目的:探讨T2WI联合DCE-MRI的影像组学特征术前预测浸润性乳腺癌腋窝淋巴结转移的价值。方法:回顾性分析经手术病理证实的168例浸润性乳腺癌病人的临床病理资料及MRI图像资料。根据手术病理结果,将其分为淋巴结转移组(n=64)和无淋巴结转...目的:探讨T2WI联合DCE-MRI的影像组学特征术前预测浸润性乳腺癌腋窝淋巴结转移的价值。方法:回顾性分析经手术病理证实的168例浸润性乳腺癌病人的临床病理资料及MRI图像资料。根据手术病理结果,将其分为淋巴结转移组(n=64)和无淋巴结转移组(n=104),并按8∶2的比例将病人随机分为训练组(n=134)与验证组(n=34)。在T2WI和DCE两个序列手动勾画ROI进行图像分割和影像组学特征提取,利用Select K Best、LASSO回归及迭代筛选特征对高维组学特征进行降维,保留与腋窝淋巴结转移高度相关的特征。采用logistic回归建立T2WI、DCE和T2WI联合DCE三个影像组学预测模型,利用ROC曲线下面积(AUC)评估模型的效能,并以最优模型生成列线图。结果:T2WI、DCE和T2WI联合DCE的影像组学预测模型在训练组的AUC分别为0.75、0.75和0.80;验证组的AUC分别为0.75、0.73和0.79。T2WI联合DCE模型的预测效能最佳。结论:T2WI联合DCE影像组学预测模型在术前对浸润性乳腺癌腋窝淋巴结转移的预测具有一定的价值,能够无创、准确地预测腋窝淋巴结转移状态。展开更多
Objective:To investigate the effects of Pien Tze Huang(PZH) on the migration and invasion of HCC cells and underlying molecular mechanism.Methods:Cell counting kit-8(CCK-8) was applied to evaluate the cell viabilities...Objective:To investigate the effects of Pien Tze Huang(PZH) on the migration and invasion of HCC cells and underlying molecular mechanism.Methods:Cell counting kit-8(CCK-8) was applied to evaluate the cell viabilities of SMMC-7721,SK-Hep-1,C3A and HL-7702(6 × 10^(3)cells/well) co-incubated with different concentrations of PZH(0,0.2,0.4,0.6,0.8 mg/mL) for 24 h.Transwell,wound healing assay,CCK-8and Annexin V-FITC/PI staining were conducted to investigate the effects of PZH on the migration,invasion,proliferation and apoptosis of SK-Hep-1 and SMMC-7721 cells(650 μg/mL for SK-Hep-1 cells and 330 μg/mL for SMMC-7721 cells),respectively.In vivo,lung metastasis mouse model constructed by tail vein injection of HCC cells was used for evaluating the anti-metastasis function of PZH.SK-Hep-1 cells(10^(6)cells/200 μL per mice) were injected into B-NDG mice via tail vein.Totally 8 mice were randomly divided into PZH and control groups,4 mice in each group.After 2-d inoculation,mice in the PZH group were administered with PZH(250 mg/kg,daily) and mice in the control group received only vehicle(PBS) from the 2nd day after xenograft to day 17.Transcriptome analysis based on RNA-seq was subsequently used for deciphering anti-tumor mechanism of PZH.Quantitative real-time polymerase chain reaction(qRT-PCR) and Western blot were applied to verify RNA-seq results.Luciferase reporter assay was performed to examine the transcriptional activity of yes-associated protein(YAP).Results:PZH treatment significantly inhibited the migration,invasion,proliferation and promoted the apoptosis of HCC cells in vitro and in vivo(P<0.01).Transcriptome analysis indicated that Hippo signaling pathway was associated with anti-metastasis function of PZH.Mechanical study showed PZH significantly inhibited the expressions of platelet derived growth factor receptor beta(PDGFRB),YAP,connective tissue growth factor(CCN2),N-cadherin,vimentin and matrix metallopeptidase 2(MMP2,P<0.01).Meanwhile,the phosphorylation of YAP was also enhanced by PZH treatment 展开更多
BACKGROUND Hepatocellular carcinoma(HCC)is a primary contributor to cancer-related mortality on a global scale.However,the underlying molecular mechanisms are still poorly understood.Long noncoding RNAs are emerging m...BACKGROUND Hepatocellular carcinoma(HCC)is a primary contributor to cancer-related mortality on a global scale.However,the underlying molecular mechanisms are still poorly understood.Long noncoding RNAs are emerging markers for HCC diagnosis,prognosis,and therapeutic target.No study of LINC01767 in HCC was published.AIM To conduct a multi-omics analysis to explore