BioFactors最新文献

{"title":"Exploring vimentin's role in breast cancer via PICK1 alternative polyadenylation and the miR-615-3p-PICK1 interaction","authors":"Xinyan Jia BD,&nbsp;Lujing Shao MD,&nbsp;Hong Quan MD,&nbsp;Zhixian Zhong BD,&nbsp;Chunyan Dong PhD","doi":"10.1002/biof.2147","DOIUrl":"10.1002/biof.2147","url":null,"abstract":"<p>Breast cancer continues to be a major health issue for women worldwide, with vimentin (VIM) identified as a crucial factor in its progression due to its role in cell migration and the epithelial-to-mesenchymal transition (EMT). This study focuses on elucidating VIM's regulatory mechanisms on the miR-615-3p/PICK1 axis. Utilizing the 4T1 breast cancer cell model, we first used RNA-seq and proteomics to investigate the changes in the APA of PICK1 following VIM knockout (KO). These high-throughput analyses aimed to uncover the underlying transcriptional and proteomic alterations associated with VIM's influence on breast cancer cells. RNA-seq and proteomic profiling revealed significant APA in PICK1 following VIM KO, suggesting a novel mechanism by which VIM regulates breast cancer progression. Validation experiments confirmed that VIM KO affects the miR-615-3p-PICK1 axis, with miR-615-3p's regulation of PICK1 being contingent upon the APA of PICK1. These findings highlight the complex interplay between VIM, miR-615-3p, and PICK1 in the regulation of breast cancer cell behavior. This study reveals that vimentin affects the miR-615-3p-PICK1 axis through APA, revealing the key role of VIM in cancer progression. Opened up new avenues for targeted cancer therapy, with a focus on regulating the interaction between APA and miR-615-3p-PICK1.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11712540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943730","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":"FAM49B drives colorectal cancer progression by stabilizing c-Myc through NEK9 phosphorylation","authors":"Chen Lu,&nbsp;Tianyu Liu,&nbsp;E. Yimin,&nbsp;Lin Miao,&nbsp;Chunzhao Yu,&nbsp;Jianping Zhang,&nbsp;Xiagang Luo","doi":"10.1002/biof.2158","DOIUrl":"10.1002/biof.2158","url":null,"abstract":"<p>Colorectal cancer (CRC) ranks as the third most prevalent cancer globally and is the second leading cause of cancer mortality. FAM49B, a member of the FAM49 gene family, is a recently identified, evolutionarily conserved gene. Emerging studies indicate that FAM49B plays a role in various cancers, though its specific mechanism in CRC remains largely unexplored. In this study, we observed that FAM49B was abnormally expressed in CRC tissues and cell lines, with elevated expression correlating with poor patient prognosis. FAM49B knockdown markedly suppressed CRC cell proliferation by arresting the cell cycle and reducing cell migration and invasion. Single-cell RNA-seq (ScRNA-seq) analysis revealed that high FAM49B expression in malignant epithelial cell clusters was strongly linked to c-Myc oncogene activation. Further, FAM49B knockdown significantly reduced c-Myc expression by enhancing its K48 ubiquitination. We identified NEK9 as a direct interacting partner of FAM49B, with FAM49B knockdown inhibiting NEK9-Thr210 phosphorylation. Similarly, high NEK9 expression was linked to unfavorable prognosis in CRC. In FAM49B-overexpressing CRC cells, NEK9 knockdown significantly suppressed c-Myc expression, c-Myc-ser62 phosphorylation, and reduced cell proliferation, migration, and invasion. Thus, directly targeting the FAM49B/NEK9/c-Myc pathway presents a promising therapeutic approach for c-Myc positive CRC patients.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943732","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":"Echinacoside promotes collagen synthesis and survival via activation of IGF-1 signaling to alleviate UVB-induced dermal fibroblast photoaging","authors":"Su-Ying Wen,&nbsp;Shang-Chuan Ng,&nbsp;Lloyd Noriega,&nbsp;Tzu-Jung Chen,&nbsp;Chih-Jung Chen,&nbsp;Shin-Da Lee,&nbsp;Chih-Yang Huang,&nbsp;Wei-Wen Kuo","doi":"10.1002/biof.2152","DOIUrl":"10.1002/biof.2152","url":null,"abstract":"<p>Ultraviolet (UV) irradiation is a major factor contributing to skin photoaging, including the formation of reactive oxygen species (ROS), collagen breakdown, and overall skin damage. Insulin-like growth factor-I (IGF-1) is a polypeptide hormone that regulates dermal survival and collagen synthesis. Echinacoside (Ech), a natural phenylethanoid glycoside, is the most abundant active compound in Cistanches. However, its potential benefits for the skin and the underlying molecular mechanisms remain unclear. The objective of this research is to investigate the protective effect of Ech on human dermal fibroblast cells (HDFs) against