中华胃肠外科杂志
中華胃腸外科雜誌
중화위장외과잡지
CHINESE JOURNAL OF GASTROINTESTINAL SURGERY
2014年
6期
594-597
,共4页
钟宝元%刘清泉%刘艳秀%熊小亮%刘瑶
鐘寶元%劉清泉%劉豔秀%熊小亮%劉瑤
종보원%류청천%류염수%웅소량%류요
结直肠肿瘤%上皮细胞间质化%蛋白,STAT3%蛋白, 磷酸化STAT3%E钙黏蛋白
結直腸腫瘤%上皮細胞間質化%蛋白,STAT3%蛋白, 燐痠化STAT3%E鈣黏蛋白
결직장종류%상피세포간질화%단백,STAT3%단백, 린산화STAT3%E개점단백
Colore ctal neoplasms%Epithelial mesenchymal transition%Protein,STAT3%Protein,p-STAT3%Protein,E-cadherin
目的:探讨结直肠癌组织中STAT3及其磷酸化STAT3(p-STAT3)和E钙黏蛋白(E-cadherin)表达的相关性及其与肿瘤浸润转移的关系。方法用免疫组织化学ElivisionTM plus法检测江西赣南医学院第一附属医院病理科存档的50例结直肠癌组织及相应癌旁组织中 STAT3、P-STAT3及上皮细胞间质化(EMT)相关蛋白E-cadherin的表达,并分析其与结直肠癌临床病理特征的关系。结果50例结直肠癌组织中STAT3和p-STAT3及E-cadherin的阳性表达率分别为72%(36/50)、76%(38/50)和26%(13/50),相应癌旁组织中的表达则分别为24%(12/50)和26%(13/50)及68%(34/50),结直肠癌组织STAT3和p-STAT3的表达明显高于相应癌旁组织,而E-cadherin的表达则明显低于癌旁组织(均P<0.05)。STAT3、p-STAT3及E-cadherin表达与肿瘤浸润深度、分化程度、肿瘤大小、淋巴结转移及TNM分期有关(均P<0.05)。 STAT3和p-STAT3蛋白在结直肠癌中的表达与E-cadherin呈显著负相关(均P<0.05)。结论 STAT3和p-STAT3可能通过对E-cadherin的抑制作用进而引起EMT现象,从而导致结直肠肿瘤的发生和进展。
目的:探討結直腸癌組織中STAT3及其燐痠化STAT3(p-STAT3)和E鈣黏蛋白(E-cadherin)錶達的相關性及其與腫瘤浸潤轉移的關繫。方法用免疫組織化學ElivisionTM plus法檢測江西贛南醫學院第一附屬醫院病理科存檔的50例結直腸癌組織及相應癌徬組織中 STAT3、P-STAT3及上皮細胞間質化(EMT)相關蛋白E-cadherin的錶達,併分析其與結直腸癌臨床病理特徵的關繫。結果50例結直腸癌組織中STAT3和p-STAT3及E-cadherin的暘性錶達率分彆為72%(36/50)、76%(38/50)和26%(13/50),相應癌徬組織中的錶達則分彆為24%(12/50)和26%(13/50)及68%(34/50),結直腸癌組織STAT3和p-STAT3的錶達明顯高于相應癌徬組織,而E-cadherin的錶達則明顯低于癌徬組織(均P<0.05)。STAT3、p-STAT3及E-cadherin錶達與腫瘤浸潤深度、分化程度、腫瘤大小、淋巴結轉移及TNM分期有關(均P<0.05)。 STAT3和p-STAT3蛋白在結直腸癌中的錶達與E-cadherin呈顯著負相關(均P<0.05)。結論 STAT3和p-STAT3可能通過對E-cadherin的抑製作用進而引起EMT現象,從而導緻結直腸腫瘤的髮生和進展。
목적:탐토결직장암조직중STAT3급기린산화STAT3(p-STAT3)화E개점단백(E-cadherin)표체적상관성급기여종류침윤전이적관계。방법용면역조직화학ElivisionTM plus법검측강서공남의학원제일부속의원병이과존당적50례결직장암조직급상응암방조직중 STAT3、P-STAT3급상피세포간질화(EMT)상관단백E-cadherin적표체,병분석기여결직장암림상병리특정적관계。결과50례결직장암조직중STAT3화p-STAT3급E-cadherin적양성표체솔분별위72%(36/50)、76%(38/50)화26%(13/50),상응암방조직중적표체칙분별위24%(12/50)화26%(13/50)급68%(34/50),결직장암조직STAT3화p-STAT3적표체명현고우상응암방조직,이E-cadherin적표체칙명현저우암방조직(균P<0.05)。STAT3、p-STAT3급E-cadherin표체여종류침윤심도、분화정도、종류대소、림파결전이급TNM분기유관(균P<0.05)。 STAT3화p-STAT3단백재결직장암중적표체여E-cadherin정현저부상관(균P<0.05)。결론 STAT3화p-STAT3가능통과대E-cadherin적억제작용진이인기EMT현상,종이도치결직장종류적발생화진전。
Objective To investigate the correlation of expressions of STAT3 and p-STAT3 with epithelial mesenchymal transition (EMT)-associated protein E-cadherin in colorectal cancer, and to examine the association of above expressions with tumor invasion and metastasis of colorectal cancer. Methods Immunohistochemistry assay ElivisionTM plus was used to detect the expressions of STAT3, p-STAT3 and E-cadherin protein in colorectal cancer tissue samples of 50 cases and their corresponding adjacent non-tumor tissues. Association of these protein expressions with tumor invasion and metastasis was analyzed with χ2 test. Correlation of STAT3 and p-STAT3 with E-cadherin was analyzed with Spearman method. Results Positive expression rates of STAT3, p-STAT3 and E-cadherin protein in colorectal cancer tissues were 72%(36/50), 76%(38/50) and 26%(13/50), which were significantly higher compared to adjacent normal intestinal mucosa tissues [24%(12/50), 26%(13/50) and 68%(34/50), all P<0.05]. STAT3, p-STAT3 and E-cadherin expressions were associated with tumor differentiation, tumor invasion depth, tumor size, lymph node metastasis, TNM staging (all P<0.05). In colorectal cancer tissues, STAT3 protein expression was positively correlated with p-STAT3 expression. STAT3 and p-STAT3 expressions in colorectal cancer tissues were negatively correlated with E-cadherin expression (P<0.05). Conclusion STAT3 and p-STAT3 may be involved in tumor EMT through inhibition of E-cadherin expression, leading to the development of colorectal cancer.