中国肿瘤临床
中國腫瘤臨床
중국종류림상
CHINESE JOURNAL OF CLINICAL ONCOLOGY
2010年
3期
142-145
,共4页
周进明%钟大平%周琪%彭秋平%潘凤%何颖%王雪%梁后杰
週進明%鐘大平%週琪%彭鞦平%潘鳳%何穎%王雪%樑後傑
주진명%종대평%주기%팽추평%반봉%하영%왕설%량후걸
结肠癌%糖皮质激素受体%地塞米松%奥沙利铂%氟脲嘧啶
結腸癌%糖皮質激素受體%地塞米鬆%奧沙利鉑%氟脲嘧啶
결장암%당피질격소수체%지새미송%오사리박%불뇨밀정
Colon carcinoma%Glucocorticoid receptor%Dexamethasone%Oxaliplatin%5-fluorouracil
目的:检测糖皮质激素受体在结肠癌组织及细胞株中的表达,探讨地塞米松共处理或预处理24h,结肠癌细胞株对奥沙利铂和氟脲嘧啶化疗敏感性的变化.方法:采用免疫组化检测糖皮质激素受体在61例结肠癌组织标本及4种结肠癌细胞株中的表达;Hoechst33342染色、流式细胞仪检测体外地塞米松对结肠癌细胞株的凋亡诱导作用;以MTT法检测地塞米松共处理或预处理24h后.结肠癌Lovo细胞株对奥沙利铂和氟脲嘧啶化疗敏感性的变化.结果:在57.3%的结肠癌组织标本中糖皮质激素受体呈阳性表达,在四种结肠癌细胞株中仅Lovo和HCT-116表达糖皮质激素受体,HT-29和SW-480细胞不表达.单独应用地塞米松后,对糖皮质激素受体阳性的Lovo和HCT-116细胞有较强的促凋亡作用,对不表达糖皮质激素受体的HT-29和SW-480细胞作用则不明显.以1×10~(-4)mol/L的地塞米松处理Lovo细胞24h,或与奥沙利铂共处理可使奥沙利铂的IC50从(13.7±1.3)μg/mL降低至(5.9±0.6)μg/mL和(4.8±0.7)μg/mL;同样处理可使氟脲嘧啶的IC50从(72.2±8.1)μg/mL降低至(21.1±4.1)μg/mL和(18.6±4.0)μg/mL.结论:部分结肠癌组织及细胞株表达糖皮质激素受体.地基米松体外作用能够促进糖皮质激素受体阳性的结肠癌细胞发生凋亡,与奥沙利铂和氟脲嘧啶预处理或共处理后可以增加结肠癌细胞的化疗敏感性.
目的:檢測糖皮質激素受體在結腸癌組織及細胞株中的錶達,探討地塞米鬆共處理或預處理24h,結腸癌細胞株對奧沙利鉑和氟脲嘧啶化療敏感性的變化.方法:採用免疫組化檢測糖皮質激素受體在61例結腸癌組織標本及4種結腸癌細胞株中的錶達;Hoechst33342染色、流式細胞儀檢測體外地塞米鬆對結腸癌細胞株的凋亡誘導作用;以MTT法檢測地塞米鬆共處理或預處理24h後.結腸癌Lovo細胞株對奧沙利鉑和氟脲嘧啶化療敏感性的變化.結果:在57.3%的結腸癌組織標本中糖皮質激素受體呈暘性錶達,在四種結腸癌細胞株中僅Lovo和HCT-116錶達糖皮質激素受體,HT-29和SW-480細胞不錶達.單獨應用地塞米鬆後,對糖皮質激素受體暘性的Lovo和HCT-116細胞有較彊的促凋亡作用,對不錶達糖皮質激素受體的HT-29和SW-480細胞作用則不明顯.以1×10~(-4)mol/L的地塞米鬆處理Lovo細胞24h,或與奧沙利鉑共處理可使奧沙利鉑的IC50從(13.7±1.3)μg/mL降低至(5.9±0.6)μg/mL和(4.8±0.7)μg/mL;同樣處理可使氟脲嘧啶的IC50從(72.2±8.1)μg/mL降低至(21.1±4.1)μg/mL和(18.6±4.0)μg/mL.結論:部分結腸癌組織及細胞株錶達糖皮質激素受體.地基米鬆體外作用能夠促進糖皮質激素受體暘性的結腸癌細胞髮生凋亡,與奧沙利鉑和氟脲嘧啶預處理或共處理後可以增加結腸癌細胞的化療敏感性.
