AIM:To study the potential value and specificity of plasma miR-216a as a marker for pancreatic injury.METHODS:Two rat models were applied in this article:L-arginine-induced acute pancreatitis was used as one model to ...AIM:To study the potential value and specificity of plasma miR-216a as a marker for pancreatic injury.METHODS:Two rat models were applied in this article:L-arginine-induced acute pancreatitis was used as one model to explore the potential value of plasma miR-216a for detection of pancreatic injury;nonlethal sepsis induced in rats by single puncture cecal ligation and puncture(CLP)was used as the other model to evaluate the specificity of plasma miR-216a compared with twocommonly used markers(amylase and lipase)for acute pancreatitis.Plasmas were sampled from rats at indicated time points and total RNA was isolated.Real-Time Quantitative reverse transcriptase-polymerase chain reaction was used to quantify miR-216a in plasmas.RESULTS:In the acute pancreatitis model,among five time points at which plasmas were sampled,miR-216a concentrations were significantly elevated 24 h after arginine administration and remained significantly increased until 48 h after operation(compared with 0 h time point,P<0.01,Kruskal-Wallis Test).In the CLP model,plasma amylase and lipase,two commonly used biomarkers for acute pancreatitis,were significantly elevated 24 h after operation(compared with 0 h time point,P<0.01 and 0.05 respectively,Pairwise Bonferroni corrected ttests),while miR-216a remained undetectable among four tested time points.CONCLUSION:Our article showed for the first time that plasma miR-216a might serve as a candidate marker of pancreatic injury with novel specificity.展开更多
Esophageal squamous cell carcinoma （ESCC） is one of the most common and deadly cancers in the world, Currently, clinical therapy of ESCC remains limited and the five-year survival rate is poor. The function of miR-4...Esophageal squamous cell carcinoma （ESCC） is one of the most common and deadly cancers in the world, Currently, clinical therapy of ESCC remains limited and the five-year survival rate is poor. The function of miR-425 has been reported in multiple human cancers. However. the tumorigenic role and clinical significance of miR-425 in ESCC remains unclear. We found that enhanced expression of miR- 425 in ESCC cell lines not only promoted cell proliferation and colony formation, but also increased cellular metastasis. Furthermore, we revealed the mechanism that miR-425 inhibited the expression of SMAD2 by targeting the second binding site in the 3＇-untranslated region （3＇-UTR） in ESCC. This mode of action influenced not only SMAD2 rnRNA expression but also protein expression. In addition, we detected the expression of miR-425 in ESCC tissues and plasma. Moreover, we analyzed the relationship between miR-425 expression and SMAD2 mRNA expression. We found that miR-425 was overexpressed in ESCC tissues and the plasma relative to adjacent normal tissues and plasma of healthy individuals. Furthermore, there was a negative correlation between miR-425 expression and SMAD2, Taken together, our results show that miR-425 functions as an oncogene by targeting the 3＇-UTR of SMAD2 and indicate the potential utility of plasma miR-425 as a novel biomarker for ESCC diagnosis.展开更多
Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of eff...Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of effective therapeutic targets to prevent breast cancer metastasis is urgently needed. The function of mi R-503-3p has been investigated in other cancers, but its role in breast cancer remains undefined.Here, we found that mi R-503-3p was overexpressed in breast cancer tissue and plasma compared with adjacent normal breast tissue and with plasma from healthy individuals. Moreover, we identified mi R-503-3p to be an oncogene of breast cancer cell proliferation, migration and invasion. Upregulation of mi R-503-3p in breast cancer cells inhibited expression of epithelialemesenchymal transition（EMT）-related protein SMAD2 and the epithelial marker protein E-cadherin by directly binding to their m RNA30 untranslated region, whereas increased expression of mesenchymal marker proteins, including vimentin and N-cadherin. Taken together, our findings support a critical role for mi R-503-3p in induction of breast cancer EMT and suggest that plasma mi R-503-3p may be a useful diagnostic biomarker for breast cancer.展开更多
目的研究利用miRNA-1诊断急性心肌梗死,在分子生物学层面拓展急性心肌梗死法医病理学诊断指标方法通过大鼠A M I动物模型,利用实时定量P C R技术检测急性心梗发生后血浆m iRN A-1表达变化水平,并与免疫组化指标Connexin 43进行对比;利...目的研究利用miRNA-1诊断急性心肌梗死,在分子生物学层面拓展急性心肌梗死法医病理学诊断指标方法通过大鼠A M I动物模型,利用实时定量P C R技术检测急性心梗发生后血浆m iRN A-1表达变化水平,并与免疫组化指标Connexin 43进行对比;利用实时定量P C R技术检测死亡早期m iR N A-1变化趋势结果A M I发生30min,血浆m iR N A-1含量开始升高,A M I发生丨h、2 h后,血浆中m iR N A-1相对含量平均值分别是对照组的3倍、5倍;而免疫组化指标Comiexin 43在AM丨发生30m in后的表达部位发生改变,表达量升高;在死后稳定性方面,大鼠死亡Oh、3h、6h、12h后,血浆miRNA-1含量没有统计学差异(p>0.05),但在24 h后,血浆miRNA-1明显升高,其平均值约为Oh组的42倍(p<0.05)。结论在心梗发生早期,血浆m iR N A-1含量特异性升高,并能在死亡早期保持稳定,有望作为法医病理诊断急性心肌梗死辅助分子指标。展开更多
基金Supported by National Nature Science Foundation of China,No.30971344Innovative Fund for PhD granted by the Second Military Medical University
文摘AIM:To study the potential value and specificity of plasma miR-216a as a marker for pancreatic injury.METHODS:Two rat models were applied in this article:L-arginine-induced acute pancreatitis was used as one model to explore the potential value of plasma miR-216a for detection of pancreatic injury;nonlethal sepsis induced in rats by single puncture cecal ligation and puncture(CLP)was used as the other model to evaluate the specificity of plasma miR-216a compared with twocommonly used markers(amylase and lipase)for acute pancreatitis.Plasmas were sampled from rats at indicated time points and total RNA was isolated.Real-Time Quantitative reverse transcriptase-polymerase chain reaction was used to quantify miR-216a in plasmas.RESULTS:In the acute pancreatitis model,among five time points at which plasmas were sampled,miR-216a concentrations were significantly elevated 24 h after arginine administration and remained significantly increased until 48 h after operation(compared with 0 h time point,P<0.01,Kruskal-Wallis Test).In the CLP model,plasma amylase and lipase,two commonly used biomarkers for acute pancreatitis,were significantly elevated 24 h after operation(compared with 0 h time point,P<0.01 and 0.05 respectively,Pairwise Bonferroni corrected ttests),while miR-216a remained undetectable among four tested time points.CONCLUSION:Our article showed for the first time that plasma miR-216a might serve as a candidate marker of pancreatic injury with novel specificity.
