中华普通外科杂志
中華普通外科雜誌
중화보통외과잡지
CHINESE JOURNAL OF GENERAL SURGERY
2009年
6期
496-499
,共4页
周敏%刘骅%沈志勇%赵文毅%曹晖
週敏%劉驊%瀋誌勇%趙文毅%曹暉
주민%류화%침지용%조문의%조휘
胃肿瘤%气腹,人工%肿瘤侵润%肿瘤转移
胃腫瘤%氣腹,人工%腫瘤侵潤%腫瘤轉移
위종류%기복,인공%종류침윤%종류전이
Stomach neoplasmas%Pneumoperitoneum,artificial%Neoplasm invasiveness%Neoplasm metastasis
目的 探讨不同压强持续性CO2气腹环境对胃癌细胞黏附与侵袭转移的影响.方法 建立体外CO2气腹模型,选用3种不同分化程度的胃癌细胞株MKN-45(低分化腺癌细胞)、SGC-7901(中分化腺癌细胞)和MKN-28(高分化腺痛细胞),分别在9 mm Hg、15 mm Hg以及常规条件下(0 mm Hg,对照组)作用2 h和4 h后,用RT-PCR法、CytoMatrixTM细胞黏附试剂盒和ECMatrixTM细胞侵袭试剂盒检测黏附分子E钙黏蛋白(E-cadherin)和细胞间黏附分子1(intercellular adhesionmolecule-1,ICAM-1)以及侵袭分子基质金属蛋白酶2(matrix metalloproteinases,MMP-2)和血管内皮生长因子A(vascular endothelial growth factor A,VEGF-A)的表达.将胃癌细胞注入裸鼠腹腔(2×106个细胞/只),每组10只.4周后每组取5只处死,记录腹腔成瘤情况,观察其余裸鼠的生存时间.结果 RT-PCR结果显示3种胃癌细胞株经CO2处理后,随着时程的延长及压强的升高,E-cadherin表达有下降的趋势(MKN-45:2.26→2.19、SGC-7901:2.16→2.09、MKN-28:2.06→1.99),而ICAM-1(MKN-45:2.20→2.28、SGC-7901:2.10→2.18、MKN-28:2.00→2.08)、MMP-2(MKN-45:2.05→2.13、SGC-7901:1.95→2.03、MKN-28:1.85→1.93)和VEGF-A(MKN-45:2.10→2.16、SGC-7901:2.00→2.06、MKN-28:1.90→1.96)则有升高的趋势,但是各实验组之间比较或实验组与对照组之间比较差异均无统计学意义(P>0.05).黏附侵袭实验也得出类似的结果.裸鼠模型显示3种胃癌细胞株在不同CO2气腹环境及对照条件下,腹腔成瘤个数随着时程的延长及压强的升高而增加(MKN-45:22→23、SGC-7901:20→22、MKN-28:21→22),存活天数则减少(MKN-45:23→21、SGC-7901:22→21、MKN-28:22→21),但各组的腹腔成瘤个数和存活时间之间相比差异均尤统计学意义(P>0.05).结论 在不高于15 mm Hg 压强以及不超过4 h的情况下,不同压强与时程的CO2对3种胃癌细胞株的黏附和侵袭能力并无显著影响,且不增加肿瘤的转移风险.
目的 探討不同壓彊持續性CO2氣腹環境對胃癌細胞黏附與侵襲轉移的影響.方法 建立體外CO2氣腹模型,選用3種不同分化程度的胃癌細胞株MKN-45(低分化腺癌細胞)、SGC-7901(中分化腺癌細胞)和MKN-28(高分化腺痛細胞),分彆在9 mm Hg、15 mm Hg以及常規條件下(0 mm Hg,對照組)作用2 h和4 h後,用RT-PCR法、CytoMatrixTM細胞黏附試劑盒和ECMatrixTM細胞侵襲試劑盒檢測黏附分子E鈣黏蛋白(E-cadherin)和細胞間黏附分子1(intercellular adhesionmolecule-1,ICAM-1)以及侵襲分子基質金屬蛋白酶2(matrix metalloproteinases,MMP-2)和血管內皮生長因子A(vascular endothelial growth factor A,VEGF-A)的錶達.將胃癌細胞註入裸鼠腹腔(2×106箇細胞/隻),每組10隻.4週後每組取5隻處死,記錄腹腔成瘤情況,觀察其餘裸鼠的生存時間.結果 RT-PCR結果顯示3種胃癌細胞株經CO2處理後,隨著時程的延長及壓彊的升高,E-cadherin錶達有下降的趨勢(MKN-45:2.26→2.19、SGC-7901:2.16→2.09、MKN-28:2.06→1.99),而ICAM-1(MKN-45:2.20→2.28、SGC-7901:2.10→2.18、MKN-28:2.00→2.08)、MMP-2(MKN-45:2.05→2.13、SGC-7901:1.95→2.03、MKN-28:1.85→1.93)和VEGF-A(MKN-45:2.10→2.16、SGC-7901:2.00→2.06、MKN-28:1.90→1.96)則有升高的趨勢,但是各實驗組之間比較或實驗組與對照組之間比較差異均無統計學意義(P>0.05).黏附侵襲實驗也得齣類似的結果.裸鼠模型顯示3種胃癌細胞株在不同CO2氣腹環境及對照條件下,腹腔成瘤箇數隨著時程的延長及壓彊的升高而增加(MKN-45:22→23、SGC-7901:20→22、MKN-28:21→22),存活天數則減少(MKN-45:23→21、SGC-7901:22→21、MKN-28:22→21),但各組的腹腔成瘤箇數和存活時間之間相比差異均尤統計學意義(P>0.05).結論 在不高于15 mm Hg 壓彊以及不超過4 h的情況下,不同壓彊與時程的CO2對3種胃癌細胞株的黏附和侵襲能力併無顯著影響,且不增加腫瘤的轉移風險.
