Molecular Carcinogenesis最新文献_第3页

GPR87 Promotes Angiogenesis in Esophageal Squamous Cell Carcinoma via VEGFA Regulation.

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-26 DOI: 10.1002/mc.23909

Dengyan Zhu, Donglei Liu, Kai Wu, Xingdong Cheng, Yang Yang

{"title":"GPR87 Promotes Angiogenesis in Esophageal Squamous Cell Carcinoma via VEGFA Regulation.","authors":"Dengyan Zhu, Donglei Liu, Kai Wu, Xingdong Cheng, Yang Yang","doi":"10.1002/mc.23909","DOIUrl":"https://doi.org/10.1002/mc.23909","url":null,"abstract":"The role and underlying mechanisms of G protein-coupled receptor 87 (GPR87) in esophageal squamous cell carcinoma (ESCC) remain unclear, despite its established oncogenic functions in other malignancies. This study examined the expression of GPR87 and its association with survival rate in ESCC using online databases. The expression of GPR87 in ESCC tissues was identified using immunohistochemistry, and a correlation analysis was carried out using ki-67 data. ESCC cells were transfected with GPR87 knockdown or overexpression plasmids, followed by functional assays such as, CCK-8 for cell viability, colony formation for proliferation, wound healing for migration, Transwell for invasion, and tube formation for angiogenesis. Western blot analysis was used to assess STAT3 phosphorylation and VEGFA expression. Additionally, a xenograft tumor model was established to investigate the effect of GPR87 on tumor growth in vivo. The findings demonstrated that GPR87 was highly expressed in ESCC tissues and its overexpression was associated with a poor patient survival. Transfection with a GPR87 overexpression plasmid increases the cell viability, invasion, proliferation, and angiogenesis of ESCC cells, while transfection with sh-GPR87 reversed these effects. Additionally, GPR87 controlled VEGFA expression levels by promoting STAT3 phosphorylation. Rescue trials further verified that GPR87 promotes the growth of ESCC by modulating STAT3. Moreover, in vivo studies validated that GPR87 knockdown suppressed tumor growth. In conclusion, the findings highlight GPR87 as a key regulator of VEGFA expression via STAT3 activation, contributing to ESCC malignancy. Targeting GPR87 may provide a potential therapeutic strategy for ESCC.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710796","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}

引用次数: 0

Hsa_circ_0000231 Accelerates Cell Autophagy and Promotes Cell Proliferation and Invasion of Colorectal Cancer via miR-140-3p/Bcl-2 Axis.

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-26 DOI: 10.1002/mc.23906

Long Zhao, Haoran Zhang, Shuo Wang, Yushi Zhou, Kewei Jiang, Shan Wang, Yingjiang Ye, Bo Wang, Zhanlong Shen

{"title":"Hsa_circ_0000231 Accelerates Cell Autophagy and Promotes Cell Proliferation and Invasion of Colorectal Cancer via miR-140-3p/Bcl-2 Axis.","authors":"Long Zhao, Haoran Zhang, Shuo Wang, Yushi Zhou, Kewei Jiang, Shan Wang, Yingjiang Ye, Bo Wang, Zhanlong Shen","doi":"10.1002/mc.23906","DOIUrl":"https://doi.org/10.1002/mc.23906","url":null,"abstract":"Accumulating evidence indicated that circular RNAs (circRNAs) directly sponge to microRNAs (miRNAs),(miRNAs), which in turn regulate the gene expression and affect the malignancy behavior at the posttranscriptional level. However, the expression levels, function, and mechanism of circ_0000231 in colorectal cancer (CRC) are largely unknown. The expression levels of circ_0000231, miR-140-3p, and Bcl-2 in 110 CRC tissues and matched normal colorectal tissues were detected by qRT-PCR method. circ_0000231 and Bcl-2 were suppressed by siRNA, and miR-140-3p was overexpressed by RNA mimics in CRC cell lines. The function-based experiments were conducted to detect the proliferation and migratory abilities in CRC cell lines. RNA pull-down, RNA immunoprecipitation (RIP), and dual-fluorescence reporter assay were conducted to verify the association among circ_0000231, miR-140-3p, and Bcl-2. Western blot analysis and mRFP-GFP-LC3 adenovirus were used to detect the autophagy level affected by circ_0000231, miR-140-3p, and Bcl-2 axis. Downregulated circ_0000231 significantly suppressed the proliferation and migratory abilities of CRC cells by suppressing autophagy and promoting G0/G1 phase arrest. Furthermore, RNA pull-down, RIP, and dual-fluorescence reporter assays confirmed that circ_0000231 regulates the expression of Bcl-2 by directly targeting miR-140-3p. More importantly, circ_0000231 promoted the levels of autophagy via the miR-140-3p/Bcl-2 axis in CRC. Our study demonstrated that circ_0000231, as a tumor promotor, enhances the level of autophagy by regulating Bcl-2 via targeting miR-140-3p. Moreover, circ_0000231 might serve as a diagnostic and prognostic indicator and a novel molecular target for CRC therapy.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710799","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}