UVB-induced skin photodamage. In this study, we demonstrated that Ech promotes IGF-1/IGF-1R/ERK-mediated collagen synthesis and IGF-1/IGF-1R/PI3K-mediated survival pathways, as well as induces IGF-1 secretion to counteract UVB-induced aging in HDFs. Furthermore, UVB-induced accumulation of SA-β-gal-positive cells, ROS, and impaired collagen synthesis were attenuated following Ech treatment. However, the protective effects of Ech were significantly diminished when IGF-1 and IGF-1R expression was silenced using small interfering RNA, indicating that Ech exerts its antiaging effects primarily by activating the IGF-1/IGF-1R signaling pathway. Our findings provide evidence of the antiaging effects of Ech on UVB-induced skin photodamage and suggest its potential development as a supplement in cosmetic dermal protective products.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943729","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":"Long non-coding RNA LINC01224 plays an oncogenic role in endometrial cancer via miR-4673/TPX2 axis and activating Wnt/β-catenin signaling pathway","authors":"Shuqing Lv,&nbsp;Xinlu Zhang,&nbsp;Fangfang Lang,&nbsp;Yanmei Wu,&nbsp;Cancan Zhang,&nbsp;Qi Qi,&nbsp;Jie Jiang","doi":"10.1002/biof.2153","DOIUrl":"10.1002/biof.2153","url":null,"abstract":"<p>Endometrial cancer (EC) is a prevalent gynecological malignancy with a rising incidence and poor prognosis in advanced cases. Long non-coding RNAs (lncRNAs) have been implicated in various cancers, including EC. This study explores the role of lncRNA Linc01224 in EC. Analyzing TCGA data, we found Linc01224 expression significantly elevated in EC tissues, correlating with poor prognosis. Clinical samples validated these findings, showing higher Linc01224 levels in tumor tissues. Knockdown of Linc01224 in EC cell lines (Hec-1-B and Ishikawa) inhibited proliferation, migration, and promoted apoptosis, alongside increased Bax and decreased BCL2 expression. Furthermore, Linc01224 knockdown notably reduced Wnt2/β-catenin pathway activation. We identified TPX2 as a target of miR-4673, which is regulated by Linc01224 through a competing endogenous RNA (ceRNA) mechanism. Dual-luciferase reporter assays confirmed miR-4673 binding to Linc01224 and TPX2. Rescue experiments revealed that TPX2 knockdown reversed Linc01224-induced proliferation and migration, highlighting TPX2's pivotal role in Linc01224's oncogenic function. In vivo, Linc01224 knockdown significantly impeded tumor growth and metastasis in a xenograft model, with decreased expression of c-Myc, Cyclin D1, and β-catenin. These findings reveal a novel ceRNA regulatory axis involving Linc01224, miR-4673, and TPX2, elucidating Linc01224's role in EC progression through the Wnt2/β-catenin pathway. Linc01224 emerges as a potential biomarker and therapeutic target for EC prognosis and treatment.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943747","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":"Comprehensive analysis of the value of angiogenesis and stemness-related genes in the prognosis and immunotherapy of ovarian cancer","authors":"Linsen Zhou,&nbsp;Yu Min,&nbsp;Qiqi Cao,&nbsp;Xun Tan,&nbsp;Yongfen Cui,&nbsp;Jiawei Wang","doi":"10.1002/biof.2155","DOIUrl":"10.1002/biof.2155","url":null,"abstract":"<p>Tumor angiogenesis and the presence of cancer stem cells (CSCs) are critical characteristics of tumors. Previous research has demonstrated that cancer stem cells promote tumor angiogenesis, while increased vascularity, in turn, fosters the growth of cancer stem cells. This creates a detrimental cycle that contributes to tumor progression. However, studies investigating the angiogenesis and stemness characteristics in ovarian cancer (OV) are limited. In this study, we employed cluster analysis and LASSO methods to assess the significance of angiogenesis- and stemness-related genes in the efficacy of OV immunotherapy. Through multivariate Cox regression analysis and Friends analysis, we identified TNFSF11 as the most significant prognostic gene associated with angiogenesis and stemness. Additionally, molecular docking results confirmed that TNFSF11 exhibits a high affinity for sorafenib and sunitinib. In summary, for the first time, we conducted a comprehensive analysis of the roles of angiogenesis and stemness-related genes in the prognosis and immunotherapy of OV patients, revealing TNFSF11 as a novel therapeutic target.