基金supported by the funding from the National High Technology Research and Development Program of China (863 Program) (Nos. 2012AA02A206 and 2011AA02A110)the National Key Basic Research Program of China (973 Program) (Nos. 2011CB910801 and 2011CB911004)the National Key Special Program on Infection diseases (No. 2013ZX10002009)
文摘Esophageal squamous cell carcinoma （ESCC） is one of the most common and deadly cancers in the world, Currently, clinical therapy of ESCC remains limited and the five-year survival rate is poor. The function of miR-425 has been reported in multiple human cancers. However. the tumorigenic role and clinical significance of miR-425 in ESCC remains unclear. We found that enhanced expression of miR- 425 in ESCC cell lines not only promoted cell proliferation and colony formation, but also increased cellular metastasis. Furthermore, we revealed the mechanism that miR-425 inhibited the expression of SMAD2 by targeting the second binding site in the 3＇-untranslated region （3＇-UTR） in ESCC. This mode of action influenced not only SMAD2 rnRNA expression but also protein expression. In addition, we detected the expression of miR-425 in ESCC tissues and plasma. Moreover, we analyzed the relationship between miR-425 expression and SMAD2 mRNA expression. We found that miR-425 was overexpressed in ESCC tissues and the plasma relative to adjacent normal tissues and plasma of healthy individuals. Furthermore, there was a negative correlation between miR-425 expression and SMAD2, Taken together, our results show that miR-425 functions as an oncogene by targeting the 3＇-UTR of SMAD2 and indicate the potential utility of plasma miR-425 as a novel biomarker for ESCC diagnosis.
基金supported by funding from the National Key Basic Research Program of China(973 Program,No.2012CB967003)the National Natural Science Foundation of China(Nos.81472661,21335007,and 81402463)the National High Technology Research and Development Program of China(863 Program,No.2015AA020104)
文摘Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of effective therapeutic targets to prevent breast cancer metastasis is urgently needed. The function of mi R-503-3p has been investigated in other cancers, but its role in breast cancer remains undefined.Here, we found that mi R-503-3p was overexpressed in breast cancer tissue and plasma compared with adjacent normal breast tissue and with plasma from healthy individuals. Moreover, we identified mi R-503-3p to be an oncogene of breast cancer cell proliferation, migration and invasion. Upregulation of mi R-503-3p in breast cancer cells inhibited expression of epithelialemesenchymal transition（EMT）-related protein SMAD2 and the epithelial marker protein E-cadherin by directly binding to their m RNA30 untranslated region, whereas increased expression of mesenchymal marker proteins, including vimentin and N-cadherin. Taken together, our findings support a critical role for mi R-503-3p in induction of breast cancer EMT and suggest that plasma mi R-503-3p may be a useful diagnostic biomarker for breast cancer.
文摘目的研究利用miRNA-1诊断急性心肌梗死,在分子生物学层面拓展急性心肌梗死法医病理学诊断指标方法通过大鼠A M I动物模型,利用实时定量P C R技术检测急性心梗发生后血浆m iRN A-1表达变化水平,并与免疫组化指标Connexin 43进行对比;利用实时定量P C R技术检测死亡早期m iR N A-1变化趋势结果A M I发生30min,血浆m iR N A-1含量开始升高,A M I发生丨h、2 h后,血浆中m iR N A-1相对含量平均值分别是对照组的3倍、5倍;而免疫组化指标Comiexin 43在AM丨发生30m in后的表达部位发生改变,表达量升高;在死后稳定性方面,大鼠死亡Oh、3h、6h、12h后,血浆miRNA-1含量没有统计学差异(p>0.05),但在24 h后,血浆miRNA-1明显升高,其平均值约为Oh组的42倍(p<0.05)。结论在心梗发生早期,血浆m iR N A-1含量特异性升高,并能在死亡早期保持稳定,有望作为法医病理诊断急性心肌梗死辅助分子指标。
