浅蓝菌素诱导口腔鳞状细胞癌细胞凋亡的实验研究

目的 :观察浅蓝菌素诱导口腔鳞状细胞癌细胞凋亡作用 ,探讨浅蓝菌素抗癌的可能性。方法 :TCA 83细胞经浅蓝菌素 (10 μg/ml)处理 2 4h后 ,提取基因组DNA ,行DNA凝胶电泳。舌癌新鲜组织经浅蓝菌素(10 μg/ml)处理 2 4h后 ,行原位细胞凋亡染色 (TUNEL)。 结果 :DNA凝胶电泳得到典型的梯状DNA电泳图 ,TUNEL分析显示 ,浅蓝菌素处理组癌细胞凋亡率明显高于未经浅蓝菌素处理的癌细胞凋亡率 (P <0 .0 0 0 1) ,浅蓝菌素诱导高分化鳞状细胞癌凋亡的作用更强。结论 :浅蓝菌素可直接诱导口腔鳞状细胞癌细胞发生凋亡 ,为脂肪酸合酶抑制剂的临床应用提供了直接的参考。     

头颈部鳞状细胞癌增殖活性研究现状

肿瘤增殖活性是反映肿瘤细胞动力学一个重要指标。本文综述了头颈部鳞状细胞癌增殖活性研究的主要方法及其优缺点，展示了增殖活性检测与头颈部鳞癌恶性程度，治疗及预后关系的研究现状。     

头颈部鳞状细胞癌干细胞的研究进展

肿瘤干细胞假说认为,只有一小部分细胞可维持肿瘤的生长,这一小部分细胞被称为“肿瘤干细胞”,其他的大部分细胞只有有限的或根本没有生长潜能。在头颈部鳞状细胞癌在内的多种肿瘤中已经初步鉴定和分离出了肿瘤干细胞。本文就CD44阳性细胞、醛脱氢酶阳性细胞、侧群细胞和八聚体4／nanog／CD133阳性细胞等与头颈部鳞状细胞癌干细胞相关的研究现状作一综述。     

信号转导蛋白P65与放疗诱导口腔鳞状细胞癌细胞凋亡的关系

目的 探讨不同剂量的X射线对口腔鳞状细胞癌(OSCC)细胞中信号转导蛋白P65表达的影响以及P65与放疗诱导口腔鳞状细胞癌细胞凋亡的关系.方法 人舌鳞癌Tca8113细胞复苏后,在37℃,5%CO2的孵箱中培养.共分对照组、2、4、6、8、10 Gy剂量组,待细胞长至对数生长期后,对细胞分别应用上述照射剂量一次性照射....     

减毒5-氟尿嘧啶乳糖苷衍生物的合成及抗口腔鳞状细胞癌活性的实验研究

目的 为降低5-氟尿嘧啶(5-FU)毒性,设计并合成了5-FU乳糖苷衍生物,并初步探究其抗肿瘤活性.方法 采用Vorbrüggen法合成5-FU乳糖苷衍生物,通过高分辨质谱(HRMS)、核磁共振氢谱(1HNMR)、核磁共振碳谱(13CNMR)、异核多量子相干谱(HMQC)及异核多键相关谱(HMBC)表征其结构,并用细胞...     

头颈部鳞状细胞癌及口腔癌的杂色体畸变

头颈部鳞状细胞癌和口腔癌的发生涉及到遗传物质的畸变。许多染色体和基因发生了畸变。这些畸变在肿瘤的发生中起着重要作用。细胞遗传学研究证实第３,９,１１,１３和１７号的染色体出现染色体的畸变。这些研究发现在临床上能提高检测潜在恶性病损的敏感性,有利于疾病的诊断和预后的预测,并为基因治疗提供了理论依据。     

染色体异常与口腔和头颈部鳞状细胞癌

现已查明在口腔癌和头颈部鳞状细胞癌中存在着多种肿瘤相关基因的异常改变,特别是染色体1,3,8,9,11,13,17区域的基因改变,包括杂合子丢失、等位基因失调以及相应的抑癌基因和癌基因的异常表达等。     

白花丹素通过ROS介导的JNK通路诱导舌鳞状细胞癌细胞凋亡

目的: 探究白花丹素诱导舌鳞状细胞癌细胞凋亡的分子机制。方法: CCK-8实验检测白花丹素对舌鳞状细胞癌细胞增殖的影响,流式细胞术检测舌鳞状细胞癌细胞凋亡率和细胞内活性氧水平,Western blot 检测Bcl-2、Bax和p-JNK蛋白的表达。 结果: CCK-8显示白花丹素有显著的抗舌鳞状细胞癌细胞增殖作用(P<0.001)。流式细胞术显示白花丹素可呈剂量依赖性地促进舌鳞状细胞癌细胞凋亡(P＜0.001),有效刺激舌鳞状细胞癌细胞内产生活性氧(P＜0.001)。Western blot结果显示,白花丹素作用后Bax/Bcl-2的比值升高(P<0.01,P<0.001),p-JNK蛋白表达随着作用时间延长逐渐升高(P＜0.05,P＜0.01,P＜0.001)。然而,当我们使用活性氧清除剂NAC后,p-JNK蛋白表达和细胞凋亡率都被显著逆转(P<0.001,P<0.001)。 结论: 白花丹素可以有效抑制舌鳞状细胞癌细胞的增殖,此外白花丹素可以通过活性氧介导的JNK途径诱导舌鳞状细胞癌细胞凋亡。     

