Cellular Oncology最新文献

{"title":"RAB37 suppresses the EMT, migration and invasion of gastric cancer cells by mediating autophagic degradation of β-catenin.","authors":"Jiangling Duan, Xiuyin Guan, Jiaxin Xue, Jiayu Wang, Zhiwei Wang, Xuan Chen, Wen Jiang, Wannian Sui, Yongfang Song, Tianshu Li, Dewang Rao, Xueyan Wu, Ming Lu","doi":"10.1007/s13402-024-01028-3","DOIUrl":"10.1007/s13402-024-01028-3","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer, characterized by its high morbidity and mortality rates, exhibits low levels of RAB37. The role and molecular mechanisms of RAB37, a small GTPase, in the pathogenesis of gastric cancer are still unclear.</p><p><strong>Methods: </strong>We assessed RAB37 expression in gastric cancer cells using quantitative Polymerase Chain Reaction (qPCR), Western blot, and immunohistochemical staining (IHC), and analyzed EMT marker proteins and autophagy changes via Western blot, immunofluorescence (IF), and transmission electron microscopy (TEM). Co-immunoprecipitation (co-IP) was used to identify protein-protein interactions. We studied the migration and invasion of gastric cancer cells using wound healing and transwell assays in vitro and a mouse pulmonary metastasis model in vivo.</p><p><strong>Results: </strong>Overexpression of RAB37 suppressed EMT, invasion, and migration while enhancing autophagy in gastric cancer cells, which was dependent on its GTPase activity. However, all these effects could be reversed by the autophagy inhibitor chloroquine. Regarding the molecular mechanism, RAB37 strengthened the interaction between p62 and β-catenin, which consequently enhanced the p62-mediated autophagic degradation of β-catenin. Furthermore, RAB37 curbed the pulmonary metastasis of both general and cisplatin-resistant gastric cancer cells.</p><p><strong>Conclusion: </strong>The low level of RAB37 reduces interaction between p62 and β-catenin and then the autophagic degradation of β-catenin, thereby promoting the EMT, invasion, and migration in gastric cancer cells. The low expression of RAB37 in gastric cancer suggests a potential therapeutic target, especially for cisplatin-resistant gastric cancer.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2407-2421"},"PeriodicalIF":4.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-canonical function of PHGDH promotes HCC metastasis by interacting with METTL3.","authors":"Bin Cheng, Jing Ma, Ni Tang, Rui Liu, Pai Peng, Kai Wang","doi":"10.1007/s13402-024-01029-2","DOIUrl":"10.1007/s13402-024-01029-2","url":null,"abstract":"<p><strong>Purpose: </strong>Phosphoglycerate dehydrogenase (PHGDH), a pivotal enzyme in serine synthesis, plays a key role in the malignant progression of tumors through both its metabolic activity and moonlight functions. This study aims to elucidate the non-canonical function of PHGDH in promoting hepatocellular carcinoma (HCC) metastasis through its interaction with methyltransferase-like 3 (METTL3), potentially uncovering a novel therapeutic target.</p><p><strong>Methods: </strong>Western blot was used to study PHGDH expression changes under anoikis and cellular functional assays were employed to assess its role in HCC metastasis. PHGDH-METTL3 interactions were explored using GST pull-down, Co-immunoprecipitation and immunofluorescence assays. Protein stability and ubiquitination assays were performed to understand PHGDH's impact on METTL3. Flow cytometry, cellular assays and nude mice model were used to confirm PHGDH's effects on anoikis resistance and HCC metastasis in vitro and in vivo.</p><p><strong>Results: </strong>PHGDH is upregulated under anoikis conditions, thereby enhancing the metastatic potential of HCC cells. By interacting with METTL3, PHGDH prevents its ubiquitin-dependent degradation, resulting in higher METTL3 protein levels. This interaction upregulates epithelial-mesenchymal transition related genes, contributing to anoikis resistance and HCC metastasis. Nude mice model confirms that PHGDH's interaction with METTL3 is crucial for driving HCC metastasis.</p><p><strong>Conclusion: </strong>Our research presents the first evidence that PHGDH promotes HCC metastasis by interacting with METTL3. The PHGDH-METTL3 axis may serve as a potential clinical therapeutic target, offering new insights into the multifaceted roles of PHGDH in HCC metastasis.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2427-2438"},"PeriodicalIF":4.