引用次数: 0

C1QBP Promotes Prostate Cancer Progression and Lipid Accumulation by Negatively Regulating ALDH9A1.

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23904

Xinyu Liu, Jiaxin Li, Runxuan Du, Qiufang Qiao, Shuang Liu, Zhihao Bo, Ruibing Chen, Yihan Dong, Xuesong Xiao, Yuejing Pan, Huamao Jiang, Rui Wang, Yong Wang, Dan Yue

{"title":"C1QBP Promotes Prostate Cancer Progression and Lipid Accumulation by Negatively Regulating ALDH9A1.","authors":"Xinyu Liu, Jiaxin Li, Runxuan Du, Qiufang Qiao, Shuang Liu, Zhihao Bo, Ruibing Chen, Yihan Dong, Xuesong Xiao, Yuejing Pan, Huamao Jiang, Rui Wang, Yong Wang, Dan Yue","doi":"10.1002/mc.23904","DOIUrl":"https://doi.org/10.1002/mc.23904","url":null,"abstract":"Prostate cancer (PCa) relies heavily on lipid metabolism for energy acquisition, and lipid metabolic reprogramming plays a crucial role in its progression. Here, we utilized publicly available PCa databases and immunohistochemistry to evaluate C1QBP expression in PCa. We found that C1QBP is highly expressed in PCa, potentially due to promoter hypomethylation. Functional assays showed that C1QBP promotes cell proliferation, migration, and lipid accumulation in PCa cells. We identified differentially expressed proteins associated with C1QBP by using liquid chromatography-tandem mass spectrometry. Functional enrichment analysis revealed that C1QBP affects lipid metabolism and negatively regulates the lipid metabolism-related molecule ALDH9A1. Furthermore, ALDH9A1 intervention rescued the tumor suppression and lipid reduction caused by C1QBP knockdown. RNA sequencing (RNA-seq) was performed to explore C1QBP regulatory pathways at the mRNA level, revealing that C1QBP also affects the MAPK and p53 pathways, as well as the expression of lipid metabolism-related molecules. In conclusion, these findings suggest that C1QBP influences PCa progression and lipid deposition by regulating ALDH9A1, while other potential mechanisms may also be involved, indicating that C1QBP is a promising target for PCa treatment.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657751","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}

引用次数: 0

CtBP2 Regulates Wnt Signal Through EGR1 to Influence the Proliferation and Apoptosis of DLBCL Cells.