常见免疫抑制剂在头颈部鳞状细胞癌的应用进展

头颈部鳞状细胞癌是头颈部最常见的恶性肿瘤,因其发病率和病死率逐年增高,并且目前传统的治疗方式仍然存在着许多并发症,因此研究一种新的治疗方式来提高头颈部鳞状细胞癌的治疗效果,并降低并发症出现的可能性是很有必要的.随着免疫检查点抑制剂的发展,将其运用到肿瘤免疫治疗中提供了长期控制一些恶性肿瘤的可能性.本文将介绍几种目前最常...     

骨桥蛋白与头颈部鳞癌的相关研究进展

骨桥蛋白（osteopontin,OPN）属于小整合素结合配体N端联结糖蛋白（small integrin binding ligand N-linked glycoprotein,SIBLING）家族。1979年,作为一种恶性转化上皮细胞的分泌蛋白首次被Senger等发现并分离。此后,发现该蛋白具有多种生物学功能,因其具有连接骨细胞和骨细胞外基质的功能,最终被命名为骨桥蛋白。近年来,     

1,25(OH)2Vitamin D3 induces elevated expression of the cell cycle inhibitor p18 in a squamous cell carcinoma cell line of the head and neck

BACKGROUND: 1Alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2) Vitamin D(3)] induces growth inhibition in squamous cell carcinoma (SCC) cell lines of the head and neck by arresting the cells in the G0/G1 phase of the cell cycle, probably due to an enhanced expression of p21, which could be demonstrated in other cell lines (JPPA, SCC9) before. In SCC25, a SCC cell line isolated from tongue, growth inhibition but no overexpression of p21 was detected. The retinoblastoma gene, as a direct target of G1 cyclin-CDK complexes, showed an obvious shift from the hyperphosphorylated to the hypophosphorylated form under 1,25(OH)(2)Vitamin D(3), which indicates that the growth inhibition takes place in the G0/G1 phase. To explore the possible pathway of growth inhibition in SCC25 we investigated other cell cycle inhibitors (p18, p19, p27). METHODS: Synchronized cells were treated with 1,25(OH)(2)Vitamin D(3) over 96 h. The cell cycle status and expression of cell cycle-regulating proteins was determined by fluorescence-activated cell sorting (FACS) and Western blotting. An overexpression of p18 in 1,25(OH)(2)Vitamin D(3) vs. ethanol-treated cells was determined until 30 h in SCC25. No influence was detectable on the expression of p27 and p19. CONCLUSION: One mechanism by which 1,25(OH)(2)Vitamin D(3) controls cell growth might be the upregulation of p21. As p21 was unsusceptible to 1,25(OH)(2)Vitamin D(3) in SCC25, other inhibiting proteins were necessary to be tested. The proven upregulation of p18 seems to be the responsible step for growth inhibition of 1,25(OH)(2)Vitamin D(3) in SCC25.     

Apoptotic mechanism of paclitaxel-induced cell death in human head and neck tumor cell lines

Background:  Paclitaxel (taxol) is clinically used to treat various human tumors. However, the cellular and molecular mechanism regarding apoptotic effect of paclitaxel on head and neck squamous cell carcinoma (HNSCC) remains elusive.
Methods:  The apoptotic effect and the mechanism of paclitaxel on FaDu hypopharyngeal cancer cell line, OEC-M1 gingival cancer cell line, and OC3 betel quid chewing-related buccal cancer cell lines were investigated by morphological observations, cell viability assay, flow cytometry assay and Western blotting methods.
Results:  Rounded-up cell number increased with membrane blebbing as the treatment of paclitaxel (50–500 nM) increased from 24 to 48 h among these cell lines. In cell viability assay, cell surviving rate significantly decreased from 87 to 27% as the dosage and duration of paclitaxel treatment increased ( P  <   0.05). Flow-cytometry analysis further demonstrated that 50 nM paclitaxel induced G2/M phase cell arrest among these cell lines within 8 h treatment, and then G2/M phase cell fraction significantly decreased as subG1 phase cell fraction significantly increased after 24 h treatment ( P  <   0.05), suggesting that cells underwent apoptosis. Furthermore, the activated caspases-8, -9, -3, -6 and poly ADP-ribose polymerase cleavage could all be significantly detected in FaDu, OEC-M1 and OC3 cells ( P  <   0.05).
Conclusion:  Paclitaxel activated cell cycle arrest and caspase protein expressions to induce apoptosis in HNSCC cell lines.     

