Molecular Carcinogenesis最新文献

{"title":"CircST6GALNAC6 Inhibits Glycolysis of Bladder Cancer by Regulating PRKN/HK1 Signaling Pathway.","authors":"Yali Zuo, Da Ren, Haiqing He, Changkun Huang, Xuan Zhu","doi":"10.1002/mc.23894","DOIUrl":"10.1002/mc.23894","url":null,"abstract":"<p><p>Bladder cancer (BCa) is an aggressive malignancy of urinary system. Aerobic glycolysis refers to the phenomenon wherein cancer cells increase glucose consumption and produce lactic acid. Our study focused on the role and mechanism of circST6GALNAC6 in BCa glycolysis. The 24 h glucose intake was detected using flow cytometry. Lactic acid and ATP were detected in BCa cells utilizing commercially provided kits. Extracellular acidification rate was measured using Seahorse XF-96p Extracellular Flux Analyzer. Cell proliferation was determined using colony formation assay. RNA immunoprecipitation and co-immunoprecipitation experiments were adopted to validate molecular interactions. BALB/C nude mice were utilized to establish xenograft tumor model. CircST6GALNAC6 was decreased in BCa cells, and overexpression of circST6GALNAC6 inhibited glycolysis and proliferation of BCa cells. Additionally, overexpression of circST6GALNAC6 promoted the degradation of glycolytic regulatory protein HK1 and decreased its expression, and PRKN facilitated ubiquitination-related degradation of HK1. CircST6GALNAC6 enhanced the mRNA stability and expression of PRKN by recruiting FUS. Furthermore, the inhibitory impact of circST6GALNAC6 overexpression on glycolysis in BCa cells was reversed by PRKN knockdown. Finally, overexpression of circST6GALNAC6 suppressed tumor growth through increasing PRKN in nude mice. CircST6GALNAC6 suppressed glycolysis in BCa through FUS/PRKN/HK1 axis. Targeting circST6GALNAC6 holds promise as a novel approach for treating BCa.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"870-882"},"PeriodicalIF":3.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143441531","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":"Integrated Genomics Reveal Potential Resistance Mechanisms of PANoptosis-Associated Genes in Acute Myeloid Leukemia.","authors":"Cong Liang, Zhiqing Long, Mengjie Lei, Ran Ding, Mengke Chen","doi":"10.1002/mc.23886","DOIUrl":"10.1002/mc.23886","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is marked by the proliferation of abnormal myeloid progenitor cells in the bone marrow and blood, leading to low cure rates despite new drug approvals from 2017 to 2018. Current therapies often fail due to the emergence of drug resistance mechanisms, such as those involving anti-apoptotic pathways and immune evasion, highlighting an urgent need for novel approaches to overcome these limitations. Programmed cell death (PCD) is crucial for tissue homeostasis, with PANoptosis-a form of PCD integrating pyroptosis, apoptosis, and necroptosis-recently identified. This process, regulated by the PANoptosome complex, could be key to overcoming AML drug resistance. Targeting multiple PCD pathways simultaneously may prove more effective than single-target therapies. Research suggests that disrupting anti-apoptotic mechanisms, such as those involving Bcl-2, can enhance drug sensitivity in AML. This study hypothesizes that PANoptosis-associated resistance genes (PARGs) play a critical role in AML drug resistance by modulating immune responses and offers a multi-faceted approach to tackle this challenge. Using RNA sequencing data from the Cancer Genome Atlas and Gene Expression Omnibus databases, we performed differential expression analysis to identify significantly dysregulated PARGs in AML. Regression analysis identified prognostic PARGs, bridging a key gap in understanding how these genes contribute to treatment resistance. We then verified their expression in AML cell lines and cell samples treated with cytarabine using RT-qPCR. Hierarchical clustering revealed distinct PARG expression patterns, and functional enrichment analysis highlighted their involvement in immune-related pathways. The combination of bioinformatics and experimental validation underscores how these genes may mediate immune modulation in drug resistance, providing a robust framework for further study. Our findings suggest that PARGs contribute to AML resistance by modulating immune responses and provide potential targets for therapeutic intervention. This study highlights the potential of targeting PARGs to improve treatment outcomes in AML. By analyzing the expression changes of these genes in response to standard clinical treatments, we provide a framework for developing multi-target therapeutic strategies that simultaneously disrupt multiple programmed cell death pathways. Such an approach directly addresses the limitations of current treatments by offering a method to enhance drug sensitivity and mitigate resistance, potentially improving survival rates. Our findings underscore the importance of a comprehensive understanding of PCD mechanisms and pave the way for innovative treatments that could significantly impact AML management.