Knock-down of ABCE1 gene induces G1/S arrest in human oral cancer cells

Purpose: This study aims to explore the clinical characteristics of ATP binding cassette E1 (ABCE1) in oral squamous cell carcinomas (OSCC) and its roles in the proliferation, invasiveness, migration and apoptosis of the human oral squamous cell carcinoma cells CAL-27. Methods: The expression of ABCE1 and its target protein-RNase L, were first studied in tumor tissues of OSCC and adjacent non-tumor tissues. Moreover, CAL-27cells were transfected by ABCE1-specific shRNA, then MTT assay, the transwell and scratch assay were used to study cell proliferation and migration activity; the apoptosis rate and cell cycle distribution were tested by flow cytometry. Western blot and RT-PCR assay were adopted to measure their silencing efficacy. Results: ABCE1 expression is low in the adjacent non-tumor tissues while the expression is high in the oral cancer; the expression is reversely proportional to the differentiation degrees. The expression of RNaseL was in contrary to ABCE1. After transfected with ABCE1-siRNA, the proliferation, invasiveness and migration capabilities of cells decreased significantly whilst the apoptosis rate enhanced greatly (P < 0.01). Meanwhile, the expression of ABCE1 in CAL-27 cells was blocked (P < 0.01) while the expression of RNase L increased significantly (P < 0.01). Conclusion: ABCE1 is closely connected with the pathogenesis and development of oral cancer, which acts through the cellular pathways of 2-5A/RNase L.     

小剂量丙泊酚对食管鳞癌细胞Eca109生物学行为的影响

目的:探讨低剂量丙泊酚对食管鳞癌细胞Eca109的增殖、凋亡、迁移及侵袭等生物学行为的影响。方法:根据预实验结果设置低剂量丙泊酚组,干预食管鳞癌细胞Eca109后,利用MTT、流式细胞术、transwell检测对增殖、凋亡、迁移及侵袭的影响,应用实时荧光定量PCR检测血红素氧合酶1(HO-1)的表达变化。结果:低剂量Eca109可以促进Eca109的增殖、迁移与侵袭并抑制凋亡,实时荧光定量PCR显示干预后HO-1的表达增加且随浓度的增加而增加。结论:低剂量丙泊酚可以促进Eca109的增殖、迁移与侵袭并抑制凋亡,可能与促进HO-1的表达相关。     

Expression of cystatin C and its effect on EC9706 cells in esophageal carcinoma

Objective: To investigate the expression of cystatin C gene and its effect on the proliferation, apoptosis and invasiveness of EC9706 cells in esophageal carcinoma. Methods: 56 cases of esophageal carcinoma were randomly collected from our hospital. Samples of human esophageal carcinomas and matched normal esophageal mucosal epithelium were selected by resection operation from these patients. Expression of cathepsin B and cystatin C in these specimens were determined by immunohistochemistry and qRT-PCR. Next, lentiviral vectors of over-expression and interference for cystatin C gene were constructed, and both were transfected into EC9706 cells, and then the levels of cystatin C mRNA and protein were detected by qRT-PCR and Western blot. The effect of over and low-expressed cystatin C on the proliferation, apoptosis and invasiveness of esophageal carcinoma cells were detected by MTT assay, flow cytometry and Transwell assay. Results: Compared with normal esophageal epithelial tissues, mRNA and protein levels of cathepsin B and cystatin C in esophageal carcinoma tissues were significantly increased (P<0.05). Lentiviral vectors of over-expression and interference for cystatin C gene were successfully transfected into EC9706 cells. Over or low-expression cystatin C had no effect on EC9706 cells proliferation but had a reverse relationship with the apoptosis. However, cystatin C over-expression significantly decreased tumor invasiveness (P<0.05) while the invasiveness of EC9706 cells was significantly enhanced by RNAi-mediated abrogation of cystatin C gene expression (P<0.05). Conclusion: Over-expressed cystatin C could inhibit the invasiveness of esophageal carcinoma cells.     

