目的:探讨S100A4基因在膀胱移行细胞癌(Transitional cell carcinoma of the bladder,TCCB)中的表达及意义。方法:通过逆转录聚合酶链反应(RT-PCR)方法检测38例膀胱移行细胞癌组织及其相应癌旁组织中S100A4基因的表达情况,结合临床及组...目的:探讨S100A4基因在膀胱移行细胞癌(Transitional cell carcinoma of the bladder,TCCB)中的表达及意义。方法:通过逆转录聚合酶链反应(RT-PCR)方法检测38例膀胱移行细胞癌组织及其相应癌旁组织中S100A4基因的表达情况,结合临床及组织病理学特点探讨S100A4基因与膀胱癌发生及发展的关系。结果:S100A4基因在膀胱移行细胞癌及正常膀胱移行上皮组织中的阳性表达率分别为60.5%(23/38)和0%(0/38)。膀胱移行细胞癌组织中S100A4基因的表达率明显高于正常膀胱移行上皮组织(P<0.005)。其中膀胱移行细胞癌组织中S100A4基因的表达率随肿瘤分级、分期的增高及淋巴结转移而相应增高(P<0.05)。结论:S100A4基因表达与移行膀胱癌分化有关,癌组织S100A4基因有可能成为膀胱癌的一个新的肿瘤标记物;S100A4基因差异表达与移行膀胱癌侵袭和转移明显相关,移行膀胱癌组织中S100A4基因可望作为移行膀胱癌的病情发展及指导临床治疗的标记物之一。展开更多
AIM:To investigate a potential role of S100A4 in esophagus squamous cell carcinoma metastasis (ESCCs).METHODS:Expression of S100A4 and E-cadherin were analyzed in frozen sections from ESCCs (metastasis,n=28;non-metast...AIM:To investigate a potential role of S100A4 in esophagus squamous cell carcinoma metastasis (ESCCs).METHODS:Expression of S100A4 and E-cadherin were analyzed in frozen sections from ESCCs (metastasis,n=28;non-metastasis,n=20) by reverse transcription-polymerase chain reaction,quantitative polymerase chain reaction and immunohistochemistry.To explore the influence of S100A4 on esophageal cancer invasion and metastasis,S100A4 was overexpressed or silenced by S100A4 siRNA in TE-13 or Eca-109 cells in vitro and in vivo.RESULTS:We found the mRNA and protein levels of S100A4 expression in ESCCs was significantly upregulated,and more importantly,that expression of S100A4 and E cadherin are strongly negatively correlated in patients who had metastasis.It was indicated that overexpression of S100A4 in TE-13 and Eca-109 cells downregulates the expression of E-cadherin,leading to increased cell migration in vitro,whereas knockdown of S100A4 inhibited cell migration and upregulation of E-cadherin expression.Moreover,the loss of cell metastatic potential was rescued by overexpression of E-cadherin completely.In addition,nude mice inoculated with S100A4 siRNA-transfected cells exhibited a significantly decreased invasion ability in vivo.CONCLUSION:S100A4 may be involved in ESCC progression by regulate E-cadherin expression,vectorbased RNA interference targeting S100A4 is a potential therapeutic method for human ESCC.展开更多
文摘目的:探讨S100A4基因在膀胱移行细胞癌(Transitional cell carcinoma of the bladder,TCCB)中的表达及意义。方法:通过逆转录聚合酶链反应(RT-PCR)方法检测38例膀胱移行细胞癌组织及其相应癌旁组织中S100A4基因的表达情况,结合临床及组织病理学特点探讨S100A4基因与膀胱癌发生及发展的关系。结果:S100A4基因在膀胱移行细胞癌及正常膀胱移行上皮组织中的阳性表达率分别为60.5%(23/38)和0%(0/38)。膀胱移行细胞癌组织中S100A4基因的表达率明显高于正常膀胱移行上皮组织(P<0.005)。其中膀胱移行细胞癌组织中S100A4基因的表达率随肿瘤分级、分期的增高及淋巴结转移而相应增高(P<0.05)。结论:S100A4基因表达与移行膀胱癌分化有关,癌组织S100A4基因有可能成为膀胱癌的一个新的肿瘤标记物;S100A4基因差异表达与移行膀胱癌侵袭和转移明显相关,移行膀胱癌组织中S100A4基因可望作为移行膀胱癌的病情发展及指导临床治疗的标记物之一。
文摘AIM:To investigate a potential role of S100A4 in esophagus squamous cell carcinoma metastasis (ESCCs).METHODS:Expression of S100A4 and E-cadherin were analyzed in frozen sections from ESCCs (metastasis,n=28;non-metastasis,n=20) by reverse transcription-polymerase chain reaction,quantitative polymerase chain reaction and immunohistochemistry.To explore the influence of S100A4 on esophageal cancer invasion and metastasis,S100A4 was overexpressed or silenced by S100A4 siRNA in TE-13 or Eca-109 cells in vitro and in vivo.RESULTS:We found the mRNA and protein levels of S100A4 expression in ESCCs was significantly upregulated,and more importantly,that expression of S100A4 and E cadherin are strongly negatively correlated in patients who had metastasis.It was indicated that overexpression of S100A4 in TE-13 and Eca-109 cells downregulates the expression of E-cadherin,leading to increased cell migration in vitro,whereas knockdown of S100A4 inhibited cell migration and upregulation of E-cadherin expression.Moreover,the loss of cell metastatic potential was rescued by overexpression of E-cadherin completely.In addition,nude mice inoculated with S100A4 siRNA-transfected cells exhibited a significantly decreased invasion ability in vivo.CONCLUSION:S100A4 may be involved in ESCC progression by regulate E-cadherin expression,vectorbased RNA interference targeting S100A4 is a potential therapeutic method for human ESCC.