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IRE1α inhibitor reduces cisplatin resistance in ovarian cancer by modulating IRE1α/XBP1 pathway.","authors":"Shiyi Lv, Lin Zhang, Min Wu, Shuangshuang Zhu, Yixue Wang, Layang Liu, Yunxuan Li, Ting Zhang, Yujie Wu, Huang Chen, Mingyao Liu, Zhengfang Yi","doi":"10.1007/s13402-024-01010-z","DOIUrl":"10.1007/s13402-024-01010-z","url":null,"abstract":"<p><p>Ovarian cancer, a leading cause of gynecological cancer deaths globally, poses significant treatment challenges. Cisplatin (CDDP) is the first treatment choice for ovarian cancer and it is initially effective. However, 80% of ovarian cancer patients eventually relapse and develop resistance, resulting in chemotherapy failure. Therefore, finding new treatment combinations to overcome ovarian cancer resistance can provide a new tactic to improve the ovarian cancer patients' survival rate. We first identified activation of the Unfolded Protein Response (UPR) in CDDP-resistant ovarian cancer cells, implicating the IRE1α/XBP1 pathway in promoting resistance. Our findings demonstrate that inhibiting IRE1α signaling can re-sensitizes resistant cells to CDDP in vivo and in vitro, suggesting that IRE1α inhibitor used in conjunction with CDDP presumably could merge as a novel therapeutic strategy. Here, our research highlights the critical role of IRE1α signaling in mediating CDDP resistance, and paves the way for improved treatment options through combinatorial therapy.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2233-2246"},"PeriodicalIF":4.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142677501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatic arterial infusion chemotherapy (HAIC) combined with Tislelizumab and Lenvatinib for unresectable hepatocellular carcinoma: a retrospective single-arm study.","authors":"Ruirui Sun, Yang Gou, Long Pan, Qiang He, Yin Zhou, Yi Luo, Chenrui Wu, Yaowu Zhao, Zixuan Fu, Ping Huang","doi":"10.1007/s13402-024-01015-8","DOIUrl":"10.1007/s13402-024-01015-8","url":null,"abstract":"<p><strong>Purpose: </strong>We aimed to explore the curative effects of hepatic arterial infusion chemotherapy (HAIC) combined with Tislelizumab and Lenvatinib on unresectable hepatocellular carcinoma (HCC).</p><p><strong>Patients and methods: </strong>From September 2021 to September 2023, 42 patients with unresectable HCC who were treated in the First Affiliated Hospital of Chongqing Medical University were enrolled in this retrospective single-arm study. They received HAIC combined with Tislelizumab and lenvatinib. Baseline characteristics, laboratory indicators before and after treatment, and imaging findings were collected from medical records. The primary endpoint was objective response rate (ORR), and the secondary endpoints included disease control rate (DCR), overall survival (OS), progression-free survival (PFS), and safety indicators.</p><p><strong>Results: </strong>A total of 199 HAIC treatments were performed, with a median of 5.5 times (3.75-6.0 times). Based on the mRECIST and RECIST1.1 criterion, the ORR was 71.4% and 57.1%, the DCR was 92.9% and 92.9%. Up to the follow-up date of October 1, 2024, the median PFS was 14.0 months (95% CI, 11.6-16.4 months), and the median OS was 26.0 months.The incidence of any grade of adverse events was 97.6%. The most commonly reported treatment-related grade 3-4 adverse events included thrombocytopenia (28.6%), elevated total bilirubin (19%), and abdominal pain (16.7%). There was no treatment-related death.</p><p><strong>Conclusion: </strong>For unresectable HCC, HAIC combined with tirelizumab and lenvatinib has good anti-tumor efficacy and acceptable adverse reactions.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2265-2276"},"PeriodicalIF":4.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Triggering immunogenic death of cancer cells by nanoparticles overcomes immunotherapy resistance.","authors":"Ting Mei, Ting Ye, Dingkun Huang, Yuxiu Xie, Ying Xue, Dongfang Zhou, Weimin Wang, Jing Chen","doi":"10.1007/s13402-024-01009-6","DOIUrl":"10.1007/s13402-024-01009-6","url":null,"abstract":"<p><p>Immunotherapy resistance poses a significant challenge in oncology, necessitating novel strategies to enhance the therapeutic efficacy. Immunogenic cell death (ICD), including necroptosis, pyroptosis and ferroptosis, triggers the release of tumor-associated antigens and numerous bioactive molecules. This release can potentiate a host immune response, thereby overcoming resistance to immunotherapy. Nanoparticles (NPs) with their biocompatible and immunomodulatory properties, are emerging as promising vehicles for the delivery of ICD-inducing agents and immune-stimulatory adjuvants to enhance immune cells tumoral infiltration and augment immunotherapy efficacy. This review explores the mechanisms underlying immunotherapy resistance, and offers an in-depth examination of ICD, including its principles and diverse modalities of cell death that contribute to it. We also provide a thorough overview of how NPs are being utilized to trigger ICD and bolster antitumor immunity. Lastly, we highlight the potential of NPs in combination with immunotherapy to revolutionize cancer treatment.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2049-2071"},"PeriodicalIF":4.