmented cell proliferation, whereas the upregulation of NEP using the HDAC1 inhibitors resulted in decreased cancer proliferation. These results suggest an inverse correlation between the NEP levels and GBM proliferation. The tumor suppression exhibited by NEP could be attributed to its degradation of mitogenic proteins such as FGF-2, IGFs etc. In conclusion, NEP can be a promising biomarker and a drug target against GBM.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528919","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}

{"title":"Effects of Lacticaseibacillus rhamnosus LB1.5 as potential probiotic supplement on the liver and adipose tissue of adult male mice to a high-fat diet.","authors":"Natália Perin Schmidt, Milena Henrique Ferri, Patrícia Molz, Brenda Santos Fraga, Priscila Dutra Silveira, Daiana Rodrigues Dos Santos, Juan Andres Cuadro Montanez, Gabriela Merker Breyer, Amanda de Souza da Motta, Marilene Porawski, Alethea Gatto Barschak, Renata Padilha Guedes, Márcia Giovenardi","doi":"10.1007/s11010-025-05344-6","DOIUrl":"https://doi.org/10.1007/s11010-025-05344-6","url":null,"abstract":"<p><p>This study aimed to investigate the effects of Lacticaseibacillus rhamnosus LB1.5 supplementation on liver and adipose tissue morphology, oxidative stress, and the relative gene expression of Sirt1, Gpx1, and Il6 in the liver of HFD-fed mice. Male C57BL/6 mice received: (i) a control diet (CONT), (ii) a control diet with probiotics (Lact. rhamnosus LB1.5, 1.3 × 10⁸ CFU/mL, three times a week; CONT + PROB), (iii) a high-fat diet (HFD), or (iv) a high-fat diet with probiotics (HFD + PROB) for 13 weeks. The HFD group showed significant liver alterations, including lipid accumulation, severe steatosis, hepatocellular ballooning, and an increase in Il6 relative gene expression, as well as an interaction effect on Sirt1 relative gene expression (p < 0.05). Nevertheless, these changes were not mitigated by probiotic supplementation (p > 0.05). Additionally, HFD-fed mice exhibited significant alterations in adipose tissue (p < 0.05), such as increased tissue weight, a lower number of adipocytes per area, and larger adipocyte size per area, with no significant effect of the probiotic observed (p > 0.05). In the liver, high TBARS levels were found in the HFD group, and a probiotic supplementation effect on sulfhydryl levels was observed only in the HFD + PROB group (p < 0.05). Unlike, in adipose tissue, redox status was not affected by diet or supplementation (p > 0.05). In conclusion, our results demonstrated the pro-inflammatory effects of an obesogenic diet and suggest that Lact. rhamnosus LB1.5 supplementation contributes only to the enhancement of liver redox status, improving antioxidant defenses by increasing sulfhydryl levels.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528916","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}

{"title":"Elexacaftor/tezacaftor/ivacaftor (ETI) therapy modifies the expression of interferon beta and inflammatory genes in the airways of adult patients with cystic fibrosis: a pilot study.","authors":"Camilla Bitossi, Federica Frasca, Alessandra D'Auria, Matteo Fracella, Giulia Radocchia, Maria Trancassini, Laura Petrarca, Domenico La Regina, Patrizia Troiani, Massimo Gentile, Valeria Pietropaolo, Fabio Midulla, Giuseppe Cimino, Guido Antonelli, Alessandra Pierangeli, Carolina Scagnolari","doi":"10.1007/s11010-025-05331-x","DOIUrl":"https://doi.org/10.1007/s11010-025-05331-x","url":null,"abstract":"<p><p>Cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapies have revolutionized the treatment of cystic fibrosis (CF) by targeting the underlying protein defect. Investigating how elexacaftor/tezacaftor/ivacaftor (ETI) therapy affects interferon (IFN) signalling and inflammatory cytokine production in CF airway epithelial cells may clarify its role in alleviating the dysregulated innate immune response. Clinical efficacy was evaluated in 26 modulator-naive CF patients with at least one F508del mutation before and after 3 and 6 months of ETI treatment. Type I/III IFNs, IFNLR1, IFN-stimulated genes (ISG15, ISG56), interleukin 8 (IL-8) and IL-1β mRNA levels were analysed by RT real-time PCR in CF airway samples (n = 74). Patients showed significant improvements in pulmonary function (ppFEV1, 3 months: 12.5%, 6 months: 17.6%), BMI (3 months: 0.9 kg/m², 6 months: 1.4 kg/m²), and sweat chloride (3 months: - 32.1 mEq/L, 6 months: - 44.4 mEq/L) compared to baseline (all p ≤ 0.001). The total number of exacerbations was also reduced (p = 0.002). Increased levels of IFNβ (p < 0.001) were found after 6 months of ETI therapy, whilst ISG15 and ISG56 decreased significantly (p = 0.022, p = 0.004). After 3 months, CF patients produced reduced levels of IL-8 and IL-1β (p = 0.001, p = 0.011) and even significantly lower levels after 6 months (p < 0.001, p < 0.001). ETI treatment appears to restore IFNβ expression and reduce levels of inflammatory genes (ISGs, IL-8 and IL-1β) in the airways, highlighting the potential of ETI to improve the dysregulated inflammatory status in CF.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144485116","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}