Concomitant leukoplakia in patients with oral squamous cell carcinoma

OBJECTIVE: There is an ongoing debate on the prevalence of premalignant lesions, in particular leukoplakia, at the time of diagnosis of an oral squamous cell carcinoma (OSCC). The aim of the present study was to determine the presence of concomitant leukoplakia in 100 patients with OSCC, and to evaluate possible differences in clinical and histopathological parameters of the OSCC between those with or without concomitant leukoplakia.PATIENTS AND METHODS: One hundred consecutive patients, 61 men and 39 women, with a histologically proven OSCC were screened on the presence of leukoplakia. Four groups were distinguished: (I) leukoplakia adjacent to the OSCC, (II) combination of leukoplakia adjacent to the OSCC, and leukoplakia at another oral site, (III) leukoplakia present at another oral site, but not adjacent to the OSCC, and (IV) no leukoplakia present.RESULTS: In 47 (47%) patients with OSCC the presence of concomitant leukoplakia was observed. Thirty-six (36%) patients had a leukoplakia adjacent to the OSCC (groups I and II), of which eight (8%) patients (group II) also had a leukoplakia present at another oral site. Eleven (11%) patients (group III) had no leukoplakia adjacent to the OSCC, but a leukoplakia present at another oral site. Fifty-three (53%) patients (group IV) with OSCC had no concomitant leukoplakia present. No differences were noted between men and women, nor was there any preference for an oral subsite with regard to the carcinoma. There were no statistically significant differences in clinical and histopathological presentation of OSCC's between those with or without concomitant leukoplakia.CONCLUSION: Almost 50% of oral squamous cell carcinomas are presumably associated with or preceded by leukoplakia. Early detection and active management of patients with oral leukoplakia may prevent the true development of a number of oral squamous cell carcinomas.     

二甲双胍治疗头颈部鳞状细胞癌机制的研究进展

头颈部鳞状细胞癌是全球第六大常见癌症,尽管治疗方法逐渐改善,其5年生存率仍仅为约63%。目前的治疗策略均带有不同程度的不良反应影响患者的生存质量。因此,找到一种毒性低、安全性高的治疗方法至关重要。二甲双胍是双胍类降糖药。研究表明,除降糖作用外,二甲双胍还可抑制多种癌症的发生与发展。二甲双胍抗头颈部鳞状细胞癌的机制可能包括降低胰岛素水平、抑制mTOR信号通路、抑制癌症干细胞、诱导细胞周期停滞并促进凋亡、免疫调节及增强辅助治疗效果等。本文结合现有文献就二甲双胍抗头颈部鳞状细胞癌可能的机制进行综述。     

基于Oncomine数据库的数据挖掘在头颈鳞状细胞癌研究中的应用实例

目的：利用Oncomine数据库结合自身样本验证,获取靶分子钙调蛋白在头颈鳞状细胞癌（HNSCC）中的表达信息。方法???利用Oncomine数据库挖掘钙调蛋白在HNSCC中转录水平的变化,采用反转录聚合酶链反应、免疫印迹技术在本地区小样本队列中验证其转录及蛋白表达水平。结果钙调蛋白在Oncomine数据库大多数HNSCC队列中呈现转录水平的高表达,少部分呈现低表达;本地区样本结果显示,钙调蛋白在转录及蛋白表达水平均呈现高表达。结论??Oncomine数据库大样本量数据的挖掘并结合本地区样本的验证,能迅速准确地获取钙调蛋白在HNSCC中表达的相关信息,为后续的深入研究奠定基础。     

MYO5A 35号外显子跳跃对头颈鳞状细胞癌患者的预后相关研究

目的:探讨MYO5A基因在头颈鳞状细胞癌(head and neck squamous cell carcinoma, HNSCC)中作为预后分子标志物的潜力。方法:从TCGA数据库下载HNSCC队列的RNA-Seq数据及相应的临床数据,单变量Cox回归分析MYO5A与患者预后之间的关系。从TCGA SpliceSeq数据库下载MYO5A基因的可变剪接类型,根据剪接百分比(percent spliced in,PSI)值识别差异性表达的MYO5A基因的可变剪接,并分析其与HNSCC患者预后的相关性。最后通过RT-PCR和Sanger测序在细胞系及徐州医科大学附属医院临床样本中进一步验证。结果:MYO5A基因在HNSCC队列中显著高表达,但MYO5A基因整体表达水平并不能作为独立的HNSCC预后风险指标。MYO5A 35号外显子跳跃在HNSCC中发生频率增加,且与预后密切相关。MYO5A 35号外显子跳跃在细胞系及临床样本中均得到了验证。结论:MYO5A 35号外显子跳跃而不是MYO5A基因整体表达水平可作为HNSCC预后独立的分子标志物。