miR-219在舌鳞状细胞癌中的表达及意义研究

目的 探讨miR-219在舌鳞状细胞癌(Tongue squamous cell carcinoma,TSCC)中的表达及其在TSCC发生发展中的作用。方法 利用qRT-PCR检测miR-219在26例TSCC组织及对应癌旁组织标本、舌磷癌细胞SCC-15及正常口腔黏膜细胞中的表达。在舌磷癌细胞SCC-15中转染miR-219基因,用MTT法、克隆形成实验、Transwell细胞迁移及侵袭实验检测miR-219过表达对舌磷癌细胞SCC-15增殖、克隆形成、迁移及侵袭的影响。结果 qRT-PCR结果显示,miR-219在TSCC组织中的表达水平明显低于对应正常癌旁组织(P＜0.001),舌磷癌细胞SCC-15中miR-219的表达水平亦低于正常口腔黏膜细胞(P＜0.05)。MTT结果表明,转染miR-219后,与对照组相比,舌磷癌细胞SCC-15的增殖受到明显抑制(P＜0.05)。克隆形成实验发现,miR-219过表达明显抑制了SCC-15细胞的克隆形成能力(P＜0.05)。同时miR-219上调也明显抑制了舌磷癌细胞SCC-15迁移及侵袭能力(P＜0.05)。结论 在TSCC中miR-219表达降低;miR-219上调可抑制舌磷癌细胞SCC-15的增殖、克隆、迁移及侵袭能力。     

miR -22抑制食管鳞状细胞癌细胞侵袭和转移

目的:探讨微小RNA-22(miR-22)对食管鳞状细胞癌细胞侵袭和转移的影响。方法:采用实时定量RT-PCR检测miR-22在食管鳞状细胞癌细胞系中的表达。过表达miR-22后应用Transwell小室、MTT增殖及划痕试验分析对食管鳞状细胞癌细胞侵袭和转移能力的影响。结果:在食管鳞状细胞癌细胞系中miR-22的表达比正常对照明显降低。此外,过表达miR-22可明显抑制食管鳞状细胞癌细胞系Eca109和TE-1细胞增殖、侵袭和转移能力。结论:miR-22作为肿瘤抑制小片段RNA可以抑制食管癌细胞的侵袭和转移。本研究有助于了解miR-22在食管鳞状细胞癌中的功能,为食管鳞状细胞癌治疗提供新靶点。     

EZH2基因在子宫颈鳞状细胞癌中的表达及其意义

 目的　探讨EZH2基因在子宫颈鳞状细胞癌（简称：鳞癌）组织中的表达及其临床意义。方法　采用反转录-聚合酶链反应（RT-PCR）方法检测21例正常子宫颈组织、27例子宫颈上皮内瘤变（CIN）及48例子宫颈鳞癌组织中EZH2 mRNA的表达,并分析EZH2与各临床病理参数之间的关系。结果　EZH2 mRNA在子宫颈鳞癌中的表达为（1.67±0.01）,明显高于正常子宫颈组织（0）和CIN组织（0.36±0.02）（均P＜0.01）;EZH2 mRNA在子宫颈鳞癌中表达与患者年龄无明显相关性（P＞0.05）,而与组织学分期、临床病理分期、浸润深度及淋巴结转移有显著相关性（均P＜0.01）。结论　EZH2在子宫颈鳞癌中高表达,提示其在子宫颈鳞癌发生、发展过程中可能起重要作用,有可能成为子宫颈鳞癌一种新的肿瘤标志物。     

