BACKGROUND Aberrant expression of stanniocalcin 2 (STC2) is implicated in colon adenocarcinoma (COAD). A previous study identified that STC2 functions as a tumor promoter to drive development of some cancers, but the ...BACKGROUND Aberrant expression of stanniocalcin 2 (STC2) is implicated in colon adenocarcinoma (COAD). A previous study identified that STC2 functions as a tumor promoter to drive development of some cancers, but the role of its overexpression in the development of COAD remains unclear. AIM To evaluate the regulation mechanism of STC2 overexpression in COAD. METHODS The expression of STC2 in COAD was assessed by TCGA COAD database and GEO (GSE50760). Methylation level of the STC2 promoter was evaluated with beta value in UALCAN platform, and the correlation between STC2 expression and survival rate was investigated with TCGA COAD. Transcription binding site prediction was conducted by TRANSFAC and LASAGNA, and a luciferase reporter system was used to identify STC2 promoter activity in several cell lines, including HEK293T, NCM460, HT29, SW480, and HCT116. Western blotting was performed to evaluate the role of Sp1 on the expression of STC2. RESULTS The central finding of this work is that STC2 is overexpressed in COAD tissues and positively correlated with poor prognosis. Importantly, the binding site of the transcription factor Sp1 is widely located in the promoter region of STC2. A luciferase reporter system was successfully constructed to analyze the transcription activity of STC2, and knocking down the expression of Sp1 significantly inhibited the transcription activity of STC2. Furthermore, inhibition of Sp1 remarkably decreased protein levels of STC2. CONCLUSION Our data provide evidence that the transcription factor Sp1 is essential for the overexpression of STC2 in COAD through activation of promoter activity. Taken together, our finding provides new insights into the mechanism of oncogenic function of COAD by STC2.展开更多
Objective This study aimed to investigate how macrophage migration inhibitory factor(MIF)regulates the interaction of signal transducer and activator of transcription 1(STAT1)with CD74,and affects colon cancer prolife...Objective This study aimed to investigate how macrophage migration inhibitory factor(MIF)regulates the interaction of signal transducer and activator of transcription 1(STAT1)with CD74,and affects colon cancer proliferation and invasion.Methods After transfecting MIF small interfering RNA into the SW480 cell line,the expression of STAT1 and CD74 mRNA was detected by qRT-PCR and western blotting.Transwell and MTT assays were performed to detect the colon cancer cell invasion and proliferation ability.Co-immunoprecipitation was used to detect the interaction between CD74 and STAT1 proteins in the treated and control groups.Results The cellular biological assays(MTT and Transwell)showed that the proliferation and invasion ability of colon cancer cells decreased after MIF knockdown;the results showed significant statistical difference(P<0.05).The results of the co-immunoprecipitation assay suggested that MIF knockdown in colon cancer cells could inhibit the binding of CD74 and STAT1 proteins;statistical difference was observed between the two groups(P<0.05).Conclusion MIF can increase the proliferation and invasion of colon cancer cells by promoting the combination of CD74 and STAT1.展开更多