목적 탐토불동압강지속성CO2기복배경대위암세포점부여침습전이적영향.방법 건입체외CO2기복모형,선용3충불동분화정도적위암세포주MKN-45(저분화선암세포)、SGC-7901(중분화선암세포)화MKN-28(고분화선통세포),분별재9 mm Hg、15 mm Hg이급상규조건하(0 mm Hg,대조조)작용2 h화4 h후,용RT-PCR법、CytoMatrixTM세포점부시제합화ECMatrixTM세포침습시제합검측점부분자E개점단백(E-cadherin)화세포간점부분자1(intercellular adhesionmolecule-1,ICAM-1)이급침습분자기질금속단백매2(matrix metalloproteinases,MMP-2)화혈관내피생장인자A(vascular endothelial growth factor A,VEGF-A)적표체.장위암세포주입라서복강(2×106개세포/지),매조10지.4주후매조취5지처사,기록복강성류정황,관찰기여라서적생존시간.결과 RT-PCR결과현시3충위암세포주경CO2처리후,수착시정적연장급압강적승고,E-cadherin표체유하강적추세(MKN-45:2.26→2.19、SGC-7901:2.16→2.09、MKN-28:2.06→1.99),이ICAM-1(MKN-45:2.20→2.28、SGC-7901:2.10→2.18、MKN-28:2.00→2.08)、MMP-2(MKN-45:2.05→2.13、SGC-7901:1.95→2.03、MKN-28:1.85→1.93)화VEGF-A(MKN-45:2.10→2.16、SGC-7901:2.00→2.06、MKN-28:1.90→1.96)칙유승고적추세,단시각실험조지간비교혹실험조여대조조지간비교차이균무통계학의의(P>0.05).점부침습실험야득출유사적결과.라서모형현시3충위암세포주재불동CO2기복배경급대조조건하,복강성류개수수착시정적연장급압강적승고이증가(MKN-45:22→23、SGC-7901:20→22、MKN-28:21→22),존활천수칙감소(MKN-45:23→21、SGC-7901:22→21、MKN-28:22→21),단각조적복강성류개수화존활시간지간상비차이균우통계학의의(P>0.05).결론 재불고우15 mm Hg 압강이급불초과4 h적정황하,불동압강여시정적CO2대3충위암세포주적점부화침습능력병무현저영향,차불증가종류적전이풍험.
Objective To investigate the influence of CO2 pneumoperitoneum on the adhesive and invasive ability of gastric cancer cells based on the expression of adhesive and invasive molecules. Methods With an artificial CO2 pneumoperitoneum model in vitro, human gastric cancer cells MKN-45, SGC-7901 and MKN-28 were exposed to 3 different CO2 gradients: 9 mm Hg, 15 mm Hg and control group (0 mm Hg). The expression of E-cadherin, ICAM-1, MMP-2 and VEGF-A were measured at 2 and 4 hours exposure by using RT-PCR, CytoMatrixTM kit and ECMatrixTM kit. The pretreated gastric cancer cells were injected into abdominal cavity of nude mice(2×106 cells per mouse). Five mice in each group were sacrificed 4 weeks later to record the number of tumor nodules in abdominal cavity. The remaining mice were kept for observation of survival time. Results The expression of E-cadherin (MKN-45: from 2.26 to 2.19, SGC-7901 :from 2.16 to 2.09、MKN-28 :from 2.06 to 1.99), ICAM-1 (MKN-45 : from 2.20 to 2.28、SGC-7901: from 2.10 to 2.18、MKN-28: from 2.00 to 2.08), MMP-2 (MKN-45:from 2.05 to 2.13、SGC-7901: from 1.95 to 2.03、MKN-28: from 1.85 to 1.93) and VEGF-A(MKN-45 : from 2.10 to 2.16、SGC-7901 :from 2.00 to 2.06、MKN-28: from 1.90 to 1.96) didn't change significantly with increasing pressure and time (P>0.05). The expression of adhesive and invasive molecules didn't change significantly between the experimental groups and the control group. There was no statistical significance of tumor metastasis in abdominal cavity of nude mice(MKN-45:from 22 to 23、SGC-7901 :from 20 to 22、MKN-28:from 21 to 22) and survival time(MKN-45 :from 23 to 21、SGC-7901 :from 22 to 21、MKN-28 :from 22 to 21) among all the groups. Conclusion Under low pressure and short time of CO2 exposure, the adhesive and invasive capacity of gastric cancer cells did not change significantly hence did not increase the possibility of neoplasm metastasis.