목적:검측당피질격소수체재결장암조직급세포주중적표체,탐토지새미송공처리혹예처리24h,결장암세포주대오사리박화불뇨밀정화료민감성적변화.방법:채용면역조화검측당피질격소수체재61례결장암조직표본급4충결장암세포주중적표체;Hoechst33342염색、류식세포의검측체외지새미송대결장암세포주적조망유도작용;이MTT법검측지새미송공처리혹예처리24h후.결장암Lovo세포주대오사리박화불뇨밀정화료민감성적변화.결과:재57.3%적결장암조직표본중당피질격소수체정양성표체,재사충결장암세포주중부Lovo화HCT-116표체당피질격소수체,HT-29화SW-480세포불표체.단독응용지새미송후,대당피질격소수체양성적Lovo화HCT-116세포유교강적촉조망작용,대불표체당피질격소수체적HT-29화SW-480세포작용칙불명현.이1×10~(-4)mol/L적지새미송처리Lovo세포24h,혹여오사리박공처리가사오사리박적IC50종(13.7±1.3)μg/mL강저지(5.9±0.6)μg/mL화(4.8±0.7)μg/mL;동양처리가사불뇨밀정적IC50종(72.2±8.1)μg/mL강저지(21.1±4.1)μg/mL화(18.6±4.0)μg/mL.결론:부분결장암조직급세포주표체당피질격소수체.지기미송체외작용능구촉진당피질격소수체양성적결장암세포발생조망,여오사리박화불뇨밀정예처리혹공처리후가이증가결장암세포적화료민감성.
Objective: To examine the expression of glucocorticoid receptor in human colon cancinoma tis-sues and call lines and to explore the survival of colon cancer cell lines treated with dexamethasone alone or in combination with 5-Fu and L-OHP in a way of dexamethasone pretreatment or co-administration in vitro.Methods: The expression of glucocorticoid receptor was detected in 61 cases of colon cancer tissue samples and 4 types of colon cancer cell lines by immunohistochemistry. Apoptosis was detected by Hoechst33342 staining and flow cytometry. MTT assay was employed to detect the chemosensitivity of colon carcinoma cells to L-OHP and 5-Fu with dexamethasone pretreatment for 24 hours or co-administretion. Results: Positive GR expression was found in 57.3% colon cancer tissue samples and in Lovo and HCT-116 cell lines, not in HT-29 and SW-480. Apoptosis was detected in GR-expressed Lovo and HCT-116 cells at 72 hours after 1×10~(-4)mol/L Dex treatment, and the rates of apoptosis were higher than those in the control groups without Dex (P<0.01),GR-negative cells, HT-29 and SW-480 even treated with 1 × 10~(-4)mol/L Dex for 72 hours. Pretreatment and co-administration for Lovo cells with 1×10~(-4)mol/L Dex could decrease the IC50 of L-OHP from 13.7±1:1.3μg/mL to 5.9±0.6μg/mL and 4.8±0.7μg/mL, respectively. IC50 of 5-Fu was decreased from 72.2±8.1 μg/mL to 21.1±4.1μg/mL and 18.6±4.0μg/mL, respectively. Conclusion: There is expression of glucocorticoid receptor in part of colon carcinoma tissue samples and cell lines. Apoptosis does occur in GR-expressed Lovo and HCT-116 cells induced by dexamethasone in vitro. Pretreatment for 24h and co-administration with Dex can increase the chemosensitivity of Lovo cells to L-OHP and 5-Fu.