Cancer Biology & Therapy最新文献

{"title":"Lenvatinib promotes hepatocellular carcinoma pyroptosis by regulating GSDME palmitoylation.","authors":"Yuan Yuan, Mu-Ru Wang, Yang Ding, Ya Lin, Ting-Ting Xu, Xing-Xing He, Pei-Yuan Li","doi":"10.1080/15384047.2025.2532217","DOIUrl":"10.1080/15384047.2025.2532217","url":null,"abstract":"<p><p>Lenvatinib, as a multi-kinase inhibitor, has been approved as a first-line drug for patients with advanced hepatocellular carcinoma (HCC). Gasdermin E (GSDME)-mediated pyroptosis, a form of programmed cell death, can be induced by chemotherapy drugs or certain kinase inhibitors. However, the role of Lenvatinib in inducing pyroptosis in HCC warrants further investigation. Phase contrast microscopy, LDH assays, and gain- and loss-of-function strategies were used to evaluate Lenvatinib-induced pyroptosis in HCC cells. GSDME palmitoylation was assessed via the acyl-biotin exchange method. In vivo, a subcutaneous HCC xenograft model in nude mice were established to assess the effects of interfering with GSDME on the sensitivity of HCC to Lenvatinib. Lenvatinib induced pyroptosis in HCC cells in a dose- and time-dependent manner. Additionally, Lenvatinib promoted GSDME cleavage, with upregulation of GSDME enhancing pyroptosis and downregulation reducing this effect. The ABE method revealed that GSDME is palmitoylated, and Lenvatinib increased its palmitoylation, promoting plasma membrane localization and enhancing protein stability. Inhibition of GSDME palmitoylation by 2-BP blocked Lenvatinib-induced pyroptosis. In vivo, upregulation of GSDME increased HCC sensitivity to Lenvatinib and inhibited tumor growth. Lenvatinib induces pyroptosis in HCC by promoting the palmitoylation of GSDME, enhancing its localization to the plasma membrane and increasing its protein stability. Interfering with GSDME, both in vitro and in vivo, affects Lenvatinib-induced pyroptosis, thereby altering the therapeutic sensitivity of HCC to Lenvatinib. Targeting GSDME palmitoylation represents a potential therapeutic strategy for HCC, as it enhances Lenvatinib-induced pyroptosis and improves the therapeutic response.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2532217"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comparison of cell death pathways in three different kinds of human lung cancer cell lines following hematoporphyrin derivative-mediated photodynamic therapy.","authors":"Yijiang Ma, Baohong Xiao, Aihua Sui, Xiaohui Yang, Shichao Cui, Yiwei Cao, Cunzhi Lin","doi":"10.1080/15384047.2025.2542011","DOIUrl":"https://doi.org/10.1080/15384047.2025.2542011","url":null,"abstract":"<p><p>This study was conducted to investigate the in vitro differences in killing effects and cellular death pathways in human bronchial epithelial BEAS-2B cells, human lung adenocarcinoma A549 cells, human lung squamous carcinoma H520 cells, and human lung small cell carcinoma H446 cells mediated by hematoporphyrin derivative (HPD) at 630 nm laser wavelength. Our results showed that the viability of the BEAS-2B, A549, H520, and H446 cells gradually decreased with increasing HPD concentration after HPD-PDT. HPD-PDT induced an increase in intracellular ROS production (<i>p</i> < 0.05), with H520 > A549 > H446 > BEAS-2B. HPD-PDT resulted in intracellular chromatin fixation and dense nuclear staining and induced apoptosis, with apoptosis rates of H520 > A549 > H446 > BEAS-2B. The western blotting (WB) results showed that HPD-PDT could lead to reduced BCL-2 protein levels, upregulate BAX protein expression and activate caspase-3 protein, and induce autophagy, as evidenced by the increased expression of the autophagy-related proteins ATG5, Beclin-1 and LC3B in all cells tested. However, apoptosis-inducing proteins and autophagy proteins were statistically different in these four cell types. Our study confirms that HPD-mediated phototoxicity varied in the different cell lines, indicating that lung cancer cells die due to the interactions of different cell death pathways rather than the same well-defined mechanisms.