miR-219调控PRKCI表达在舌鳞状细胞癌中作用和机制

目的 探讨PRKCI与miR-219表达的相关性以及对舌鳞状细胞癌的细胞增殖、侵袭和转移的影响。方法 利用双荧光素酶报告基因实验对预测的靶基因进行验证, 用qRT-PCR和Western blot实验检测外源过表达miR-219对舌鳞状细胞癌细胞中转染的PRKCI基因和蛋白表达的影响。最后在过表达miR-219的稳转细胞系中再过表达PRKCI, 利用MTT法、细胞平板克隆实验、划痕实验和Transwell小室法分析PRKCI对miR-219抑制舌鳞状细胞癌细胞增殖、克隆形成能力、迁移能力和侵袭能力的逆转效果。通过qRT-PCR法检测舌鳞状细胞癌组织中PRKCI基因的表达情况并进一步分析PRKCI和miR-219之间的关系。结果 通过生物信息学分析预测得到miR-219下游靶基因为PRKCI。双荧光素酶报告基因实验结果显示miR-219能够降低野生型PRKCI报告基因载体的荧光活性。此外qRT-PCR实验和Western blot实验也显示miR-219能够下调PRKCI在舌鳞状细胞癌细胞中的表达。MTT结果显示过表达PRKCI能够逆转miR-219对舌鳞状细胞癌细胞增殖活性的抑制效应, 进一步通过细胞平板克隆实验、划痕实验以及Transwell实验证明PRKCI过表达能够逆转miR-219对TSCC细胞增殖、侵袭和转移的抑制效应。结论 miR-219通过直接靶向PRKCI、负调控PRKCI的表达发挥抑制肿瘤的作用。在舌鳞状细胞癌组织中, miR-219与PRKCI的表达呈负相关。     

JMJD3和EZH2在45例喉鳞状细胞癌中的表达及其临床意义分析

摘 要：［目的］ 研究JMJD3及EZH2在喉鳞状细胞癌中的表达及其临床意义。［方法］ 收集45例喉鳞状细胞癌患者的喉癌、癌旁组织切片及相关临床特征数据,采用免疫组化染色法检测标本。采用?字2检验或Fisher确切概率法分析JMJD3与EZH2在喉鳞状细胞癌中的表达及其与临床特征的相关性。Kaplan-Meier分析JMJD3及EZH2与喉鳞状细胞癌3年总生存率的关联。［结果］ JMJD3及EZH2在喉癌组织中表达阳性率明显高于癌旁组织（?字2=9.800、10.766,P均<0.01）。在喉癌组织中,JMJD3及EZH2的表达与患者肿瘤分化程度、肿瘤部位、淋巴结转移、临床分期相关。JMJD3阳性表达及阴性表达患者的3年生存率分别为68.2%、87.0%（?字2=2.631,P=0.105）;EZH2阳性表达及阴性表达患者的3年生存率分别为70.8%、85.7%（?字2=1.688,P=0.194）。JMJD3和EZH2在喉癌中的表达呈正相关（P=0.02）。［结论］ 在喉鳞状细胞癌中JMJD3和EZH2均起了促癌基因的作用。JMJD3及EZH2的高表达与喉鳞状细胞癌的发生、转移、恶性程度存在显著关联,两者的失衡共同促进了喉癌的发生发展。     

舌鳞状细胞癌生物学特性及其防治实验研究

上海第二医科大学附属第九人民医院口腔医学研究所何荣根、邱蔚六教授等科研人员，于1981年率先在国内建立了第一株口腔癌——人舌鳞状细胞癌Tea8113细胞系。该成果获得1994年度国家教委科技进步一等奖（甲类）。该项目具体科学技术内容可归纳如下：1．建立了人舌鳞癌Tea8113细胞系：于1981年建立，该细胞系组织来源明确，取材病期早，临床经过单纯，未经任何放疗、化疗处理，对于研究人体口腔鳞癌生物学特性具有良好的代表性，已于1982年通过专家鉴定。该细胞生长稳定，至今已13年以上，群体倍增时间38小时，分裂指数高峰值为61．‰。2．…     

miR-4465调控EZH2的表达抑制胃癌细胞增殖、侵袭和迁移的机制探讨

目的:探讨miR-4465通过调控EZH2的表达对胃癌细胞增殖、侵袭和迁移的影响。方法:qRT-PCR检测胃癌组织和细胞系中miR-4465的表达水平;在MKN45细胞中过表达miR-4465或沉默EZH2,采用CCK-8和Transwell检测MKN45细胞增殖活力、迁移和侵袭能力;Western blotting检测EZH2、E-cadherin、N-cadherin和Vimentin的表达情况;双荧光素酶报告基因检测miR-4465与EZH2的相互作用。结果:与癌旁组织相比,miR-4465在胃癌组织中的表达降低,在胃癌细胞系(MCC-803、SGC7901、MKN45)中的表达水平显著低于人永生化胃细胞RGM-1,且在MKN45细胞系中的表达低于其他细胞。过表达miR-4465明显抑制MKN45细胞增殖、迁移、侵袭和上皮间质转化(epithelial-mesenchymal transition, EMT);双荧光素酶报告基因结果证实,miR-4465直接靶向作用于EZH2的3’-UTR;进一步实验证明,同时沉默miR-4465和EZH2能够恢复沉默EZH2对MKN45细胞增殖...     