{"title":"Synthetic inhibition of the SUMO pathway by targeting the SAE1 component via TAK-981 compound impairs growth and chemosensitizes embryonal and alveolar rhabdomyosarcoma cell lines.","authors":"Silvia Codenotti, Volker M Lauschke, Emma V Casella, Daniel C Andersson, Alessandro Fanzani, Stefano Gastaldello","doi":"10.1007/s11010-025-05336-6","DOIUrl":"https://doi.org/10.1007/s11010-025-05336-6","url":null,"abstract":"<p><p>Rhabdomyosarcoma (RMS) is a highly aggressive pediatric soft tissue sarcoma with limited therapeutic options, particularly for cases resistant to conventional treatments. The SUMOylation pathway, which plays a key role in regulating the cell cycle, apoptosis, and transcription, has emerged as a potential therapeutic target in RMS. Elevated levels of SUMO1 and SUMO2/3 conjugates in RMS cell lines, compared to normal human skeletal muscle cells, underscore the association between upregulated SUMOylation and aggressive cancer phenotypes. Understanding these molecular underpinnings is critical for the development of innovative and effective treatments. The investigation encompassed transcriptomic and protein analyses to profile SUMOylation pathway components across alveolar and embryonal RMS subtypes, aiming to identify heterogeneity that could guide personalized therapy approaches. TAK-981, a small molecule that selectively inhibits the SUMOylation of target proteins, was evaluated in combination with chemotherapeutic agents for additive or synergistic effects. Additionally, its impact on radiosensitivity and key signaling pathways, such as AKT, ERK and CAV1 phosphorylation, was assessed to elucidate its mechanism of action. Transcriptomic and proteomic analyses revealed distinct expression profiles of SUMOylation pathway components across RMS subtypes, highlighting heterogeneity that could guide personalized therapeutic strategies. Notably, SAE1 protein was overexpressed in RMS tissues and cells, positioning it as a potential biomarker for this cancer. Its activity was effectively counteracted by TAK-981, a SUMO inhibitor that demonstrated significant therapeutic potential by suppressing RMS cell proliferation and migration, and enhancing the cytotoxic effects of chemotherapeutic agents actinomycin D and doxorubicin. However, TAK-981 did not increase radiosensitivity, suggesting its selective action through chemical inhibition mechanisms. Mechanistically, TAK-981 reduced phosphorylation of key signaling proteins, including AKT, ERK and CAV1, which are critical for RMS cell survival. The findings of this study establish TAK-981 as a promising therapeutic agent for RMS. The results also provide foundational insights into the role of SUMOylation associated with the new biomarker SAE1 in RMS and its subtypes, paving the way for the development of personalized treatment strategies that leverage SUMO pathway inhibition.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475980","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}

{"title":"Correction to: miR-143 decreases prostate cancer cells proliferation and migration and enhances their sensitivity to docetaxel through suppression of KRAS.","authors":"Bin Xu, Xiaobing Niu, Xiangxiang Zhang, Jun Tao, Deyao Wu, Zidun Wang, Pengchao Li, Wei Zhang, Hongfei Wu, Ninghan Feng, Zengjun Wang, Lixin Hua, Xinru Wang","doi":"10.1007/s11010-025-05333-9","DOIUrl":"https://doi.org/10.1007/s11010-025-05333-9","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475977","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}