目的 :分析结肠癌相关转录因子1(CCAT-1)m RNA在结直肠癌患者外周血中的表达水平与临床病理特征及预后生存的关联,探讨CCAT-1在结直肠癌早期筛查及病程预后评估中的作用。方法:采用实时定量PCR法(q PCR)检测结直肠癌(60例)、结直肠腺瘤...目的 :分析结肠癌相关转录因子1(CCAT-1)m RNA在结直肠癌患者外周血中的表达水平与临床病理特征及预后生存的关联,探讨CCAT-1在结直肠癌早期筛查及病程预后评估中的作用。方法:采用实时定量PCR法(q PCR)检测结直肠癌(60例)、结直肠腺瘤(30例)及健康志愿者(30例)外周血中CCAT-1 m RNA表达,采用ROC曲线判断CCAT-1对结直肠癌的诊断价值,计算Youden指数确定CCAT-1对结直肠癌的诊断阈值;采用双变量相关(bivariate correlation)Pearson检验分析CCAT-1m RNA表达水平与结直肠癌患者临床病理特征;采用Kaplan-Meier生存分析(Log-rank检验)分析CCAT-1 m RNA表达与结直肠癌患者3年生存率的相关性,绘制生存曲线。结果:结直肠癌患者外周血CCAT-1 m RNA水平相对于结直肠腺瘤患者(P<0.01)、健康志愿者(P<0.01)显著高表达,CCAT-1 m RNA在健康志愿者、结直肠腺瘤及结直肠癌患者外周血中的表达量呈逐渐递增趋势;结直肠癌患者外周血CCAT-1 m RNA表达量与肿瘤直径(P<0.05)、分化程度(P<0.01)、原发灶浸润深度(P<0.01)、淋巴结转移数(P<0.01)、远处转移(P<0.05)及TNM分期(P<0.05)呈显著正相关,与3年生存率呈负相关(P<0.05);CCAT-1 m RNA高表达组生存时间显著低于低表达组(P<0.01)。结论:CCAT-1可作为一种有价值的结直肠癌早期筛查及预后评估的标志物。展开更多
Long non-coding RNAs(lncRNAs)are a family of non-protein-coding RNAs that span a length of over 200 nucleotides.Research reports have illustrated that lncRNAs are involved in various cellular processes and that their ...Long non-coding RNAs(lncRNAs)are a family of non-protein-coding RNAs that span a length of over 200 nucleotides.Research reports have illustrated that lncRNAs are involved in various cellular processes and that their abnormal expression leads to the occurrence and development of various tumors.Colon cancer-associated transcript 2(CCAT2)was first reported as an oncogene in colon cancer.LncRNA CCAT2 is abnormally expressed in hepatocellular carcinoma,cholangiocarcinoma,lung cancer,breast cancer,ovarian cancer,glioma,and other tumors.In tumor tissues,abnormally overexpressed CCAT2 can affect cell proliferation,migration,epithelial-mesenchymal transition,apoptosis,and other biological behaviors through endogenous RNAs mechanisms,various signaling pathways,transcriptional regulation,and other complex mechanisms.Additionally,the overexpression of CCAT2 is also closely related to the tumor size,tumor node metastasis(TNM)stage,survival time,and other prognostic factors,suggesting that it is a potential prognostic indicator.This article reviews the biological functions of CCAT2 and its mechanisms of action in tumors from previous studies.In this review,we attempt to provide a molecular basis for future clinical applications of lncRNA CCAT2.展开更多
基金the Natural Science Foundation of Liaoning Province,China,No.20180550769
文摘BACKGROUND Aberrant expression of stanniocalcin 2 (STC2) is implicated in colon adenocarcinoma (COAD). A previous study identified that STC2 functions as a tumor promoter to drive development of some cancers, but the role of its overexpression in the development of COAD remains unclear. AIM To evaluate the regulation mechanism of STC2 overexpression in COAD. METHODS The expression of STC2 in COAD was assessed by TCGA COAD database and GEO (GSE50760). Methylation level of the STC2 promoter was evaluated with beta value in UALCAN platform, and the correlation between STC2 expression and survival rate was investigated with TCGA COAD. Transcription binding site prediction was conducted by TRANSFAC and LASAGNA, and a luciferase reporter system was used to identify STC2 promoter activity in several cell lines, including HEK293T, NCM460, HT29, SW480, and HCT116. Western blotting was performed to evaluate the role of Sp1 on the expression of STC2. RESULTS The central finding of this work is that STC2 is overexpressed in COAD tissues and positively correlated with poor prognosis. Importantly, the binding site of the transcription factor Sp1 is widely located in the promoter region of STC2. A luciferase reporter system was successfully constructed to analyze the transcription activity of STC2, and knocking down the expression of Sp1 significantly inhibited the transcription activity of STC2. Furthermore, inhibition of Sp1 remarkably decreased protein levels of STC2. CONCLUSION Our data provide evidence that the transcription factor Sp1 is essential for the overexpression of STC2 in COAD through activation of promoter activity. Taken together, our finding provides new insights into the mechanism of oncogenic function of COAD by STC2.
