中华口腔医学杂志
中華口腔醫學雜誌
중화구강의학잡지
Chinese Journal of Stomatology
2014年
3期
171-176
,共6页
张舒%王博%周旋%岳恺%王旭东
張舒%王博%週鏇%嶽愷%王旭東
장서%왕박%주선%악개%왕욱동
受体,CXCR-4%口腔鳞状细胞癌%淋巴转移
受體,CXCR-4%口腔鱗狀細胞癌%淋巴轉移
수체,CXCR-4%구강린상세포암%림파전이
Receptors,CXCR-4%Oral sprays%Lymphatic metastasis
目的 探讨趋化因子CXC亚家族受体4(CXC subfamily receptor4,CXCR.4)调控口腔鳞状细胞癌上皮间质转化(epithelial-mesenchymal transition,EMT)介导淋巴转移的作用和机制.方法 应用免疫组化SP法检测CXCR-4及EMT相关因子在60例口腔鳞状细胞癌中的表达,分析CXCR-4的表达与口腔鳞状细胞癌患者临床病理特征之间的关系及其与EMT相关因子的相关性.利用小干扰RNA(small interfering RNA,siRNA)沉默CXCR-4在人舌鳞状细胞癌细胞Tscca中的表达,应用PCR及蛋白质印迹法检测沉默效果.通过Transwell、划痕实验、流式细胞术、蛋白质印迹法检测沉默后细胞侵袭、迁移能力、凋亡及EMT相关因子表达的情况.结果 CXCR-4、神经钙黏素、Twist、Snail在淋巴转移组高表达,β-联蛋白、钙黏着蛋白在非淋巴结转移组中高表达.且CXCR-4与Twist、Snail、神经钙黏素的表达呈正相关(相关系数分别为0.300、0.256、0.333,P＜0.05),与β-联蛋白的表达呈负相关(相关系数为-0.497,P＜0.05).沉默CXCR-4的舌癌细胞迁移、侵袭能力减弱,凋亡率增加,神经钙黏素、基质金属蛋白酶2、9表达下降(神经钙黏素:F=20.999,P=0.002;基质金属蛋白酶2:F=47.156,P=0.000;基质金属蛋白酶9:F=142.317,P=0.000),钙黏着蛋白表达升高(F=111.022,P =0.000).结论 CXCR-4可能通过调控EMT的发生,促进口腔鳞状细胞癌的淋巴转移.
目的 探討趨化因子CXC亞傢族受體4(CXC subfamily receptor4,CXCR.4)調控口腔鱗狀細胞癌上皮間質轉化(epithelial-mesenchymal transition,EMT)介導淋巴轉移的作用和機製.方法 應用免疫組化SP法檢測CXCR-4及EMT相關因子在60例口腔鱗狀細胞癌中的錶達,分析CXCR-4的錶達與口腔鱗狀細胞癌患者臨床病理特徵之間的關繫及其與EMT相關因子的相關性.利用小榦擾RNA(small interfering RNA,siRNA)沉默CXCR-4在人舌鱗狀細胞癌細胞Tscca中的錶達,應用PCR及蛋白質印跡法檢測沉默效果.通過Transwell、劃痕實驗、流式細胞術、蛋白質印跡法檢測沉默後細胞侵襲、遷移能力、凋亡及EMT相關因子錶達的情況.結果 CXCR-4、神經鈣黏素、Twist、Snail在淋巴轉移組高錶達,β-聯蛋白、鈣黏著蛋白在非淋巴結轉移組中高錶達.且CXCR-4與Twist、Snail、神經鈣黏素的錶達呈正相關(相關繫數分彆為0.300、0.256、0.333,P＜0.05),與β-聯蛋白的錶達呈負相關(相關繫數為-0.497,P＜0.05).沉默CXCR-4的舌癌細胞遷移、侵襲能力減弱,凋亡率增加,神經鈣黏素、基質金屬蛋白酶2、9錶達下降(神經鈣黏素:F=20.999,P=0.002;基質金屬蛋白酶2:F=47.156,P=0.000;基質金屬蛋白酶9:F=142.317,P=0.000),鈣黏著蛋白錶達升高(F=111.022,P =0.000).結論 CXCR-4可能通過調控EMT的髮生,促進口腔鱗狀細胞癌的淋巴轉移.
목적 탐토추화인자CXC아가족수체4(CXC subfamily receptor4,CXCR.4)조공구강린상세포암상피간질전화(epithelial-mesenchymal transition,EMT)개도림파전이적작용화궤제.방법 응용면역조화SP법검측CXCR-4급EMT상관인자재60례구강린상세포암중적표체,분석CXCR-4적표체여구강린상세포암환자림상병리특정지간적관계급기여EMT상관인자적상관성.이용소간우RNA(small interfering RNA,siRNA)침묵CXCR-4재인설린상세포암세포Tscca중적표체,응용PCR급단백질인적법검측침묵효과.통과Transwell、화흔실험、류식세포술、단백질인적법검측침묵후세포침습、천이능력、조망급EMT상관인자표체적정황.결과 CXCR-4、신경개점소、Twist、Snail재림파전이조고표체,β-련단백、개점착단백재비림파결전이조중고표체.차CXCR-4여Twist、Snail、신경개점소적표체정정상관(상관계수분별위0.300、0.256、0.333,P＜0.05),여β-련단백적표체정부상관(상관계수위-0.497,P＜0.05).침묵CXCR-4적설암세포천이、침습능력감약,조망솔증가,신경개점소、기질금속단백매2、9표체하강(신경개점소:F=20.999,P=0.002;기질금속단백매2:F=47.156,P=0.000;기질금속단백매9:F=142.317,P=0.000),개점착단백표체승고(F=111.022,P =0.000).결론 CXCR-4가능통과조공EMT적발생,촉진구강린상세포암적림파전이.
Objective To sutdy the effect and mechanism of CXC chemokine receptor 4(CXCR-4) modulating oral squanmous cell carcinoma(OSCC) epithelial-mesenchymal transition(EMT) to mediate tumor lymphatic metastasis.Methods Immunohistochemistry was used to detect the CXCR-4 and EMT related proteins among 60 OSCC samples with different lymph node metastasis status and the relationship with clinicopathological features and EMT related factors were analyzed.The small interfering RNA (siRNA) was applied to silence CXCR-4 in Tscca cell.Reverse transcription-PCR and Western blotting were used to observe the inhibitory effect.The wound healing assay,transwell invasion assay and flow cotometry were used to detect Tscca cell migration,invasion ability and apoptosis.Results In lymph node metastasis group,the expression of CXCR-4,N-cadherin,Twist,Snail were higher than those in non-lymph node metastasis group.CXCR-4 showed a positive correlation with Twist,Snail,N-cadherin (correlation coefficient:0.300,0.256,0.333,P ＜ 0.05),but negatively correlated with β-catenin (correlation coefficient:-0.497,P ＜ 0.05).CXCR-4 silencing inhibited the migration and invasion of Tscca cell and induced apoptosis of the cell.Western blotting results indicated that N-cadherin,matrix metalloproteina-2/9 (MMP-2/9) was decreased (N-cadherin:F =20.999,P =0.002 ;MMP-2:F =47.156,P =0.000; MMP-9:F =142.317,P =0.000) while E-cadherin was up-regulated (F =111.022,P =0.000).Conclusions CXCR-4 might play a critical role in the metastasis of OSCC via modulating EMT.