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/biof.2155","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142862955","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":"Issue Information - Cover","authors":"","doi":"10.1002/biof.1972","DOIUrl":"https://doi.org/10.1002/biof.1972","url":null,"abstract":"","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"50 6","pages":""},"PeriodicalIF":5.0,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/biof.1972","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142868315","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":"Cannabidiol effects in stem cells: A systematic review","authors":"Cristina Mesas,&nbsp;Javier Moreno,&nbsp;Kevin Doello,&nbsp;Mercedes Peña,&nbsp;Juan M. López-Romero,&nbsp;Jose Prados,&nbsp;Consolación Melguizo","doi":"10.1002/biof.2148","DOIUrl":"10.1002/biof.2148","url":null,"abstract":"<p>Stem cells play a critical role in human tissue regeneration and repair. In addition, cancer stem cells (CSCs), subpopulations of cancer cells sharing similar characteristics as normal stem cells, are responsible for tumor metastasis and resistance to chemo- and radiotherapy and to tumor relapse. Interestingly, all stem cells have cannabinoid receptors, such as cannabidiol (CBD), that perform biological functions. The aim of this systematic review was to analyze the effect of CBD on both somatic stem cells (SSCs) and CSCs. Of the 276 articles analyzed, 38 were selected according to the inclusion and exclusion criteria. A total of 27 studied the effect of CBD on SSCs, finding that 44% focused on CBD differentiation effect and 56% on its protective activity. On the other hand, 11 articles looked at the effect of CBD on CSCs, including glioblastoma (64%), lung cancer (27%), and breast cancer (only one article). Our results showed that CBD exerted a differentiating and protective effect on SCCs. In addition, this molecule demonstrated an antiproliferative effect on some CSCs, although most of the analyses were performed in vitro. Therefore, although in vivo studies should be necessary to justify its clinical use, CBD and its receptors could be a specific target to act on both SSCs and CSCs.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681305/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799350","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":"Knockdown of integrin β1 inhibits proliferation and promotes apoptosis in bladder cancer cells","authors":"Jin-feng Wang,&nbsp;Jian-she Wang,&nbsp;Yang Liu,&nbsp;Bo Ji,&nbsp;Bei-chen Ding,&nbsp;Ya-xuan Wang,&nbsp;Ming-hua Ren","doi":"10.1002/biof.2150","DOIUrl":"10.1002/biof.2150","url":null,"abstract":"<p>Bladder cancer (BC) is the most common urinary tract malignancy. Identifying biomarkers that predict prognosis and immune function in patients with BC can enhance our understanding of its pathogenesis and provide valuable guidance for diagnosis and treatment. Our findings indicate that increased ITGB1 expression is associated with higher clinical grade and stage, establishing ITGB1 as an independent prognostic risk factor for BC. Enrichment analysis revealed that the function of ITGB1 in BC was linked to the extracellular matrix. The experimental results showed that ITGB1 knockdown in the BC cell lines 5637 and RT112 reduced their proliferation, migration, and invasion. Furthermore, ITGB1 suppression promotes apoptosis in BC cells by inhibiting the PI3K-AKT pathway. A prognostic risk model incorporating CES1, NTNG1, SETBP1, and AIFM3 was developed based on ITGB1, this model can accurately predict patient prognosis based on immunological status. In conclusion, this study shows that knockdown of ITGB1 can restrain the migratory and invasive capabilities of BC cells and accelerate apoptosis, and this role might be associated with PI3K-AKT, highlighting its potential as a diagnostic marker and therapeutic target for BC.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791159","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 potential molecular mechanisms in clear cell renal cell carcinoma based on the ubiquitin-conjugating enzyme E2 related genes: Identifying UBE2C correlates to infiltration of regulatory T cells","authors":"Xiaoqiang Feng,&nbsp;Zhenwei Wang,&nbsp;Meini Cen,&nbsp;Zongtai Zheng,&nbsp;Bangqi Wang,&nbsp;Zongxiang Zhao,&nbsp;Zhihui Zhong,&nbsp;Yesong Zou,&nbsp;Qian Lv,&nbsp;Shiyu Li,&nbsp;Li Huang,&nbsp;Hai Huang,&nbsp;Xiaofu Qiu","doi":"10.1002/biof.2143","DOIUrl":"10.1002/biof.2143","url":null,"abstract":"&lt;p&gt;Renal clear cell carcinoma (ccRCC) is a highly aggressive and common form of kidney cancer, with limited treatment options for advanced stages. Recent studies have highlighted the importance of the ubiquitin-proteasome system in tumor progression, particularly the role of ubiquitin-conjugating enzyme E2 (UBE2) family members. However, the prognostic significance of UBE2-related genes (UBE2RGs) in ccRCC remains unclear. In this study, bulk RNA-sequencing and single-cell RNA-sequencing data from