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"801-815"},"PeriodicalIF":3.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046938","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 \"Plasma DNA Methylation-Based Biomarkers for MPNST Detection in Patients With Neurofibromatosis Type 1\".","authors":"","doi":"10.1002/mc.23890","DOIUrl":"10.1002/mc.23890","url":null,"abstract":"","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"953"},"PeriodicalIF":3.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12128706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of Interleukin-Related Genes Signature for Prognosis Prediction in Head and Neck Squamous Cell Carcinoma Patients.","authors":"Haojie Yang, Zihao Liu, Zicong Tan, Huimin Luo, Qin Li, Zhongqi Liu, Fengtao Ji","doi":"10.1002/mc.23880","DOIUrl":"10.1002/mc.23880","url":null,"abstract":"<p><p>This study focused on identifying the interleukin (IL)-related genes that influence the head and neck squamous cell carcinoma (HNSCC) patients' prognosis and response to anticancer therapy in patients with HNSCC. We developed a risk model that included three gene signatures, IL Enhancer Binding Factor 2 (ILF2), IL 36 alpha (IL36A), and IL10, based on differential expression analysis, survival analysis, Least Absolute Shrinkage and Selection Operator (LASSO) analysis, and Cox regression analysis. We found that the low-risk group was scored with higher immune cell infiltration, higher expression of human leukocyte antigen (HLA) family genes and immune checkpoint genes, higher cytolytic activity (CYT), tertiary lymphoid structures (TLS), and CD8A/PD-L1 ratio. In contrast, the high-risk group was scored with higher tumor immune dysfunction and exclusion (TIDE), which implied worse response to immunotherapy and worse prognosis. The results above indicated that the low-risk group had stronger antitumor immunity and better responsiveness to immunotherapy. We also observed a significantly enriched pattern of cancer-related pathways and immune pathways in the comparison of the high-risk and low-risk groups. Furthermore, the high-risk group had higher sensitivity to chemotherapy drugs, which suggested that they might benefit from chemotherapy treatment. Following the results above, we confirmed in HNSCC cell lines and clinical specimens that the level of ILF2 in tumors was significantly higher than that in adjacent tumor tissues. Besides, in vivo and in vitro results both showed that silencing ILF2 might depress tumor growth, invasion, and migration. This study not only provided novel perspectives into the immunological and molecular mechanisms of HNSCC and uncovered IL-related gene signatures for predicting HNSCC patients' prognosis and response to chemotherapy and immunotherapy, but also preliminarily suggested that ILF2 might be an important target in the treatment of HNSCC.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"842-857"},"PeriodicalIF":3.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143365271","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":"Knocking Down Ferredoxin 1 Inhibits the Progression of Colorectal Cancer and Regulates Cuproptosis via Mediating the Hippo Signaling Pathway.","authors":"Ying Hu, Haihua Liu, Xiaobin Tan, Xiongjian Wu","doi":"10.1002/mc.23897","DOIUrl":"10.1002/mc.23897","url":null,"abstract":"<p><p>Cuproptosis is a form of programmed cell death dependent on mitochondrial respiration and is crucial in cancer treatment. The study attempted to screen cuproptosis-associated genes in colorectal cancer (CRC) and reveal regulatory pathways. Weighted gene co-expression network analysis (WGCNA) was applied to screen the co-expression modules based on gene expression in CRC patients. The cuproptosis-associated genes were screened at the intersection of co-expression modules and cuproptosis gene data set. RNA sequencing was performed to assess the transcriptome changes, followed by functional enrichment analyses to reveal the potential pathways. Ferredoxin 1 (FDX1) was knocked down in in vivo and in vitro experiments to investigate the effects of FDX1 knockdown on CRC progression and cuproptosis. FDX1 was found as a cuproptosis-associated gene and was highly expressed in CRC tumor and CRC cells. Knockdown of FDX1 regulated cuproptosis in CRC cells, and inhibited CRC cell growth, migration and invasion. We screened 1956 upregulated DEGs and 2201 downregulated DEGs in si-FDX1 cells, which were mainly enriched in mitogen-activated protein kinase (MAPK) signaling pathway, tumor necrosis factor (TNF) signaling pathway and Hippo signaling pathway. Knockdown of FDX1 inhibited CRC progression by increasing the levels of dihydrolipoamide S-succinyltransferase (DLST), lipoic acid synthetase (LIAS) and phosphorylation Yes-associated protein (pYAP)/YAP, and downregulated transcriptional coactivator with a PDZ-binding domain (TAZ). The inhibitor of Hippo pathway GA-017 blocked this process. Knocking down FDX1 regulated cuproptosis and inhibited CRC progression by mediating the Hippo signaling pathway, which shed new insights into the development of biomarkers for CRC treatment.