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2542011"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MGAT4EP promotes tumor progression and serves as a prognostic marker for breast cancer.","authors":"Lin Zhong, Jianfeng Zhu, Jie Chen, Xuchu Jin, Liangquan Liu, Shufeng Ji, Jing Luo, Hong Wang","doi":"10.1080/15384047.2025.2475604","DOIUrl":"10.1080/15384047.2025.2475604","url":null,"abstract":"<p><p>Breast cancer remains a global health challenge with varied prognoses despite treatment advancements. Therefore, this study explores the pseudogene MGAT4EP as a potential biomarker and therapeutic target in breast cancer. Using TCGA data and bioinformatics, MGAT4EP was identified as significantly overexpressed in breast cancer tissues and associated with poor prognosis. Multivariate Cox regression confirmed MGAT4EP as important prognostic factor. A clinical prediction model based on MGAT4EP expression showed high accuracy for 1-, 3-, and 5-year survival rates and was translated into a nomogram for clinical application. Functional studies revealed that silencing MGAT4EP <i>via</i> siRNA promoted apoptosis, inhibited migration and invasion in breast cancer cells. RNA-seq, GSEA, and GO analyses linked MGAT4EP to apoptosis and focal adhesion pathways. Notably, knock down of MGAT4EP significantly suppressed tumor growth and metastasis in xenograft and lung metastasis models. Taken together, these findings establish MGAT4EP as an attractive target for metastatic breast cancer and provide a potential a promising therapeutic target for breast cancer treatment.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2475604"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11901376/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of extracellular vesicle ZNF280B derived from lung cancer stem cells on lung cancer progression.","authors":"Qixia Guo, Jiayan Lu, Hui Zhao, Ding Zhou, Hua Liu","doi":"10.1080/15384047.2025.2450849","DOIUrl":"10.1080/15384047.2025.2450849","url":null,"abstract":"<p><strong>Objective: </strong>The purpose of this research was to investigate the role of extracellular vesicles derived from lung cancer stem cells (lung CSCs-EVs) in lung cancer and to explore their potential mechanisms.</p><p><strong>Methods: </strong>Lung CSCs were first isolated and verified using flow cytometry and RT-qPCR assays. Lung CSCs-EVs were extracted through ultracentrifugation and further characterized using transmission electron microscopy and Western blotting. The interaction between lung CSCs-EVs and lung cancer cells was observed through PKH67 staining. Subsequently, we analyzed the differentially expressed genes in lung CSCs using bioinformatics data analysis and evaluated the prognostic value of ZNF280B in lung cancer with the Kaplan-Meier Plotter. RT-qPCR was utilized to assess the mRNA expression levels of these genes, while Western blotting was used to evaluate the protein expression levels of ZNF280B and P53. Next, CCK-8 and colony formation assays were conducted to assess the effects of lung CSCs-EVs and ZNF280B on cancer cell proliferation, migration (via wound healing assay), and invasion (using transwell assay). Additionally, subcutaneous tumor-bearing experiments in nude mice were performed to evaluate the roles of lung CSCs-EVs in lung cancer progression <i>in vivo</i>.</p><p><strong>Results: </strong>The results indicated that lung CSCs-EVs accelerated the progression of lung cancer. Mechanistically, these lung CSCs-EVs transferred ZNF280B into cancer cells, leading to the inhibition of P53 expression.</p><p><strong>Conclusions: </strong>In summary, the manuscript first describes the molecular mechanism by which lung CSCs-EVs promote pro-cancer functions in lung cancer through the ZNF280B/P53 axis.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2450849"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the potential for in vivo modulation of <i>FTH1 gene</i> expression with small peptides to restore and enhance androgen receptor pathway inhibition in prostate cancer.","authors":"Crawford Currie, Christian Bjerknes, McKayla Nicol, Sateesh Kumar, Bomi Framroze","doi":"10.1080/15384047.2025.2503417","DOIUrl":"https://doi.org/10.1080/15384047.2025.2503417","url":null,"abstract":"<p><p>Increased levels of intratumoral free iron drive more aggressive behavior with the development of treatment resistance and spread in a range of cancers including prostate cancer (PCa). This phenotype is associated with an increase in TFRC expression and a decrease in FTH1, a profile supporting increased iron acquisition. In this study we investigated the anti-oncogenic effects of two small peptides (FT-002 and FT-005) that upregulate FTH1 expression and downregulate TFRC expression when combined with standard androgen receptor pathway inhibitors (ARPIs) in xenograft models of PCa in male athymic nude mice. The PC3 cell line was used to establish xenografts representing highly aggressive, androgen-resistant PCa and the LNCaP cell line as a model of androgen-sensitive PCa. Both peptides enhanced the anti-tumor efficacy of ARPI therapy. Efficacy was more marked with the combination of the second-generation APRI enzalutamide than the first-generation agent bicalutamide, a result consistent with known resistance mechanisms to different ARPI therapy. Further, the FT-peptide/enzalutamide combination drove tumor regression whereas enzalutamide monotherapy only slowed growth, even in the hormone-sensitive xenograft. The FT-002a-enzalutamide combination was more effective than FT-005 in reducing tumor mass and volume and modulating FTH1 and TFRC expression. The reversal by the peptides of this oncogenic expression pattern points to a reduction in the tumor free iron via increased iron storage in ferritin and a reduction in iron influx via the transferrin receptor. Peptide-mediated modulation of tumor iron metabolism may therefore offer a novel means to enhance ARPI efficacy and delay resistance in advanced prostate cancer.