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23901

Jianfang Dong, Lihua Li, Xuefei Zhang, Xijing Yin, Zucong Chen

{"title":"CtBP2 Regulates Wnt Signal Through EGR1 to Influence the Proliferation and Apoptosis of DLBCL Cells.","authors":"Jianfang Dong, Lihua Li, Xuefei Zhang, Xijing Yin, Zucong Chen","doi":"10.1002/mc.23901","DOIUrl":"https://doi.org/10.1002/mc.23901","url":null,"abstract":"Diffuse large B-cell lymphoma (DLBCL) is the most prevalent form of lymphoma. The overexpression of CtBP2 in tissues may contribute to tumor occurrence and progression. The expression of EGR1 in DLBCL is elevated, suggesting its potential role as an oncogene that promotes the proliferation of DLBCL cells. Database predictions indicate that CtBP2 can bind to EGR1. The objective of the present study was to investigate whether CtBP2 can influence the proliferation and apoptosis of DLBCL cells by regulating the Wnt signaling pathway through EGR1. Western blot assay showed that CtBP2 expression was upregulated in DLBCL cells. Cell proliferation level was detected by CCK8 assay and EdU staining, and the apoptosis level and cycle distribution were analyzed through flow cytometry. Our data indicated that interference with CtBP2 and EGR1 can inhibit the proliferation and cell cycle progression of DLBCL cells while promoting apoptosis. The predictions from the HDOCK server, along with the results of Co-IP experiments, suggested that EGR1 and CtBP2 can effectively bind to each other, with EGR1 positioned downstream of CtBP2 and regulated by it. Furthermore, interference with CtBP2 could also inhibit the expression of the Wnt/β-catenin signaling pathway. Overexpression of EGR1 counteracted the effects of siRNA-CtBP2, promoting cell proliferation and cycle, inhibiting apoptosis and upregulating the expression of the Wnt/β-catenin signaling pathway. From the above experiments, we found that CtBP2 can regulate the Wnt/β-catenin signaling pathway through EGR1 to influence the proliferation and apoptosis of DLBCL cells. Therefore, EGR1 may be one of the key contributors involved in the regulation of Wnt/β-catenin signaling by CtBP2.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657754","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}

引用次数: 0

P21-Activated Kinase 1 (PAK1) Modulates Therapeutic Response to Ionizing Radiation in Head and Neck Squamous Cell Carcinoma Cells.

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23902

Swetha Rajendran, Rohan Prasad Surabhi, A Satheesh Kumar, Prarthana Gopinath, Vishnupriya Kanakaveti, Gouthaman Shanmugasundaram, M Michael Gromiha, Suresh Kumar Rayala, Ganesh Venkatraman

{"title":"P21-Activated Kinase 1 (PAK1) Modulates Therapeutic Response to Ionizing Radiation in Head and Neck Squamous Cell Carcinoma Cells.","authors":"Swetha Rajendran, Rohan Prasad Surabhi, A Satheesh Kumar, Prarthana Gopinath, Vishnupriya Kanakaveti, Gouthaman Shanmugasundaram, M Michael Gromiha, Suresh Kumar Rayala, Ganesh Venkatraman","doi":"10.1002/mc.23902","DOIUrl":"https://doi.org/10.1002/mc.23902","url":null,"abstract":"Head and neck squamous cell carcinoma (HNSCC) continues to be a formidable epithelial malignancy characterized by late-stage detection and recurrence impacting survival. P21-activated kinase-1 (PAK1) was reported to be overexpressed in head and neck cancers and activated by ionizing radiation (IR), affecting treatment outcomes. Present investigations revealed that PAK1 silencing on HNSCC cells reverted the aggressive phenotype and showed impaired DNA damage repair upon IR exposure. Further HNSCC cells were resistant to IR up to 30 Gy with elevated pPAK1 levels. Radiation-resistant (RR) HNSCC cells expressed radiation-resistant markers, namely MRE-11 and NME-1; stemness markers-OCT4 and SOX2; and EMT & metastasis markers-vimentin, snail, and α-smooth muscle actin (α-SMA). In addition, HNSCC RR cells showed increased levels of DNA damage response protein H2AX, indicative of an aggressive phenotype with an augmented DNA repair machinery and a potential target for inhibition. Since H2AX appears to be a mechanistic hub for PAK1-induced radiation resistance, using in silico methods, peptides were designed, and the PL-8 peptide was chosen to target the phosphorylation of H2AX, which could enhance the sensitivity to IR and push the cells to radiation-induced cell death. PL-8 peptide inhibited H2AX phosphorylation on HNSCC cells and triggered radiation-induced cell death as determined by functional assays. The present study reveals PAK1 induced in HNSCC cells by IR and causes resistance by enhancing DNA damage response mediated through γH2AX. To counteract this complex molecular interplay, we propose inhibiting γH2AX formation & silencing PAK1 appears to be a probable way forward in HNSCC.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657756","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}