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"911-922"},"PeriodicalIF":3.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143483707","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 FGFR Attenuates Tumor Growth in an Anal Squamous Cell Carcinoma Patient Derived Xenograft Model.","authors":"Thuc Ly, Athena E Golfinos-Owens, Naren Raja, Levi Arnold, Pachiappan Arjunan, John Ashcraft, Benjamin Martin, Shrikant Anant, Sumedha Gunewardena, Rong Wang, Huy Q Dinh, Sufi Mary Thomas","doi":"10.1002/mc.23919","DOIUrl":"https://doi.org/10.1002/mc.23919","url":null,"abstract":"<p><p>Anal squamous cell carcinoma (ASCC) is a rare malignancy with a rising incidence and limited treatment options. To identify actionable therapeutic targets, we developed a patient-derived xenograft (PDX) model using a metastatic ASCC sample and performed single-cell RNA sequencing. Our analysis confirmed previously reported genetic mutations highly expressed in the sample, along with copy number alterations, and revealed epithelial cancer cell heterogeneity. Notably, epithelial cells exhibited a low hybrid epithelial-mesenchymal transition (hEMT) signature compared to stromal cells. Among epithelial subpopulations, the most abundant cluster displayed high expression of FGFR1-2 and FGF ligands. Treatment with AZD4547, an FGFR1-3 inhibitor, resulted in a significant reduction in tumor volume over time (p = 0.0036). Immunohistochemistry staining for proliferative Ki67 and cleaved caspase 3 suggested ongoing proliferation in residual cells. Fourier-transform infrared (FTIR) spectroscopy of post-treatment residual tumors revealed significant differences in the Amide I and Amide II regions between AZD4547-treated and control groups. These findings demonstrate that FGFR inhibition effectively attenuates ASCC tumor growth and highlights the promise of precision medicine in managing this rare cancer.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019277","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":"SDCBP Orchestrated Gastric Cancer Aggression Through Epithelial- Mesenchymal Transition and Macrophages M2 Polarization.","authors":"Chan-Yuan Zhao, Feng Liu, Jia-Ming Dong, Cun-Pu Du, Chen-Li Zhang, Chen-Yu Wang, Xiao-Yu Zhang, Quan Zhou, Wei Liu, Ai-Jun Yang, Yong-Ning Zhou, Yun Dang, Li-Na Shang, Min Wang, Min Li","doi":"10.1002/mc.23923","DOIUrl":"https://doi.org/10.1002/mc.23923","url":null,"abstract":"<p><p>Gastric cancer remains a significant global health burden with limited treatment options and high mortality. Syndecan-binding protein (SDCBP), a scaffolding protein involved in tumor differentiation, has attracted attention as a potential therapeutic target in cancers. However, its precise role in gastric cancer progression is not fully understood. In this study, through bioinformatics analysis and gastric cancer samples detection, we discovered that SDCBP was highly expressed in gastric cancer tissues, which was correlated with clinicopathological features such as tumor invasion depth and distant metastasis, and exhibited heterogeneity across histological or molecular subtypes. Elevated SDCBP expression promoted the proliferation, invasion and migration of gastric cancer cells, and modulated epithelial-mesenchymal transition (EMT) via the ERK signaling pathway. Xenograft experiments in mice confirmed that inhibiting SDCBP or ERK signaling could delay cancer progression. We also found that gastric cancer cells with SDCBP knockdown were able to inhibit the M2 polarization of cocultured macrophages, reduce chemotaxis and enhance phagocytosis of macrophages. Therefore, SDCBP plays a crucial role in driving gastric cancer progression. Targeting SDCBP in gastric cancer can partially reverse the malignant phenotype, and SDCBP is expected to be a promising therapeutic target for gastric cancer.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034020","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":"Differential Response and Resistance to KRAS-Targeted Therapy.","authors":"Zhaojin Liu, Heinz-Josef Lenz, Jian Yu, Lin Zhang","doi":"10.1002/mc.23908","DOIUrl":"https://doi.org/10.1002/mc.23908","url":null,"abstract":"<p><p>KRAS is the most frequently mutated oncogene. In epithelial malignancies such as lung, colorectal, and pancreatic tumors, KRAS is mutated in 25 to above 90% cases. KRAS was considered undruggable for over three decades until the recent development of covalent inhibitors targeting the KRAS G12C mutant. The recent approval of the KRAS G12C inhibitors sotorasib and adagrasib has ushered in a new era of KRAS-targeted therapy. Despite this success, a major challenge in KRAS-targeted therapy is intrinsic and acquired resistance to KRAS inhibitors. Clinical studies have shown that many patients with KRAS G12C cancers did not respond to sotorasib and adagrasib. Colorectal cancer, in particular, has a markedly lower response rate to KRAS G12C inhibitors compared to non-small cell lung cancer. Furthermore, the therapeutic response to KRAS G12C inhibition was short-lived, with quick emergence of acquired resistance. In this review, we summarize several major themes that have emerged from recent clinical and preclinical studies on the mechanisms of intrinsic and acquired resistance to KRAS-targeted therapy in colorectal, lung, and pancreatic cancers. We also discuss various combination strategies for targeting these mechanisms to overcome resistance to KRAS inhibitors.