the roles of LINC01767 in HCC for the first time.METHODS DESeq2 Package was used to analyze different gene expressions.Receiver operating characteristic curves assessed the diagnostic performance.Kaplan-Meier univariate and Cox multivariate analyses were used to perform survival analysis.The least absolute shrinkage and selection operator(LASSO)-Cox was used to identify the prediction model.Subsequent to the validation of LINC01767 expression in HCC fresh frozen tissues through quantitative real time polymerase chain reaction,next generation sequencing was performed following LINC01767 over expression(GSE243371),and Gene Ontology/Kyoto Encyclopedia of Genes and Genomes/Gene Set Enrichment Analysis/ingenuity pathway analysis was carried out.In vitro experiment in Huh7 cell was carried out.RESULTS LINC01767 was down-regulated in HCC with a log fold change=1.575 and was positively correlated with the cancer stemness.LINC01767 was a good diagnostic marker with area under the curve(AUC)[0.801,95% confidence interval(CI):0.751-0.852,P=0.0106]and an independent predictor for overall survival(OS)with hazard ratio=1.899(95%CI:1.01-3.58,P=0.048).LINC01767 nomogram model showed a satisfied performance.The top-ranked regulatory network analysis of LINC01767 showed the regulation of genes participating various pathways.LASSO regression identified the 9-genes model showing a more satisfied performance than 5-genes model to predict the OS with AUC>0.75.LINC01767 was down-expressed obviously in tumor than para-tumor tissues in our cohort as well as in cancer cell line;the over expression of LINC01767 inhibit cell proliferation and clone formation of Huh7 in vitro.CONCL展开更多
文摘目的:探讨T2WI联合DCE-MRI的影像组学特征术前预测浸润性乳腺癌腋窝淋巴结转移的价值。方法:回顾性分析经手术病理证实的168例浸润性乳腺癌病人的临床病理资料及MRI图像资料。根据手术病理结果,将其分为淋巴结转移组(n=64)和无淋巴结转移组(n=104),并按8∶2的比例将病人随机分为训练组(n=134)与验证组(n=34)。在T2WI和DCE两个序列手动勾画ROI进行图像分割和影像组学特征提取,利用Select K Best、LASSO回归及迭代筛选特征对高维组学特征进行降维,保留与腋窝淋巴结转移高度相关的特征。采用logistic回归建立T2WI、DCE和T2WI联合DCE三个影像组学预测模型,利用ROC曲线下面积(AUC)评估模型的效能,并以最优模型生成列线图。结果:T2WI、DCE和T2WI联合DCE的影像组学预测模型在训练组的AUC分别为0.75、0.75和0.80;验证组的AUC分别为0.75、0.73和0.79。T2WI联合DCE模型的预测效能最佳。结论:T2WI联合DCE影像组学预测模型在术前对浸润性乳腺癌腋窝淋巴结转移的预测具有一定的价值,能够无创、准确地预测腋窝淋巴结转移状态。
基金Supported by Joint Funds for Innovation of Science and Technology,Fujian Province(No.2019Y9047)Joint Funds for Innovation of Science and Technology of Fujian Province(No.2017Y9117)+3 种基金Young and Middle-Aged Talent Training Project of Fujian Provincial Health and Family Planning Commission(No.2020GGA072)Natural Science Foundation of Fujian Province(No.2020J011164,2020J011170)Startup Fund for Scientific Research,Fujian Medical University(No.2019QH1298)Science and Technology Plan Project of Fuzhou(No.2019-S-87)。
文摘Objective:To investigate the effects of Pien Tze Huang(PZH) on the migration and invasion of HCC cells and underlying molecular mechanism.Methods:Cell counting kit-8(CCK-8) was applied to evaluate the cell viabilities of SMMC-7721,SK-Hep-1,C3A and HL-7702(6 × 10^(3)cells/well) co-incubated with different concentrations of PZH(0,0.2,0.4,0.6,0.8 mg/mL) for 24 h.Transwell,wound healing assay,CCK-8and Annexin V-FITC/PI staining were conducted to investigate the effects of PZH on the migration,invasion,proliferation and apoptosis of SK-Hep-1 and SMMC-7721 cells(650 μg/mL for SK-Hep-1 cells and 330 μg/mL for SMMC-7721 cells),respectively.In vivo,lung metastasis mouse model constructed by tail vein injection of HCC cells was used for evaluating the anti-metastasis function of