ccRCC patients were retrieved from the Cancer Genome Atlas and Gene Expression Omnibus databases. Differential expression analysis was performed to identify UBE2RGs associated with ccRCC. A combination of 10 machine learning methods was applied to develop an optimal prognostic model, and its predictive performance was evaluated using area under the curve (AUC) values for 1-, 3-, and 5-year overall survival (OS) in both training and validation cohorts. Functional enrichment analyses of gene ontology and Kyoto Encyclopedia of Genes and Genomes were conducted to explore the biological pathways involved. Correlation analysis was conducted to investigate the association between the risk score and tumor mutational burden (TMB) and immune cell infiltration. Immunotherapy and chemotherapy sensitivity were assessed by immunophenoscore and tumor immune, dysfunction, and exclusion scores to identify potential predictive significance. In vitro, knockdown of the key gene UBE2C in 786-O cells by specific small interfering RNA to validate its impact on apoptosis, migration, cell cycle, migration, invasion of tumor cells, and induction of regulatory T cells (Tregs). Analysis of sc-RNA revealed that UBE2 activity was significantly upregulated in malignant cells, suggesting its role in tumor progression. A three-gene prognostic model comprising UBE2C, UBE2D3, and UBE2T was constructed by Lasoo Cox regression and demonstrated robust predictive accuracy, with AUC values of 0.745, 0.766, and 0.771 for 1-, 3-, and 5-year survival, respectively. The model was validated as an independent prognostic factor in ccRCC. Patients in the high-risk group had a worse prognosis, higher TMB scores, and low responsiveness to immunotherapy. Additionally, immune infiltration and chemotherapy sensitivity analyses revealed that UBE2RGs are associated with various immune cells and drugs, suggesting that UBE2RGs could be a potential therapeutic target for ccRCC. In vitro experiments confirmed that the reduction of UBE2C led to an increase in apoptosis rate, as well as a decrease in tumor cell invasion and metastasis abilities. Additionally, si-UBE2C cells reduced the release of the cytokine Transforming Growth Factor-beta 1 (TGF-β1), leading to a decreased ratio of Tregs in the co-culture system. This study presents a novel three-gene prognostic model based on UBE2RGs that demonstrates significant predictive value for OS, immunotherapy, and chemotherapy in ccRCC patients. The findings underscore","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754497","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":"Suppression of colorectal cancer growth: Interplay between curcumin and metformin through DMT1 downregulation and ROS-mediated pathways","authors":"Hui-Yen Chuang,&nbsp;Hui-Wen Chan,&nbsp;Kuang-Chung Shih","doi":"10.1002/biof.2137","DOIUrl":"10.1002/biof.2137","url":null,"abstract":"<p>The rising incidence of colorectal cancer (CRC) poses significant healthcare challenges. This study explored the therapeutic potential of combined curcumin (CUR) and metformin (MET) treatment in CRC models. Our findings indicate that the combination treatment (COMB) effectively downregulates the expression of divalent metal transporter-1 (DMT-1), leading to a reduction in cell proliferation aligned with suppression of the pAKT/mTOR/Cyclin D1 signaling pathway. The COMB increased reactive oxygen species (ROS) production, triggering activation of the NRF2/KEAP1 pathway. This pathway elicits an antioxidant response to manage oxidative stress in CRC cell lines. Interestingly, the response of NRF2 varied between CT26 and HCT116 cells. Moreover, our study highlights the induction of apoptosis and autophagy, as evidenced by upregulations in Bax/Bcl-2 ratios and autophagy-related protein expressions. Notably, the COMB promoted lipid peroxidation and downregulated xCT levels, suggesting the induction of ferroptosis. Ferroptosis has been shown to activate autophagy, which helps eliminate cells potentially damaged by the increased oxidative stress. Furthermore, the COMB effectively diminished the migratory ability of CRC cells. In vivo experiments using CRC-bearing mouse models, the results confirmed the anti-tumor efficacy of the COMB, leading to substantial inhibition of tumor growth without inducing general toxicity. In conclusion, our study suggests that combining CUR with MET holds promise as a potential option for CRC treatment, with critical mechanisms likely involving ROS elevation, autophagy, and ferroptosis.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 1","pages":""},"PeriodicalIF":5.0,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738152","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}