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2503417"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12068333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143954609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal miR-122-5p for regulation of secretory functions of fibroblasts and promotion of breast cancer metastasis by targeting MKP-2: an experimental study.","authors":"Yun Lv, Yue Li, Jie Zhou, Xin Liu, Dandan Wang, Dongmei Wang, Dandan Tong, Shuhuai Wang, Hanxiang An, Xinmei Kang","doi":"10.1080/15384047.2025.2500104","DOIUrl":"https://doi.org/10.1080/15384047.2025.2500104","url":null,"abstract":"<p><p>Tumor metastasis is a major obstacle for the effective treatment of breast cancer. Some studies showed that exosomes could promote tumor distant metastasis by establishing pre-metastasis niches (PMN). MicroRNAs (miRNAs) in exosomes play a critical role in tumor development and invasion. We aimed to investigate the effects of exosomal miRNAs derived from breast cancer cells on metastasis. MiRNA sequencing and RT-PCR approach were used to screen potential exosomal miRNAs. We compared the levels of serum exosomal miRNAs from breast cancer patients and those from MCF10A/MCF7/MDA-MB-231 cells. We found that differential exosomal miRNAs screened from patients with metastasis have higher expression levels in exosomes secreted by MDA-MB-231 cells. Using miRNA mimics or inhibitors, exosomal miR-122-5p was found to enhance the secretion levels of chemokine MCP-1 and SDF-1 from WI-38 lung fibroblast cells. In vitro luciferase assay and western blot confirmed the targeting of 3'-untranslated region of MKP-2 and suppression of MKP-2 expression by miR-122-5p in WI-38 cells. Treatment of xenograft mice with exosomal miR-122-5p increased the levels of MCP-1 and SDF-1 in serum, and promoted lung metastasis of breast cancer. In conclusion, we identified exosomal miR-122-5p from breast cancer cells that could promote the chemokine secretion of lung fibroblasts, which might facilitate the chemotaxis and colonization of breast cancer cells in lung tissue.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2500104"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12051585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of pseudogene MT2P1 transcription induced by E2F7 inhibits hepatocellular carcinoma cell proliferation and facilitates apoptosis via preserving its parental gene.","authors":"Yiquan Lu, Yifan Zhang, Fengjie Hao, Nan Wang, Yongjun Chen, Junqing Wang","doi":"10.1080/15384047.2025.2510035","DOIUrl":"10.1080/15384047.2025.2510035","url":null,"abstract":"<p><p>The majority of the pseudogenes are inert in normal transcription. Their transcripts are mostly attributed to non-coding RNAs that play various functions in human tumorigenicity and progression. Distinctively, pseudogene MT2P1 is universally transcribed in hepatocytes and presents a significant decrease in hepatocellular carcinoma (HCC). The effect of MT2P1-RNA on HCC cell proliferation and apoptosis needs investigation. MT2P1-RNA was detected by RT-qPCR assay in HCC tissues and cell lines, combined with the exploration of the public databases. The immunohistochemistry assay was used for testing the expression profile of E2F7 and the parental gene MT2A. The clinicopathological features of the patients were collected and analyzed. Ectopic expression of MT2P1-RNA in HCC cell lines was conducted, and the CCK8 assay and flow cytometry assay were carried out. Chromatin immunoprecipitation assay and Dual-luciferase reporter assay were, respectively, applied to validate the interaction between MT2P1, E2F7, and microRNA-15b-5p. The downregulation of MT2P1-RNA in HCC is negatively correlated with dismal clinicopathological features. MT2P1-RNA significantly suppressed HCC cell proliferation and induced apoptosis. E2F7 depletion sequentially elevated the level of MT2P1-RNA and MT2A, and E2F7 was validated as a suppressive transcription factor of the MT2P1 gene. The direct interactions of either MT2P1/miR-15b-5p or miR-15b-5p/MT2A were, respectively, ascertained, enlightening the ceRNA effect of them. The pseudogene-derived MT2P1-RNA is a suppressor of HCC by exerting the ceRNA effect on preserving MT2A, and its transcription is regulated by the suppressive transcription factor E2F7.