{"title":"Emerging trends in cardiovascular diseases: the impact of ferroptosis and cuproptosis on cardiomyocyte death.","authors":"Peijian Chen, Ping He, Xuejing Rao, Minglu Ding, Jieting Liu, Yanhui Chu, Yang Xiao","doi":"10.1007/s11010-025-05340-w","DOIUrl":"https://doi.org/10.1007/s11010-025-05340-w","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) comprise a range of conditions affecting the heart and vasculature, encompassing ischemic heart disease (IHD), stroke, heart failure (HF), peripheral and aortic diseases, arrhythmias, and valvulopathy. Notably, the high prevalence rates of CVDs among younger populations warrant concern, emphasizing the importance of prevention and treatment. In recent years, ferroptosis, a novel form of cell death, has attracted significant research interest across various diseases. Similarly, cuproptosis, another cell death mechanism resulting from copper ion accumulation, has also been extensively studied. Cell death plays a crucial role in the development and maintenance of organisms, with both ferroptosis and cuproptosis closely associated with cell metabolism, signaling pathways, and drug resistance. Emerging evidence suggests that ferroptosis and cuproptosis are closely linked to the occurrence and progression of various diseases, including CVDs. The death of myocardial cells is pivotal in the pathophysiology of CVDs, with the roles of ferroptosis and cuproptosis in this process increasingly recognized. This article aims to summarize the molecular mechanisms and interactions of ferroptosis and cuproptosis, as well as their potential as novel targets for CVD treatment.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475978","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}

{"title":"High IGFL2 regulates ovarian cancer progression and the tumor immune microenvironment via the Warburg effect.","authors":"Zhizai Chen, Dalong Song, Shuting Huang, Jinyu Chao, Junhong Huang, Ming Luo, Shanyang He","doi":"10.1007/s11010-025-05328-6","DOIUrl":"https://doi.org/10.1007/s11010-025-05328-6","url":null,"abstract":"<p><p>This study aimed to explore the role and mechanism of insulin-like growth factor-like family member 2 (IGFL2) in ovarian cancer (OC) metastasis. Specifically, we focused on how IGFL2 regulates tumor cell energy metabolism and influences macrophage polarization to promote ovarian cancer metastasis. By conducting in vitro and in vivo experiments to elucidate the biological functions of IGFL2, this study aiming to identify new therapeutic targets for ovarian cancer treatment and provide a more effective treatment strategy. Our study revealed that the expression of IGFL2 was substantially upregulated in ovarian cancer metastases, and its high expression was positively correlated with the malignancy and metastatic potential of ovarian cancer. IGFL2 knockdown promoted mitochondrial oxidative phosphorylation and inhibited the Warburg effect, evidenced by increased oxygen consumption rate (OCR) and ATP production, and decreased glycolytic enzyme expression and lactate secretion. Concurrently, IGFL2 promoted M2 macrophage polarization via the STAT1/STAT6 signaling pathway, increasing the proportion of CD11b + CD206 + M2 cells and suppressing M1 polarization. In vivo, IGFL2 knockdown significantly inhibited tumor growth and metabolic reprogramming in xenograft models.These findings demonstrate that IGFL2 promotes OC metastasis through a dual mechanism: regulating metabolic reprogramming (Warburg effect) and influencing tumor-associated macrophage (TAM) polarization.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475979","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}

{"title":"The challenges and progress of CAR-T cell therapy in the treatment of solid tumors.","authors":"Kai Cui, Wanjun He, Na Huang, Songshan Zhu, Dan Jiang, Weiqiang Yang, Yiwei Zeng, Muhammad Asad Farooq, Guangxian Xu","doi":"10.1007/s11010-025-05329-5","DOIUrl":"https://doi.org/10.1007/s11010-025-05329-5","url":null,"abstract":"<p><p>Current traditional cancer treatment methods include surgery, chemotherapy, radiotherapy, etc., which lack targeted killing functions and may damage normal tissues. Immunotherapy, targeted therapy, and personalized medicine have become promising methods for cancer treatment, providing more precise and effective treatment for patients. Among them, chimeric antigen receptor (CAR)-T cell therapy utilizes the immune system's T cells to recognize and attack tumor cells, showing promising therapeutic prospects. The FDA has approved CAR-T therapy for treating B-cell acute lymphoblastic leukemia, large B-cell lymphoma, and multiple myeloma, targeting CD-19 and B-cell maturation antigens. Despite success in hematologic cancers, CAR-T technology faces challenges in solid tumors, including a lack of reliable tumor-associated antigens, hypoxic cores, immunosuppressive tumor environments, enhanced reactive oxygen species, and decreased T cell infiltration. This review covers the advantages and disadvantages of various immunotherapy methods, highlights CAR-T therapy's evolution, summarizes CAR-T therapy's current status, lists promising therapeutic targets, and emphasizes the challenges CAR-T cell therapy faces.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475981","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}