CAJ | 학술논문

目的：检测人细胞分裂控制蛋白4（hCDC4）在口腔鳞状细胞癌（OSCC）中的表达情况，分析其与临床病理参数之间的相关性。方法收集52例手术切除的 OSCC 组织及12例正常组织，运用免疫组织化学技术检测 hCDC4表达情况，分析 hC‐DC4蛋白表达与临床病理参数之间的相关性。应用 hCDC4‐siRNA 瞬时转染 OSCC 细胞系 Tca8113，M TT 及蛋白免疫印迹（Western blot）检测细胞增殖能力及 c‐Myc 和 Cyclin E 蛋白表达变化。结果 hCDC4蛋白在正常组织中的表达显著高于对应的OSCC 组织（83．3％ vs ．25．0％，P＜0．05）；hCDC4蛋白低表达与较大肿瘤直径（≥4 cm）和高临床分期（Ⅲ＋Ⅳ）显著相关（P ＜0．05）；敲低 Tca8113细胞中 hCDC4表达，导致细胞增殖能力显著增强（P＜0．05）以及 c‐Myc 和 Cyclin E 蛋白蓄积。结论 hC‐DC4表达缺失导致 c‐Myc 和 Cyclin E 蛋白蓄积可能是促进肿瘤进展的重要因素。
목적：검측인세포분렬공제단백4（hCDC4）재구강린상세포암（OSCC）중적표체정황，분석기여림상병리삼수지간적상관성。방법수집52례수술절제적 OSCC 조직급12례정상조직，운용면역조직화학기술검측 hCDC4표체정황，분석 hC‐DC4단백표체여림상병리삼수지간적상관성。응용 hCDC4‐siRNA 순시전염 OSCC 세포계 Tca8113，M TT 급단백면역인적（Western blot）검측세포증식능력급 c‐Myc 화 Cyclin E 단백표체변화。결과 hCDC4단백재정상조직중적표체현저고우대응적OSCC 조직（83．3％ vs ．25．0％，P＜0．05）；hCDC4단백저표체여교대종류직경（≥4 cm）화고림상분기（Ⅲ＋Ⅳ）현저상관（P ＜0．05）；고저 Tca8113세포중 hCDC4표체，도치세포증식능력현저증강（P＜0．05）이급 c‐Myc 화 Cyclin E 단백축적。결론 hC‐DC4표체결실도치 c‐Myc 화 Cyclin E 단백축적가능시촉진종류진전적중요인소。
Objective To investigate human cell division control protein 4(hCDC4) expression and its correlation with the clini‐copathological features in oral squamous cell carcinoma(OSCC) .Methods We freshly collected 52 samples of surgically resected OSCC tissues and 12 samples of normal tissues .hCDC4 expression in the samples was detected by immunohistochemical staining . The correlation between hCDC4 protein expression and clinicopathological feature was analysed .OSCC cells and Tca8113 were transfected with hCDC4‐siRNA ,cell proliferation and c‐Myc and Cyclin E protein expression were determined by using M TT and Western blot .Results The hCDC4 protein expression in normal tissues was significantly up‐regulated compared to those in OSCC tissues (83 .3% vs .25 .0% ,P < 0 .05) .Clinicopathological analysis revealed that reduced hCDC4 expression was associated with large tumor size ( ≥ 4 cm) and high clinic stage ( Ⅲ + Ⅳ ) (P< 0 .05) .hCDC4 knockdown by siRNA led to increased cell prolifera‐tion and c‐Myc and Cyclin E protein accumulation in Tca8113 cells .Conclusion Loss of hCDC4 may promote tumor progression by resulting in c‐Myc and Cyclin E protein accumulation in OSCC .