舌鳞状细胞癌组织中c-erbB-2异常表达的临床意义研究

目的:探讨舌鳞状细胞癌(squamouscell carcinoma, SCC)中c- erbB -2 表达的临床价值。方法:回顾性分析舌SCC -76 例临床病理资料。对常规HE染色检测证实有肿瘤及瘤旁正常黏膜同时存在的原始蜡块连续切片2张,1 张c erbB 2免疫组织化学染色, 1 张备用。结果:经免疫组织化学检测, c- erbB- 2 阳性者49 例(64 .5%),瘤旁黏膜阳性者15 例( 19. 7%)。c erbB 2基因过度表达与患者生存时间差异有统计学意义,P<0 05;c- erbB -2与舌SCC的转移差异也有统计学意义,P<0 01;c- erbB- 2基因异常表达与舌SCC分期有相关性,P<0 05;c- erbB- 2基因异常表达与舌SCC分级无相关性。c- erbB- 2基因异常表达与舌SCC大小、原发灶的控制、性别、年龄无相关性;c -erbB- 2基因异常表达与局部复发无相关性。结论:在舌SCC中c- erbB- 2基因过度表达可缩短患者的生存时间,并有促进肿瘤细胞转移的可能性。     

口腔舌鳞状细胞癌的临床分析

目的:总结口腔舌鳞状细胞癌的治疗经验以指导临床。方法:回顾性分析1975年1月～2000年12月初次在我院诊治的329例口腔舌鳞状细胞癌患者的临床资料。T1病变82例,T2病变190例,T3病变43例,T4病变14例。综合治疗186例,单纯手术84例,单纯放疗59例。结果:91例患者组织学检查颈部淋巴结转移,其中Ⅰ区淋巴结转移36例,Ⅱ区淋巴结转移65例,Ⅲ区淋巴结转移18例,Ⅳ区淋巴结转移10例。T1病变患者5年和10年累积生存率分别为72.23%和65.21%,T2分别为38.38%和33.11%,T3分别为10.63%和10.63%,T4分别为7.14%和7.14%(P=0.0000,Logrank=75.99)。单纯手术组患者5年和10年累积生存率分别为56.13%和47.28%,单纯放疗组分别为17.49%和17.49%,综合治疗组分别为43.51%和39.04%(P=0.0000,Logrank=42.23)。结论:口腔舌鳞状细胞癌早期病变可考虑单纯手术,而中晚期应给予综合治疗,对中晚期cN0患者可考虑扩大的肩胛舌骨肌上清扫术。     

舌鳞状细胞癌p53基因突变的研究

现已发现 ,ｐ５３基因的突变是人类肿瘤发生发展过程中最常见的基因事件 ,与口腔癌发生发展的关系密切。本研究采用单链构象多态性分析（ＰＣＲ -ＳＳＣＰ）技术 ,对３５例舌鳞癌组织及２０例正常舌粘膜的 ｐ５３基因第７ ,８外显子和第７内含子突变进行检测 ,并分析它与舌鳞癌的发生发展 ,包括临床分期、细胞分化程度、淋巴结转移的关系 ,探讨上述检测指标作为指导舌癌治疗及判断预后手段的可能性。１材料与方法１ １标本来源收集本科１９９３～１９９６年舌鳞状细胞癌术后新鲜组织标本３５例 ,其中５例系活检术后标本。所有标本均作常规石…     

Mesenchymal stem cell‐derived CCN2 promotes the proliferation,migration and invasion of human tongue squamous cell carcinoma cells

Recent studies have demonstrated that mesenchymal stem cells (MSC) exhibit a tropism to tumors and form the tumor stroma. In addition, we found that MSC can secrete different types of factors. However, the involvement of MSC‐derived factors in human tongue squamous cell carcinoma (TSCC) growth has not been clearly addressed. The CCN family includes multifunctional signaling molecules that affect the initiation and development events of various tumors. In our study, we report that CCN2/connective tissue growth factor (CTGF) was the most highly induced among the CCN family members in MSC that were co‐cultured with TSCC cells. To evaluate the relationship between CCN2 and TSCC growth, we downregulated MSC‐derived CCN2 expression with shRNA targeting CCN2 and found that MSC‐secreted CCN2 promotes TSCC cell proliferation, migration and invasion. We also confirmed that MSC‐derived CCN2 partially accelerated tumor growth in vitro. Taken together, these results suggest that MSC‐derived CCN2 contributes to the promotion of proliferation, migration and invasion of TSCC cells and may be a possible therapy target in the future.     