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142677507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic insights into tumor lymph node metastasis in melanoma.","authors":"Jiayi Huang, Zixu Gao, Jiangying Xuan, Ningyuan Gao, Chuanyuan Wei, Jianying Gu","doi":"10.1007/s13402-024-01027-4","DOIUrl":"10.1007/s13402-024-01027-4","url":null,"abstract":"<p><p>Although accounting for only a small amount of skin cancers, melanoma contributes prominently to skin cancer-related deaths, which are mostly caused by metastatic diseases, and lymphatic metastasis constitutes the main route. In this review, we concentrate on the metabolic mechanisms of tumor lymph node (LN) metastasis in melanoma. Two hypotheses of melanoma LN metastasis are introduced, which are the premetastatic niche (PMN) and parallel progression model. Dysregulation of oxidative stress, lactic acid concentration, fatty acid synthesis, amino acid metabolism, autophagy, and ferroptosis construct the metabolic mechanisms in LN metastasis of melanoma. Moreover, melanoma cells also promote LN metastasis by interacting with non-tumor cells through metabolic reprogramming in TIME. This review will deepen our understanding of the mechanism of lymph node metastasis in melanoma.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2099-2112"},"PeriodicalIF":4.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142865987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toxicity profiles of immunochemotherapy for gastric or gastroesophageal junction adenocarcinoma: a systematic review and meta-analysis.","authors":"Linghong Wan, Fanxuan Tian, Lei Wang, Yongying Hou, Wenkang Liu, Qin Liu, Dongfeng Chen, Xianfeng Li, Junyv Xiang, Zhong-Yi Qin, Tao Wang, Bijng Mao, Linyu Wu, Lu Hu","doi":"10.1007/s13402-024-01021-w","DOIUrl":"10.1007/s13402-024-01021-w","url":null,"abstract":"<p><strong>Purpose: </strong>Neoadjuvant immunochemotherapy is emerging as a promising regimen for patients with locally advanced gastric and gastroesophageal junction (G/GEJ) adenocarcinoma. However, it remains unclear whether immunochemotherapy will bring more adverse events (AEs) leading to a delay or even cancellation of surgeries. We aimed to provide a comprehensive analysis of the toxicity profiles for immune checkpoint inhibitors (ICIs) combined with chemotherapy among patients with G/GEJ adenocarcinoma.</p><p><strong>Methods: </strong>Published trials up to January 2024 were identified on Web of Science, Cochrane Library, Embase, and PubMed. Single-group and controlled clinical trials with ICIs in combination with chemotherapy in patients with G/GEJ adenocarcinoma were included. Two reviewers independently extracted data including incidence rate of AEs. The primary outcomes included the proportion of patients with adverse events leading to treatment discontinuation, grade 3 or higher adverse events, and serious adverse events. This study is registered with PROSPERO (CRD42023492676).</p><p><strong>Results: </strong>Twenty studies were included for a total of 6692 patients. In patients receiving immunochemotherapy, 17% (95% confidence interval (CI), 11-23%) had adverse events leading to treatment discontinuation, 23% (95% CI, 19-27%) had serious adverse events, and 64% (95% CI, 58-70%) had grade 3 or higher adverse events. Compared with patients receiving chemotherapy alone, patients with immunochemotherapy were associated with higher rates of adverse events leading to discontinuation (RR, 1.45; 95% CI, 1.32-1.60), serious adverse events (RR, 1.27; 95% CI, 1.04-1.57), and grade 3 or higher adverse events (RR, 1.15; 95% CI, 1.07-1.23).</p><p><strong>Conclusions: </strong>In conclusion, the incidence of adverse events leading to discontinuation, serious adverse events, and grade 3 or higher adverse events were higher in patients receiving immunochemotherapy compared to those with chemotherapy.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2335-2347"},"PeriodicalIF":4.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142787421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting CA9 restricts pancreatic cancer progression through pH regulation and ROS production.","authors":"Jing Yang, Xuhui Tong, Wei Wang, Xianjun Yu, Jin Xu, Si Shi","doi":"10.1007/s13402-024-01022-9","DOIUrl":"10.1007/s13402-024-01022-9","url":null,"abstract":"<p><strong>Purpose: </strong>Lactate is a key metabolite produced by glycolytic metabolism, yet it also serves as an energy source for cancer cells. Lactate accumulation in the tumor microenvironment (TME) has been demonstrated to correlate with immunosuppressive TME and tumor progression. As a highly glycolytic tumor, it is crucial to decipher the underlying mechanism in pancreatic ductal adenocarcinoma (PDAC).