文摘Objective This study aimed to investigate how macrophage migration inhibitory factor(MIF)regulates the interaction of signal transducer and activator of transcription 1(STAT1)with CD74,and affects colon cancer proliferation and invasion.Methods After transfecting MIF small interfering RNA into the SW480 cell line,the expression of STAT1 and CD74 mRNA was detected by qRT-PCR and western blotting.Transwell and MTT assays were performed to detect the colon cancer cell invasion and proliferation ability.Co-immunoprecipitation was used to detect the interaction between CD74 and STAT1 proteins in the treated and control groups.Results The cellular biological assays(MTT and Transwell)showed that the proliferation and invasion ability of colon cancer cells decreased after MIF knockdown;the results showed significant statistical difference(P<0.05).The results of the co-immunoprecipitation assay suggested that MIF knockdown in colon cancer cells could inhibit the binding of CD74 and STAT1 proteins;statistical difference was observed between the two groups(P<0.05).Conclusion MIF can increase the proliferation and invasion of colon cancer cells by promoting the combination of CD74 and STAT1.
文摘目的 :分析结肠癌相关转录因子1(CCAT-1)m RNA在结直肠癌患者外周血中的表达水平与临床病理特征及预后生存的关联,探讨CCAT-1在结直肠癌早期筛查及病程预后评估中的作用。方法:采用实时定量PCR法(q PCR)检测结直肠癌(60例)、结直肠腺瘤(30例)及健康志愿者(30例)外周血中CCAT-1 m RNA表达,采用ROC曲线判断CCAT-1对结直肠癌的诊断价值,计算Youden指数确定CCAT-1对结直肠癌的诊断阈值;采用双变量相关(bivariate correlation)Pearson检验分析CCAT-1m RNA表达水平与结直肠癌患者临床病理特征;采用Kaplan-Meier生存分析(Log-rank检验)分析CCAT-1 m RNA表达与结直肠癌患者3年生存率的相关性,绘制生存曲线。结果:结直肠癌患者外周血CCAT-1 m RNA水平相对于结直肠腺瘤患者(P<0.01)、健康志愿者(P<0.01)显著高表达,CCAT-1 m RNA在健康志愿者、结直肠腺瘤及结直肠癌患者外周血中的表达量呈逐渐递增趋势;结直肠癌患者外周血CCAT-1 m RNA表达量与肿瘤直径(P<0.05)、分化程度(P<0.01)、原发灶浸润深度(P<0.01)、淋巴结转移数(P<0.01)、远处转移(P<0.05)及TNM分期(P<0.05)呈显著正相关,与3年生存率呈负相关(P<0.05);CCAT-1 m RNA高表达组生存时间显著低于低表达组(P<0.01)。结论:CCAT-1可作为一种有价值的结直肠癌早期筛查及预后评估的标志物。
基金Anhui Province Science Foundation(No.2008085MH256).
文摘Long non-coding RNAs(lncRNAs)are a family of non-protein-coding RNAs that span a length of over 200 nucleotides.Research reports have illustrated that lncRNAs are involved in various cellular processes and that their abnormal expression leads to the occurrence and development of various tumors.Colon cancer-associated transcript 2(CCAT2)was first reported as an oncogene in colon cancer.LncRNA CCAT2 is abnormally expressed in hepatocellular carcinoma,cholangiocarcinoma,lung cancer,breast cancer,ovarian cancer,glioma,and other tumors.In tumor tissues,abnormally overexpressed CCAT2 can affect cell proliferation,migration,epithelial-mesenchymal transition,apoptosis,and other biological behaviors through endogenous RNAs mechanisms,various signaling pathways,transcriptional regulation,and other complex mechanisms.Additionally,the overexpression of CCAT2 is also closely related to the tumor size,tumor node metastasis(TNM)stage,survival time,and other prognostic factors,suggesting that it is a potential prognostic indicator.This article reviews the biological functions of CCAT2 and its mechanisms of action in tumors from previous studies.In this review,we attempt to provide a molecular basis for future clinical applications of lncRNA CCAT2.