敲低Plk1对人肝癌血管内皮细胞迁移影响研究

目的研究人Polo样激酶1(polo-like kinase 1,Plk1)在人肝癌血管内皮细胞(human hepatocellular carcinoma tumor-derived endothelial cell,TEC)迁移过程中的作用。方法用含有20%胎牛血清的RPMI1640培养基培养TEC细胞,合成Plk1和阴性对照小干扰片段。实验设置Plk1siRNA处理组和siRNA阴性组(对照组)。分别用Plk1siRNA和阴性对照siRNA转染TEC,采用蛋白质印迹法验证Plk1siRNA干扰能否有效降低TEC细胞的Plk1蛋白表达水平;采用Transwell细胞迁移实验和细胞划痕实验评估Plk1siRNA转染后TEC迁移能力的变化。结果蛋白质印迹法检测结果显示,Plk1siRNA转染后TEC细胞中Plk1蛋白表达降低。Transwell细胞迁移实验发现,Plk1siRNA处理组12h穿膜细胞数为130.9±23.0,低于siRNA阴性组的184.9±26.6,t=-5.943,P<0.001。细胞划痕实验显示,Plk1siRNA处理组细胞12h迁移距离为(17.5±7.0)像素,低于siRNA阴性组的(72.6±12.4)像素,t=-6.698,P=0.006;Plk1siRNA处理组细胞24h迁移距离为(70.9±6.9)像素,低于siRNA阴性组的(137.9±18.9)像素,t=-5.761,P=0.016。结论敲低Plk1能显著抑制人肝癌血管内皮细胞的迁移能力,提示Plk1可能在人肝癌血管内皮细胞转移中具有一定作用。     

MicroRNA-373 promotes migration and invasion in human esophageal squamous cell carcinoma by inhibiting TIMP3 expression

Esophageal squamous cell carcinoma (ESCC) is the predominant pathological type of esophageal carcinoma in Asia. MicroRNAs (miRNAs) are a class of 19-22-nucleotide non-coding RNAs acting on target mRNAs that function as either oncogenes or anti-oncogenes. It has been confirmed that miR-373 expression varies among different tumor types. However, its mechanism is still unclear in ESCC. In our current study, we found that miR-373 expression was upregulated in ESCC tissues compared with matched adjacent normal tissues, as well as in the plasma of ESCC patients compared with that of healthy volunteers. Overexpression of miR-373 in ECA109 cells enhanced proliferation, G1-phase cell proportion, migration, and invasion. On the other hand, suppression of miR-373 in KYSE410 cells decreased proliferation, G1-phase cell proportion, migration, and invasion and also improved cell apoptosis. Moreover, we found that TIMP3, which was reported to suppress invasion and metastasis of ESCC, was a direct target of miR-373. Overexpression of miR-373 in ECA109 caused a reduction of TIMP3 mRNA and protein, whereas suppression of miR-373 in KYSE410 led to an increase of TIMP3 mRNA and protein. Introducing TIMP3 in miR-373 over-expressed cells or knocking down TIMP3 in miR-373 suppressed cells could partially abrogate the effect of miR-373 on migration and invasion. Therefore, these results prove that as an oncogene, miRNA-373 would be an important and reliable biomarker for ESCC diagnosis and treatment by targeting TIMP3.     