</p><p><strong>Methods: </strong>Bioinformation analysis was used to identify lactate mediated carbonic anhydrase IX (CA9) upregulation. CCK-8, colony formation and mouse xenograft assay were utilized to study the effect of CA9 in PDAC. ECAR, OCR and pHi measurement confirmed the impacts of CA9 in Warburg phenotype. Using confocal microscopy, flow cytometry, qRT-PCR, co-IP, we validated the signaling pathways in PDAC to regulate reactive oxygen species (ROS) production.</p><p><strong>Results: </strong>We confirmed that CA9 is highly expressed in PDAC and positively regulated by lactate levels. CA9 can enhance the proliferative and migratory capabilities of PDAC cells. Pharmacologic inhibition or knockdown of CA9 significantly reduce pHi, increase the intracellular lactate and reverse the Warburg phenotype. The intracellular lactate accumulation caused by CA9 knockdown upregulates ROS and mitochondrial dysfunction. Furthermore, it was discovered that the competitive binding of CA9 with FUS inhibits the facilitation of FUS on NOX4 pre-mRNA splicing.</p><p><strong>Conclusion: </strong>Collectively, our data illustrate that CA9 has a direct regulatory role in pHi homeostasis and ROS production, providing a potential therapeutic target for PDAC treatment.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2367-2382"},"PeriodicalIF":4.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142802778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Hepatic arterial infusion chemotherapy (HAIC) combined with Tislelizumab and Lenvatinib for unresectable hepatocellular carcinoma: a retrospective single-arm study.","authors":"Ruirui Sun, Yang Gou, Long Pan, Qiang He, Yin Zhou, Yi Luo, Chenrui Wu, Yaowu Zhao, Zixuan Fu, Ping Huang","doi":"10.1007/s13402-024-01031-8","DOIUrl":"10.1007/s13402-024-01031-8","url":null,"abstract":"","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2277-2278"},"PeriodicalIF":4.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The survival prediction analysis and preliminary study of the biological function of YEATS2 in hepatocellular carcinoma.","authors":"Yao Long, Wei Wang, Shouping Liu, Xiang Wang, Yongguang Tao","doi":"10.1007/s13402-024-01019-4","DOIUrl":"10.1007/s13402-024-01019-4","url":null,"abstract":"<p><strong>Purpose: </strong>Our study aims to develop and validate a novel molecular marker for the prognosis and diagnosis of hepatocellular carcinoma (HCC) MATERIALS & METHODS: We retrospectively analyzed mRNA expression profile and clinicopathological data of HCC patients fetched from The Cancer Genome Atlas (TCGA), Gene Expression Omnibus (GEO) and The International Cancer Genome Consortium (ICGC) datasets. Univariate Cox regression analysis was performed to collect differentially expressed mRNA (DEmRNAs) from HCC and non-tumor tissues, and YEATS2, a prognostic marker, was identified by further analysis. ROC curve, survival analysis and multivariate Cox regression analysis as well as nomograms were used to evaluate the prognosis of this gene. Finally, the biological function of this gene was preliminarily discussed by using single gene Gene Set Enrichment Analysis (GSEA), and the YEATS2 overexpression and knockdown hepatoma cell line was used to verify the results in vitro and in vivo.</p><p><strong>Results: </strong>Based on the clinical information of HCC in TCGA, GEO and ICGC databases, the gene YEATS2 with significant differences from HCC was identified. There was a statistical difference in the survival prognosis between the two databases and the ROC curve showed that the survival of HCC in both TCGA, GSE14520 and ICGC groups had a satisfactory predictive effect. Univariate and multivariate Cox regression analysis showed that YEATS2 was an independent prognostic factor for HCC, and Nomograms, which combined this prognostic feature with significant clinical features, provided an important reference for the clinical prognostic diagnosis of HCC. Next, we constructed overexpression and knockdown YEATS2 cell line in Hep3B and LM3 cells, and further proved that overexpression YEATS2 promote the proliferation and migration of HCC cells by CCK8, colony formation experiment, and transwell assays, and knockdown YEATS2 inhibited the proliferation and migration of HCC cells by CCK8, colony formation experiment, and transwell assays. Finally, the biological function of YEATS2 was preliminarily explored through GSEA analysis of a single gene, and it was found that it was significantly correlated with cell cycle and DNA repair, which provided us with ideas for further analysis. Furthermore, the knockdown of YEATS2 promoted radiation-induced DNA damage, enhanced radiosensitivity, and ultimately inhibited the proliferation of hepatocellular carcinoma cells in vitro and in vivo.</p><p><strong>Conclusions: </strong>Our study identified a promising prognostic marker for hepatocellular carcinoma that is useful for clinical decision-making and individualized treatment.</p>","PeriodicalId":49223,"journal":{"name":"Cellular Oncology","volume":" ","pages":"2297-2316"},"PeriodicalIF":4.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}