引用次数: 0

Circ_0044362 Facilitates the Progression of Epithelial Ovarian Cancer via Enhancing HOXB4 Transcription to Activate the RUNX1/IGFBP3 Axis.

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23905

Shengtou Ye, Han Wu, Junjiang Liu, Jianguo Zhou, Sisi He, Na Li

{"title":"Circ_0044362 Facilitates the Progression of Epithelial Ovarian Cancer via Enhancing HOXB4 Transcription to Activate the RUNX1/IGFBP3 Axis.","authors":"Shengtou Ye, Han Wu, Junjiang Liu, Jianguo Zhou, Sisi He, Na Li","doi":"10.1002/mc.23905","DOIUrl":"https://doi.org/10.1002/mc.23905","url":null,"abstract":"Increasing numbers of studies have elucidated the emerging roles of circular RNA (circRNA) in cancer progression. However, the function of circRNAs in modulating their parental genes in ovarian cancer remains poorly understood. In this study, we identified that circ_0044362, a circRNA derived from homeobox B4 (HOXB4), significantly promotes the expression of its parental gene HOXB4 in ovarian cancer. Functionally, circ_0044362 promotes the malignant phenotypes of ovarian cancer cells. Further analysis revealed that circ_0044362 facilitates the transcriptional activation of its parental gene HOXB4 by directly guiding U1 small nuclear ribonucleoprotein (snRNP) to its promoter region, thereby enhancing the oncogenic behaviors of ovarian cancer cells. Furthermore, HOXB4 positively regulates runt-related transcription factor 1 (RUNX1) expression, with RUNX1 serving as a transcription factor to promote the transcription of insulin-like growth factor binding protein-3 (IGFBP3). Notably, inhibitors of either HOXB4, RUNX1, or IGFBP3 could reverse the oncogenic activity mediated by circ_0044362. Collectively, our findings reveal the involvement of the circ_0044362/HOXB4 pathway in ovarian cancer progression and provide potential therapeutic strategies for ovarian cancer treatment.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143657752","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}

引用次数: 0

LINC02154 Promotes Esophageal Squamous Cell Carcinoma Progression via the PI3K-AKT-mTOR Signaling Pathway by Interacting With IGF2BP2.

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23903

Mingyuan Zhang, Cai Zhang, Fuyou Zhou, Ruotong Yang, Yang Feng, Yangyang Ji, Huijun Ren, Liang Ming

引用次数: 0

Correction to "Plasma DNA Methylation-Based Biomarkers for MPNST Detection in Patients With Neurofibromatosis Type 1".

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-18 DOI: 10.1002/mc.23890

引用次数: 0

Potential Crosstalk Between ANXA1+ Epithelial Cells and FABP4+ TAM Cells of Ferroptosis-Related Molecular Clusters Promotes an Immunosuppressive Microenvironment in Non-Small Cell Lung Cancer.