CD151对人舌鳞癌细胞Tca8113迁移作用的影响

背景与目的:CD151在肿瘤组织中的高表达与肿瘤的转移和预后密切相关,但其具体机制尚不清楚。本研究旨在探讨携带全长正义和反义CD151基因的重组腺相关病毒(rAAV-CD151,rAAV-antiCD151)对人舌鳞癌细胞Tca8113细胞迁移的影响。方法:利用含酶切位点的PCR引物克隆CD151基因,分别呈正向和反向插入包装质粒pAAV,并包装成rAAV-CD151,rAAV-antiCD151,斑点杂交测定病毒滴度;rAAV-CD151与rAAV-antiCD151分别转染Tca8113细胞2周后,Westernblot检测CD151表达,通过Boyden趋化小室研究其对Tca8113细胞迁移的影响。结果:斑点杂交结果显示rAAV-CD151和rAAV-antiCD151病毒滴度分别为2.0×1011pfu/ml,1.0×1011pfu/ml;转染rAAV-CD151后,Tca8113细胞CD151的表达较未转染组增加了108%,细胞迁移数(93.6±11.6)显著高于未转染组和转染rAAV-GFP对照组(53.0±6.6和46.0±7.0,P<0.05);转染rAAV-antiCD151后,Tca8113细胞CD151的表达较未转染组减少了79%,细胞迁移数(24.0±4.4)显著低于未转染组和转染rAAV-GFP对照组(P<0.05)。结论:CD151在肿瘤细胞的迁移中起重要的作用,是肿瘤转移的重要分子基础。携带反义CD151基因的重组腺相关病毒作为一种新的治疗工具,可以特异性阻断肿瘤细胞CD151表达,抑制肿瘤细胞的迁移。     

微小RNA?224对口腔鳞状细胞癌细胞侵袭迁移和KLLN表达的影响

目的探讨微小RNA-224(miR-224)对口腔鳞状细胞癌(OSCC)细胞侵袭迁移和KLLN表达的影响。方法采用实时定量PCR(QPCR)检测正常口腔上皮细胞HOK和OSCC细胞(CAL-27、TSCCa和Tca8113)的miR-224水平,脂质体法向CAL-27细胞转染miR-224模拟物(Mimics组)或阴性对照序列(NC组),另以仅脂质体处理的细胞为对照组,活细胞计数(CCK-8)法、Transwell小室实验和划痕实验评估细胞增殖、侵袭和迁移能力,Western blotting检测KLLN、基质金属蛋白酶(MMP)-2和MMP-9的水平,双荧光素酶报告基因实验验证miR-224对KLLN的靶向调控作用。结果QPCR结果显示,OSCC细胞的miR-224水平较HOK细胞下调(P<0.05),其中CAL-27细胞的miR-224水平最低。Mimics组的miR-224水平为12.325±1.250,高于对照组的1.003±0.058和NC组的1.029±0.072(P<0.05);Mimics组转染24、48 h后的增殖活力低于对照组和NC组(P<0.05);Mimics组的划痕愈合率和穿膜细胞数分别为(23.161±3.609)%和(187.977±19.644)个,低于对照组的(47.372±4.717)%和(352.429±28.372)个及NC组的(45.094±5.651)%和(187.977±19.644)个,差异有统计学意义(P<0.05);Mimics组的KLLN、MMP-2和MMP-9水平低于对照组和NC组(P<0.05)。对照组和NC组上述指标的差异无统计学意义(P>0.05)。MiR-224模拟物对载有突变型KLLN细胞的荧光素酶活性不产生影响,而抑制了野生型KLLN细胞的荧光素酶活性(P<0.05)。结论OSCC细胞的miR-224水平降低且上调miR-224可能通过靶向KLLN来抑制OSCC细胞的迁移侵袭,该miRNA有望成为OSCC的预后生物标志物和治疗靶点。     

PRAF3 induces apoptosis and inhibits migration and invasion in human esophageal squamous cell carcinoma

Background

Diet has long been suspected to impact on breast cancer risk. In this study we evaluated whether the degree of adherence to a Mediterranean diet pattern modifies breast cancer risk amongst Greek-Cypriot women.

Methods

Subjects included 935 cases and 817 controls, all participating in the MASTOS case-control study in Cyprus. The study was approved by the Cyprus National Bioethics Committee. Information on dietary intakes was collected using an interviewer administered 32-item Food Frequency Questionnaire. Information on demographic, anthropometric, lifestyle, and other confounding factors was also collected. Adherence to the Mediterranean Diet pattern was assessed using two a-priory defined diet scores. In addition, dietary patterns specific to our population were derived using Principal Component Analysis (PCA). Logistic regression models were used to assess the association between the dietary patters and breast cancer risk.