PZH.SK-Hep-1 cells(10^(6)cells/200 μL per mice) were injected into B-NDG mice via tail vein.Totally 8 mice were randomly divided into PZH and control groups,4 mice in each group.After 2-d inoculation,mice in the PZH group were administered with PZH(250 mg/kg,daily) and mice in the control group received only vehicle(PBS) from the 2nd day after xenograft to day 17.Transcriptome analysis based on RNA-seq was subsequently used for deciphering anti-tumor mechanism of PZH.Quantitative real-time polymerase chain reaction(qRT-PCR) and Western blot were applied to verify RNA-seq results.Luciferase reporter assay was performed to examine the transcriptional activity of yes-associated protein(YAP).Results:PZH treatment significantly inhibited the migration,invasion,proliferation and promoted the apoptosis of HCC cells in vitro and in vivo(P<0.01).Transcriptome analysis indicated that Hippo signaling pathway was associated with anti-metastasis function of PZH.Mechanical study showed PZH significantly inhibited the expressions of platelet derived growth factor receptor beta(PDGFRB),YAP,connective tissue growth factor(CCN2),N-cadherin,vimentin and matrix metallopeptidase 2(MMP2,P<0.01).Meanwhile,the phosphorylation of YAP was also enhanced by PZH treatment
基金Supported by Foundation of Qingdao Postdoctoral Innovation Project,No.QDBSH20230101019Funded State Key Laboratory of Marine Food Processing&Safety Control,Qingdao,No.SKL2023M05.
文摘BACKGROUND Hepatocellular carcinoma(HCC)is a primary contributor to cancer-related mortality on a global scale.However,the underlying molecular mechanisms are still poorly understood.Long noncoding RNAs are emerging markers for HCC diagnosis,prognosis,and therapeutic target.No study of LINC01767 in HCC was published.AIM To conduct a multi-omics analysis to explore the roles of LINC01767 in HCC for the first time.METHODS DESeq2 Package was used to analyze different gene expressions.Receiver operating characteristic curves assessed the diagnostic performance.Kaplan-Meier univariate and Cox multivariate analyses were used to perform survival analysis.The least absolute shrinkage and selection operator(LASSO)-Cox was used to identify the prediction model.Subsequent to the validation of LINC01767 expression in HCC fresh frozen tissues through quantitative real time polymerase chain reaction,next generation sequencing was performed following LINC01767 over expression(GSE243371),and Gene Ontology/Kyoto Encyclopedia of Genes and Genomes/Gene Set Enrichment Analysis/ingenuity pathway analysis was carried out.In vitro experiment in Huh7 cell was carried out.RESULTS LINC01767 was down-regulated in HCC with a log fold change=1.575 and was positively correlated with the cancer stemness.LINC01767 was a good diagnostic marker with area under the curve(AUC)[0.801,95% confidence interval(CI):0.751-0.852,P=0.0106]and an independent predictor for overall survival(OS)with hazard ratio=1.899(95%CI:1.01-3.58,P=0.048).LINC01767 nomogram model showed a satisfied performance.The top-ranked regulatory network analysis of LINC01767 showed the regulation of genes participating various pathways.LASSO regression identified the 9-genes model showing a more satisfied performance than 5-genes model to predict the OS with AUC>0.75.LINC01767 was down-expressed obviously in tumor than para-tumor tissues in our cohort as well as in cancer cell line;the over expression of LINC01767 inhibit cell proliferation and clone formation of Huh7 in vitro.CONCL
