中国免疫学杂志
中國免疫學雜誌
중국면역학잡지
CHINESE JOURNAL OF IMMUNOLOGY
2015年
4期
497-501,508
,共6页
肿瘤相关成纤维细胞%口腔癌%侵袭%肿瘤生长
腫瘤相關成纖維細胞%口腔癌%侵襲%腫瘤生長
종류상관성섬유세포%구강암%침습%종류생장
Cancer associated fibroblasts%Oral carcinoma%Invasion%Tumor group
目的：探讨肿瘤相关成纤维细胞（ CAFs）对口腔癌细胞增殖、迁移、侵袭的影响，初步分析产生影响的可能原因。方法：体外培养CAFs、舌癌细胞株SCC－9和CAL－27，并建立CAFs与舌癌细胞株共同培养体系；采用红色荧光蛋白标记法观察CAFs对舌癌细胞株增殖能力的影响；利用Transwell小室建立CAFs与舌癌细胞株SCC－9或CAL－27的交互作用模型，观察CAFs对舌癌细胞株迁移和侵袭能力的影响；采用细胞因子芯片检测CAFs单独培养、SCC－9单独培养、CAFs和SCC－9共同培养上清中可溶性细胞因子水平的差异。采用裸鼠成瘤实验观察CAFs对舌癌成瘤能力的影响。结果：培养第5天SCC－9与CAFs共同培养组中SCC－9的数量是初始SCC－9量的（4．41±0．38）倍，明显高于SCC－9单独培养组（3．21±0．35）倍；CAL－27组结果相似。24 h后SSC－9＋CAFs组迁移到小室底面的SCC－9细胞与SCC－9单独培养组相比比值为2．6±0．42，CAL－27组比值为3．11±0．46。细胞侵袭研究结果与迁移研究结果类似，共同培养组穿透基质胶的OCC细胞明显增多（ P＜0．05）。细胞因子抗体芯片分析发现，与细胞单独培养相比，共同培养组培养上清中CCL2、CCL5、IL8水平明显升高。裸鼠成瘤实验结果发现，6周后，SCC－9与CAFs混合注入组的肿瘤体积明显大于SCC－9单独注入组。结论：口腔CAFs能促进舌癌细胞株SCC－9和CAL－27的增殖、迁移和侵袭和肿瘤生长，癌细胞功能的改变可能与微环境中CCL2、CCL5、IL8等细胞因子水平升高有关。
目的：探討腫瘤相關成纖維細胞（ CAFs）對口腔癌細胞增殖、遷移、侵襲的影響，初步分析產生影響的可能原因。方法：體外培養CAFs、舌癌細胞株SCC－9和CAL－27，併建立CAFs與舌癌細胞株共同培養體繫；採用紅色熒光蛋白標記法觀察CAFs對舌癌細胞株增殖能力的影響；利用Transwell小室建立CAFs與舌癌細胞株SCC－9或CAL－27的交互作用模型，觀察CAFs對舌癌細胞株遷移和侵襲能力的影響；採用細胞因子芯片檢測CAFs單獨培養、SCC－9單獨培養、CAFs和SCC－9共同培養上清中可溶性細胞因子水平的差異。採用裸鼠成瘤實驗觀察CAFs對舌癌成瘤能力的影響。結果：培養第5天SCC－9與CAFs共同培養組中SCC－9的數量是初始SCC－9量的（4．41±0．38）倍，明顯高于SCC－9單獨培養組（3．21±0．35）倍；CAL－27組結果相似。24 h後SSC－9＋CAFs組遷移到小室底麵的SCC－9細胞與SCC－9單獨培養組相比比值為2．6±0．42，CAL－27組比值為3．11±0．46。細胞侵襲研究結果與遷移研究結果類似，共同培養組穿透基質膠的OCC細胞明顯增多（ P＜0．05）。細胞因子抗體芯片分析髮現，與細胞單獨培養相比，共同培養組培養上清中CCL2、CCL5、IL8水平明顯升高。裸鼠成瘤實驗結果髮現，6週後，SCC－9與CAFs混閤註入組的腫瘤體積明顯大于SCC－9單獨註入組。結論：口腔CAFs能促進舌癌細胞株SCC－9和CAL－27的增殖、遷移和侵襲和腫瘤生長，癌細胞功能的改變可能與微環境中CCL2、CCL5、IL8等細胞因子水平升高有關。
목적：탐토종류상관성섬유세포（ CAFs）대구강암세포증식、천이、침습적영향，초보분석산생영향적가능원인。방법：체외배양CAFs、설암세포주SCC－9화CAL－27，병건립CAFs여설암세포주공동배양체계；채용홍색형광단백표기법관찰CAFs대설암세포주증식능력적영향；이용Transwell소실건립CAFs여설암세포주SCC－9혹CAL－27적교호작용모형，관찰CAFs대설암세포주천이화침습능력적영향；채용세포인자심편검측CAFs단독배양、SCC－9단독배양、CAFs화SCC－9공동배양상청중가용성세포인자수평적차이。채용라서성류실험관찰CAFs대설암성류능력적영향。결과：배양제5천SCC－9여CAFs공동배양조중SCC－9적수량시초시SCC－9량적（4．41±0．38）배，명현고우SCC－9단독배양조（3．21±0．35）배；CAL－27조결과상사。24 h후SSC－9＋CAFs조천이도소실저면적SCC－9세포여SCC－9단독배양조상비비치위2．6±0．42，CAL－27조비치위3．11±0．46。세포침습연구결과여천이연구결과유사，공동배양조천투기질효적OCC세포명현증다（ P＜0．05）。세포인자항체심편분석발현，여세포단독배양상비，공동배양조배양상청중CCL2、CCL5、IL8수평명현승고。라서성류실험결과발현，6주후，SCC－9여CAFs혼합주입조적종류체적명현대우SCC－9단독주입조。결론：구강CAFs능촉진설암세포주SCC－9화CAL－27적증식、천이화침습화종류생장，암세포공능적개변가능여미배경중CCL2、CCL5、IL8등세포인자수평승고유관。