Results

There was no association with breast cancer risk for either score, however, higher consumptions of vegetables, fish and olive oil, were independently associated with decreased risk. In addition, the PCA derived component which included vegetables, fruit, fish and legumes was shown to significantly reduce risk of breast cancer (ORs across quartiles of increasing levels of consumption: 0.89 95%CI: 0.65-1.22, 0.64 95%CI: 0.47-0.88, 0.67 95%CI: 0.49-0.92, P trend < 0.0001), even after adjustment for relevant confounders.

Conclusions

Our results suggest that adherence to a diet pattern rich in vegetables, fish, legumes and olive oil may favorably influence the risk of breast cancer. This study is the first investigation of dietary effects on breast cancer risk in Cyprus, a country whose population has traditionally adhered to the Mediterranean diet.     

EZH2和H3K27me3的表达对食管癌细胞迁移和侵袭能力的影响

目的:通过转染Zeste同源物增强子2(enhancer of zeste homolog 2,EZH2)过表达或者敲低载体,探讨EZH2和Lys27位点三甲基化组蛋白H3(histone H3 methylated Lys27,H3K27me3)对食管麟状细胞癌(esophageal squamous cell cancer,ESCC)细胞迁移和侵袭能力的影响.方法:应用实时荧光定量PCR、Western blotting法检测ESCC细胞株KYSE30、KYSE170、TE1、Eca109中EZH2 mRNA水平,以及ESCC细胞过表达或者敲低EZH2对H3 K27me3表达水平的影响.用划痕实验及Transwell侵袭实验分析过表达或者敲低EZH2后ESCC细胞的迁移侵袭能力.用实时荧光定量PCR法分析ESCC细胞过表达及敲低EZH2对MMPs mRNA水平的影响.结果:食管癌Eea109及TE1细胞中EZH2和H3K27me3 mRNA和蛋白水平明显高于KYSE30及KYSE170细胞(P＜0.05).过表达EZH2的食管癌KYSE30及KYSE170细胞H3K27me3蛋白的表达水平显著升高(P＜0.05),敲低EZH2后Eca109及TE1细胞H3 K27 me3蛋白的表达水平明显降低(P＜0.05).过表达EZH2后,KYSE30及KYSE170细胞的穿膜数目明显增多[(281.33±4.10)、(241.67 ±4.04) vs(132.00 ±4.00)、(105.33 ±3.51)个,均P＜0.05]、迁移距离明显增大[(63.6±1.2)、(62.5±2.5)vs (23.0±2.3)、(21.2±1.0) μm,P＜0.05].敲低EZH2后Eca109及TE1细胞的穿膜数目显著减少(均P＜0.05),转染shEZH2后Eca109及TE1细胞迁移的距离明显减小(均P＜0.05).结论:EZH2可增加靶基因启动子上组蛋白H3第27位赖氨酸的三甲基化,并增强ESCC细胞的迁移和侵袭能力.     

Overexpression of DDR2 contributes to cell invasion and migration in head and neck squamous cell carcinoma

BackgroundDiscoidin domain receptor 2 (DDR2) is a unique receptor tyrosine kinase (RTK) that is activated by fibrillar collagens. Although DDR2 contributes to the metastasis of some tumors, its role in head and neck squamous cell carcinoma (HNSCC) remains unknown. The aim of this study was to investigate the expression level, clinical and pathological significance, and biologic function of DDR2 in HNSCC.MethodsReal-time quantitative PCR, western blot, and immunohistochemical staining were employed to assess the expression levels of DDR2 in HNSCC specimens. Adenovirus-mediated overexpression of DDR2 was used to evaluate its consequences on cell proliferation, invasion, migration, and the process of hypoxia-induced epithelial-mesenchymal transition (EMT). Then nude mouse xenograft and tail vein metastasis models were utilized to validate the in vitro results.ResultsDDR2 was highly expressed in high grade HNSCC tissues and lowly expressed in low grade HNSCC tissues, but absent or rarely expressed in cancer-associated normal tissues. Both the frequency and expression intensity of DDR2 were significantly associated with tumor pathologic stage and lymph node metastasis. In vitro, DDR2 overexpression in HNSCC cells failed to alter cell proliferation but markedly accelerates cell invasion and migration as well as hypoxia-induced EMT. In vivo, elevated expression of DDR2 speeds up the metastasis of HNSCC cells to the lung.ConclusionDDR2 plays an important role in HNSCC metastasis, and might be a promising target for future therapies in this type of cancer.