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2510035"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction.","authors":"","doi":"10.1080/15384047.2025.2520651","DOIUrl":"10.1080/15384047.2025.2520651","url":null,"abstract":"","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2520651"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12169023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Copper death combination therapy: the innovative frontier and challenges in prostate cancer treatment.","authors":"Jia Wei He, Pei Zhen Li, Zi Xuan Huang","doi":"10.1080/15384047.2025.2532224","DOIUrl":"10.1080/15384047.2025.2532224","url":null,"abstract":"<p><p>Prostate cancer (PCA) remains a significant health challenge, necessitating the exploration of novel therapeutic strategies to enhance patient outcomes. Recent research has identified cuproptosis, a copper-dependent programmed cell death mechanism, as a promising target in PCA treatment. Elevated copper levels have been associated with tumor progression and therapeutic resistance, highlighting the need for innovative approaches. This review synthesizes current findings on the role of copper and cuproptosis in PCA, focusing on the mechanisms underlying cuproptosis, the identification of key biomarkers, and the therapeutic potential of copper complexes and ionophores. The integration of cuproptosis-related biomarkers into clinical practice may facilitate personalized treatment strategies, while ongoing research into copper-based therapies holds promise for overcoming limitations of traditional chemotherapy. Future directions should emphasize elucidating the molecular mechanisms of cuproptosis and optimizing therapeutic applications to improve patient outcomes in PCA.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2532224"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Robust prediction of glioma prognosis by hypoxia-induced ferroptosis genes: VEGFA-XBP1 co-expression for salvage therapy.","authors":"Zhou Liwei, Lu Hanwen, Zhao Wenpeng, Yu Weijie, Chen Sifang, Zhang Bingchang, Li Zhangyu, Gao Xin, Li Wenhua, Mao Jianyao, Xie Yuanyuan, Tan Guowei, Wang Zhanxiang","doi":"10.1080/15384047.2025.2529643","DOIUrl":"10.1080/15384047.2025.2529643","url":null,"abstract":"<p><p>Hypoxia as a hallmark of solid malignancies compromises therapeutic efficacy and prognosis. This study deciphers the functional role of hypoxia-induced ferroptosis in glioma prognosis. Hypoxia-related transcripts and ferroptosis markers were curated from public databases. ConsensusClusterPlus identify hypoxia-based molecular subtypes, while LASSO-penalized Cox regression integrated with limma-based differential expression analysis screened prognostic ferroptosis genes. Subsequent risk modeling was validated against clinical parameters and extended through nomogram construction. Protein-protein interaction networks centered on HIF-1αidentified high-confidence interactors, with parallel immune correlation analysis completing the systems-level investigation.Based on 27 hypoxia-associated genes, we stratified samples into three distinct hypoxic clusters. Differential analysis of 123 ferroptosis markers across clusters, combined with univariate Cox regression and LASSO regression, identified 23 hypoxia-induced ferroptosis genes for constructing a prognostic model. The model demonstrated robust predictive accuracy with AUC values of 0.80 (1-year), 0.86 (3-year), and 0.86 (5-year). GSEA revealed significant enrichment in ECM-receptor interactions, focal adhesion, JAK-STAT signaling, and p53 signaling pathways, suggesting their involvement in hypoxia-induced ferroptosis. Our risk model significantly outperformed conventional clinical parameters (pathology, grade, age, primary/recurrent status). Protein-protein interaction analysis incorporating HIF-1αand the 23-model genes identified XBP1 and VEGFA co-expression as significant positive prognostic factor. The immune infiltration analysis further indicated that M0 macrophages may participate in the regulation of the prognosis of VEGFA-XBP1.Hypoxia-induced ferroptosis modulation emerges as a prognostic factor in gliomas, with XBP1 and VEGFA representing druggable nodes for novel combination therapies.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2529643"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239816/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}