Objective:To elucidate the effects of CAFs on the proliferation,migration and invasion of oral cancer cells and those on tumor growth.Potential mechanism was discussed.Methods:CAFs and SCC-9 or CAL-27 were cocultured.The proliferation of oral cancer cells were detected by measuring the level of RFP.A interaction model between CAFs and SCC-9 or CAL-27 were established with Transwell chambers to abserve the effects of CAFs on the migration and invasion of OCCs.The conditioned medium collected from mono-cultured CAFs or SSC-9 cell,and co-culture were subjected to a cytokine antibody array.Volumes of xenografts were obtained and presented.Results:At day 5,significant difference was found in OCC proliferation between OCC-CAFs group and OCC group.The SCC-9 cell number was up to 4.41±0.38 times as many as the initial number in co-culture group and 3.21±0.35 times in SCC-9 group(P<0.05).The proliferation of CAL-27 was similar to that of SCC-9.SCC-9 cells migrated to the bottom in group SCC-9+CAFs were 2.6± 0.42 times as many as group SCC-9(P<0.05).CAL-27 cells migrated to the bottom in group CAL-27+CAFs were 3.11±0.46 times as many as group CAL-27 ( P<0.05 ) .The similar results were found in invasion analysis.OCCs invaded more quickly towards medium derived from co-cultured cells than that from OCCs alone.Three human cytokines(CCL2,CCL5 and IL-8)were significantly upregulated in conditioned medium from co-cultured cells compared with those from CAFs or SSC-9 alone.Six weeks after injection,we observed that SCC-9 mixed with CAFs generated tumors of greater volume than those generated from SCC-9 cells alone.Conclusion:CAFs Promote the Proliferation,Migration,Invasion of oral cancer cells and tumor growth.Cytokines(CCL2,CCL5 and IL-8)may responsible for the bi-ological function change of cancer cells.