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-04 DOI: 10.1002/mc.23899

Shengqiang Mao, Qingyan Li, Ying Yang, Zhiqiang Liu, Li Zhang

{"title":"Potential Crosstalk Between ANXA1+ Epithelial Cells and FABP4+ TAM Cells of Ferroptosis-Related Molecular Clusters Promotes an Immunosuppressive Microenvironment in Non-Small Cell Lung Cancer.","authors":"Shengqiang Mao, Qingyan Li, Ying Yang, Zhiqiang Liu, Li Zhang","doi":"10.1002/mc.23899","DOIUrl":"https://doi.org/10.1002/mc.23899","url":null,"abstract":"The tumor microenvironment (TME) affects tumor initiation, invasion, metastasis, and therapies. Recently, increasing evidence has demonstrated that ferroptosis plays important regulatory roles in tumourigenesis and progression. It is unclear how ferroptosis affects non-small cell lung cancer (NSCLC) progression by remodeling the TME. In this study, the single-cell RNA sequencing (scRNA-seq) data (85,562 cells, n = 18) were employed to reveal the heterogeneity of ferroptosis activation in NSCLC, and identified six ferroptosis-related molecular clusters. We found that ANXA1+ epithelial and FABP4 + TAM subpopulations were key factors in lung cancer progression and TME remodeling. In addition, the cell-cell communication analysis showed that ANXA1-FPR2/FPR1 receptor-ligand pair contributed to the formation of an immunosuppressive TME. Furthermore, we established a novel signature based on ferroptosis-related molecular clusters, and the risk score model may predict survival and response to immunotherapy. We also found that compared with responder, the expression of ANXA1 and FABP4 is higher in progressor, which indicating a higher expression of ANXA1 and FABP4 was associated with a worse response to immunotherapy. Therefore, we concluded that the molecular clusters associated with ferroptosis served as potential prognostic markers and therapeutic targets for NSCLC patients.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143557486","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}

引用次数: 0

Therapeutic Potential of IL-37 in Cervical Cancer: Suppression of Tumour Progression and Enhancement of CD47-Mediated Macrophage Phagocytosis. IL-37在宫颈癌中的治疗潜力：抑制肿瘤进展和增强cd47介导的巨噬细胞吞噬。

IF 3 2区医学

Molecular Carcinogenesis Pub Date : 2025-03-01 Epub Date: 2024-12-02 DOI: 10.1002/mc.23855

Yuan Feng, Lianlian Feng, Bingyu Wang, Teng Zhang, Baoxia Cui

{"title":"Therapeutic Potential of IL-37 in Cervical Cancer: Suppression of Tumour Progression and Enhancement of CD47-Mediated Macrophage Phagocytosis.","authors":"Yuan Feng, Lianlian Feng, Bingyu Wang, Teng Zhang, Baoxia Cui","doi":"10.1002/mc.23855","DOIUrl":"10.1002/mc.23855","url":null,"abstract":"As a promising therapeutic approach, immunotherapy is being extensively investigated in cervical cancer. Although immunotherapy has been validated to improve progression-free survival and overall survival in clinical trials, the overall response rate for cervical cancer remains inadequate, necessitating further improvement. Interleukin (IL)-37, an emerging immunomodulator, exhibits antitumour potentials by inhibiting tumour progression and regulating tumour-associated macrophage recognition. We found a significant downregulation of IL-37 expression in cervical cancer, correlated with a poor prognosis. Moreover, the upregulation of IL-37 expression exhibited a suppressive effect on various tumorigenic processes, suppressing the proliferation, invasion, migration, apoptosis and angiogenesis of tumour cells. We also found that the upregulation of IL-37 suppressed cluster of differentiation 47 (CD47) expression in tumour cells via suppression of the signal transducer and activator of transcription 3 (STAT3) expression and phosphorylation, thereby enhancing macrophage recognition and phagocytosis to tumour cells, ultimately reducing immune evasion. Overall, our study highlighted the crucial role of IL-37 in antitumour efficacy and downregulating the expression of CD47 in tumour cells to reduce immune evasion, suggesting the potential of IL-37 as a prognostic biomarker in cervical cancer and offering innovative therapeutic strategies to improve cancer treatment outcomes.","PeriodicalId":19003,"journal":{"name":"Molecular Carcinogenesis","volume":" ","pages":"425-439"},"PeriodicalIF":3.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11814915/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770380","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}

引用次数: 0