中华口腔医学杂志
中華口腔醫學雜誌
중화구강의학잡지
Chinese Journal of Stomatology
2010年
2期
85-88
,共4页
丁艳平%李曙霞%吴洪儒%张辛燕%汤晓飞%孙正
丁豔平%李曙霞%吳洪儒%張辛燕%湯曉飛%孫正
정염평%리서하%오홍유%장신연%탕효비%손정
半胱氨酸天冬氨酸蛋白酶3%口腔肿瘤%生存素%细胞凋亡
半胱氨痠天鼕氨痠蛋白酶3%口腔腫瘤%生存素%細胞凋亡
반광안산천동안산단백매3%구강종류%생존소%세포조망
Caspase 3%Mouth neoplasms%Survivin%Apoptosis
目的 探讨生存素(survivin)、半胱氨酸天冬氨酸蛋白酶3(caspase-3)在口腔癌发生中的作用,以期为口腔癌的监测和治疗提供参考.方法 选取首都医科大学口腔医学院病理科存档石蜡标本45例,其中口腔白斑伴上皮轻-中度异常增生16例,口腔白斑伴上皮重度异常增生12例,口腔高-中分化鳞状细胞癌17例;正常口腔黏膜组织10例.采用免疫组化SP法对生存素、caspase-3的表达进行检测;脱氧核糖核苷酸末端转移酶介导的原位缺口末端标记法对细胞凋亡指数进行检测.结果 生存素表达在正常黏膜、白斑伴上皮轻-中度异常增生、白斑伴上皮重度异常增生及口腔癌中逐渐增加,阳性细胞率分别为(1.05±1.21)%、(6.06 ±4.87)%、(12.49 ±8.41)%和(21.89±10.45)%;caspase-3的表达在3个病例组中逐渐下降,正常对照、白斑伴上皮轻-中度异常增生、白斑伴上皮重度异常增生及口腔鳞状细胞癌组阳性细胞率分别为(12.37 ±5.48)%、(19.51 ±13.15)%、(9.76±7.83)%和(6.08 ±6.91)%;正常对照、白斑伴轻-中度异常增生、白斑伴重度异常增生及口腔鳞状细胞癌组凋亡指数分别为(0.89 ±0.46)%、(1.29 ±0.63)%、(0.65 ±0.40)%和(0.21 ±0.12)%,前3组与口腔鳞状细胞癌组相比差异有统计学意义(P<0.05).结论 生存素在口腔癌的发生过程中起重要作用,随着生存素表达的增加,caspase-3和凋亡指数呈下降趋势;生存索可能通过抑制caspase-3的表达,从而抑制细胞的凋亡,促进口腔癌的发生.
目的 探討生存素(survivin)、半胱氨痠天鼕氨痠蛋白酶3(caspase-3)在口腔癌髮生中的作用,以期為口腔癌的鑑測和治療提供參攷.方法 選取首都醫科大學口腔醫學院病理科存檔石蠟標本45例,其中口腔白斑伴上皮輕-中度異常增生16例,口腔白斑伴上皮重度異常增生12例,口腔高-中分化鱗狀細胞癌17例;正常口腔黏膜組織10例.採用免疫組化SP法對生存素、caspase-3的錶達進行檢測;脫氧覈糖覈苷痠末耑轉移酶介導的原位缺口末耑標記法對細胞凋亡指數進行檢測.結果 生存素錶達在正常黏膜、白斑伴上皮輕-中度異常增生、白斑伴上皮重度異常增生及口腔癌中逐漸增加,暘性細胞率分彆為(1.05±1.21)%、(6.06 ±4.87)%、(12.49 ±8.41)%和(21.89±10.45)%;caspase-3的錶達在3箇病例組中逐漸下降,正常對照、白斑伴上皮輕-中度異常增生、白斑伴上皮重度異常增生及口腔鱗狀細胞癌組暘性細胞率分彆為(12.37 ±5.48)%、(19.51 ±13.15)%、(9.76±7.83)%和(6.08 ±6.91)%;正常對照、白斑伴輕-中度異常增生、白斑伴重度異常增生及口腔鱗狀細胞癌組凋亡指數分彆為(0.89 ±0.46)%、(1.29 ±0.63)%、(0.65 ±0.40)%和(0.21 ±0.12)%,前3組與口腔鱗狀細胞癌組相比差異有統計學意義(P<0.05).結論 生存素在口腔癌的髮生過程中起重要作用,隨著生存素錶達的增加,caspase-3和凋亡指數呈下降趨勢;生存索可能通過抑製caspase-3的錶達,從而抑製細胞的凋亡,促進口腔癌的髮生.
목적 탐토생존소(survivin)、반광안산천동안산단백매3(caspase-3)재구강암발생중적작용,이기위구강암적감측화치료제공삼고.방법 선취수도의과대학구강의학원병이과존당석사표본45례,기중구강백반반상피경-중도이상증생16례,구강백반반상피중도이상증생12례,구강고-중분화린상세포암17례;정상구강점막조직10례.채용면역조화SP법대생존소、caspase-3적표체진행검측;탈양핵당핵감산말단전이매개도적원위결구말단표기법대세포조망지수진행검측.결과 생존소표체재정상점막、백반반상피경-중도이상증생、백반반상피중도이상증생급구강암중축점증가,양성세포솔분별위(1.05±1.21)%、(6.06 ±4.87)%、(12.49 ±8.41)%화(21.89±10.45)%;caspase-3적표체재3개병례조중축점하강,정상대조、백반반상피경-중도이상증생、백반반상피중도이상증생급구강린상세포암조양성세포솔분별위(12.37 ±5.48)%、(19.51 ±13.15)%、(9.76±7.83)%화(6.08 ±6.91)%;정상대조、백반반경-중도이상증생、백반반중도이상증생급구강린상세포암조조망지수분별위(0.89 ±0.46)%、(1.29 ±0.63)%、(0.65 ±0.40)%화(0.21 ±0.12)%,전3조여구강린상세포암조상비차이유통계학의의(P<0.05).결론 생존소재구강암적발생과정중기중요작용,수착생존소표체적증가,caspase-3화조망지수정하강추세;생존색가능통과억제caspase-3적표체,종이억제세포적조망,촉진구강암적발생.
Objective To investigate the roles of surviving and caspase-3 in the development of oral cancer. Methods Archival tissue sections of 17 oral squamous cell carcinoma(OSCC), 28 oral leukoplakia with dysplasia, 10 normal oral mucosa were obtained from Capital Medical University School of Stomatology for immunohistochemical staining of markers of survivin and caspase-3. The cell apoptosis was detected with terminal dooxynucleotidyl transferase-mediated nucleotide shift enzyme (TdT) mediated d-UTP end labeling (TUNEL). Positively stained cells were counted and analyzed statistically to determine potential relationship between survivin, caspase-3 and cell apoptosis. Results The expression of survivin was faint or negative in normal epithelial cells. The average positive rate of survivin was (1.05± 1.21)% in control group and (21.89 ±10.45)% in OSCC. Caspase-3 was expressed in all the normal mucosa, but it obviously down-regulated in dysplasia and OSCC. The apoptosis index (AI) decreased from (0. 89 ± 0. 46) % in normal mucosa to (0. 21±0. 12)% in OSCC. Conclusions Both survivin and caspase-3 are associated with carcinogenesis of the oral mucosa. Survivin may restrain cell apoptosis by inhibiting caspase-3.