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971770","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":"Therapeutic Targeting of the Pentose Phosphate Pathway in Colorectal Cancer Using 6-Aminonicotinamide and 5-Fluorouracil.","authors":"Israa Ahmad Cheikh, Berthe Hayar, Noorhan Ghanem, Lara Al Saleh, Chirine El-Baba, Sadaf Al-Hadeethi, Riyad El-Khoury, Julnar Usta, Nadine Darwiche","doi":"10.1002/mc.23920","DOIUrl":"https://doi.org/10.1002/mc.23920","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a significant global health concern with rising incidence and mortality rates. 5-Fluorouracil (5-FU) is the standard chemotherapy for CRC but is often constrained by resistance and toxicity, highlighting the need for more efficient treatments. The pentose phosphate pathway (PPP), a glucose metabolic shunt, is significantly upregulated in CRC to support nucleotide synthesis and redox balance. Therefore, we hypothesized that targeting the PPP decreases CRC cell growth, reduces tumor progression, and improves 5-FU therapy. Consequently, we investigated the anti-tumor activities, cell death mechanism, and mode of action of the PPP inhibitor, 6-aminonicotinamide (6-AN), and 5-FU alone or in combination against CRC. We used human CRC cell lines with different p53 and 5-FU resistance statuses and a CRC xenograft model. Our findings show that 6-AN reduced the viability of human CRC cells independently of their p53 and 5-FU resistance profile, with its effect further enhanced in combination with 5-FU. The 6-AN/5-FU combination treatment synergized by reducing the total dehydrogenase activity of the PPP, inducing oxidative stress, and promoting senescence in CRC cells. Furthermore, 6-AN treatment significantly decreased tumor growth in a CRC xenograft mouse model. However, combining 6-AN with 5-FU did not reduce tumor volume significantly, highlighting the complexities of translating in vitro findings to animal models. These results suggest that interfering with the PPP activity suppresses CRC cell growth and may reduce 5-FU resistance. This study underscores targeting cancer metabolism as a novel therapeutic strategy to minimize drug resistance and to improve CRC therapeutic outcomes.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143991103","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":"SRPK1 Activation Facilitates Gli3^S664 Phosphorylation and Promotes Metastasis in Esophageal Squamous Cell Carcinoma.","authors":"Yongwei Ding, Jiace Qin, Mengjia Zhang, Huiting Wu, Chang Liu, Yaping Guo, Wenjie Wu, Yanan Jiang, Chenjuan Zhang, Yanying Ma, Xinghuan Chen, Jing Lu, Kangdong Liu, Ziming Dong, Jimin Zhao, Yan Qiao","doi":"10.1002/mc.23913","DOIUrl":"https://doi.org/10.1002/mc.23913","url":null,"abstract":"<p><p>Esophageal squamous cell carcinoma (ESCC) stands out as one of the most malignant digestive tumors, with its prognosis marred by frequent metastasis and recurrence. However, the mechanism behind ESCC metastasis remains elusive, impeding therapeutic advancements. SRPK1 emerges as an independent prognostic marker for ESCC patients. Our research illuminates the consequential role of SRPK1, where its genetic knockout led to decreased levels of transcription factors Snail and Slug, concomitant with an enhanced expression of the cell-to-cell adhesion protein E-cadherin. Conversely, reintroducing an overexpression of SRPK1 reversed the effects, highlighting its essential role in ESCC metastasis. Through bioinformatics analysis, we identified a correlation between SRPK1 and Gli3. Furthermore, increased levels of Gli3 and its phosphorylated form, p-Gli3^S664, were detected in ESCC tissues, which are implicated in promoting ESCC metastasis. Notably, our research confirmed that SRPK1 promotes migration, invasion, and epithelial-mesenchymal transition (EMT) of ESCC cells through phosphorylates Gli3 at ser 664. Additional investigations reveal that dihydroartemisinin (DHA) effectively impedes ESCC cell metastasis by suppressing SRPK1-mediated phosphorylation of Gli3^S664 both in vitro and in vivo. Consequently, our study underscores the pivotal role of the SRPK1-p-Gli3^S664 axis in ESCC metastasis and suggests DHA as a promising candidate for preventing ESCC metastasis by targeting this axis.</p>","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144008578","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}