LINC00659靶向miR-149-5p调控食管鳞癌细胞Eca-109的增殖、迁移、侵袭及放射敏感性

目的 探讨长基因间非编码RNA 00659(LINC00659)是否靶向miR-149-5p调控食管鳞癌Eca-109细胞的增殖、 迁移侵袭及放射敏感性.方法 实时定量PCR(RT-qPCR)分析30对食管鳞癌组织、 对照组织中LINC00659和miR-149-5p表达量.将Eca-109细胞分为si-NC组、si-...     

Smac基因过表达增强顺铂对食管癌Eca109细胞化疗的敏感性

目的:探讨Smac基因过表达对食管癌细胞株Eca109顺铂化疗敏感性的影响。方法:脂质体介导将带有GFP的pcDNA3.1-Smac重组体及带有GFP的pcDNA3.1空白载体转染入食管癌细胞株Eca-109,G418筛选阳性克隆,荧光显微镜下观察转染效率,Western blot检测转染前后细胞内Smac蛋白表达水平的变化。顺铂处理组(1、5、10 mg/L)和顺铂未处理组分别处理转染前后的食管癌细胞株Eca109,Annexin V/PI双染法经流式细胞术检测细胞凋亡率。结果:分别建立稳定表达Smac基因+GFP基因,新霉素抗性基因(neo)+GFP基因的食管癌亚克隆细胞株Eca109/Smac,Eca109/neo。Eca109/Smac的Smac蛋白表达水平明显高于Eca109/neo和Eca109(P<0.05)。在顺铂未处理组,Eca109/Smac、Eca109/neo和Eca109的细胞凋亡率组间无明显统计学差异。在顺铂处理组,顺铂浓度分别为1 mg/L、5 mg/L、10 mg/L,Eca109/Smac的细胞凋亡率明显高于Eca109/neo和Eca109,组间具有统计学差异(P<0.05),且随着顺铂浓度的升高,Eca109/Smac细胞凋亡率随之升高(P<0.05)。Eca109/neo和Eca109组间无明显统计学差异。结论:Smac基因转染未经顺铂处理的Eca109细胞株中不诱发凋亡,在顺铂处理组其过表达能增强Eca109对顺铂的化疗敏感性。     

miR-101 suppresses tumor proliferation and migration,and induces apoptosis by targeting EZH2 in esophageal cancer cells

Aim: To investigate the role of miR-101 in the regulation of tumor proliferation, invasion, apoptosis and to its target gene in human ESCC. Methods: The expression level of miR-101 in Eca109 cell line was determined by real-time polymerase chain reaction (PCR). After transfected with miR-101 mimics and inhibitor, proliferation, migration and apoptosis in ESCC cell line (Eca109) were detected by MTT, cell wound healing assay and flow cytometry, respectively. The expression of EZH2 in Eca109 cell was examined by immunohistochemical staining. Results: We found that miR-101 was significantly down-regulated in ESCC cell than in matched normal esophageal epithelium cell. The expression level of miR-101 was inversely correlated to EZH2 protein expression in ESCC cell. In Eca109 cells, over-expression of miR-101 significantly inhibited the migration and invasion of ESCC cells, and promotes cell apoptosis. Conclusions: These findings suggest that decreased expression of miR-101 might promote metastasis of human ESCC by inducing accumulation of EZH2 protein.     

诱导细胞凋亡青蒿琥酯抗食管癌作用机制研究

 [摘要] 目的 研究青蒿琥酯诱导食管癌细胞凋亡作用及探讨青蒿琥酯抗食管癌作用机制。方法 不同浓度的青蒿琥酯(Artesunate, Art)(0、10、20、40μg/ml) 作用Eca109细胞24h,流式细胞术（Flow cytometry, FCM）方法检测细胞凋亡、周期及细胞中bcl-2和bax蛋白的表达量。结果 青蒿琥酯作用Eca109细胞24h后,与对照组相比,细胞凋亡率显著增高P<0.05,且具有剂量依赖性。青蒿琥酯组与对照组相比,Eca109细胞中bcl-2蛋白表达水平及细胞增殖指数显著降低P<0.05,而bax蛋白表达量显著增高P<0.05,且具有剂量依赖性。结论 青蒿琥酯可以通过调节Eca109细胞中bcl-2、bax蛋白表达水平和细胞增殖,从而诱导Eca109细胞产生凋亡,起到抗食管癌作用。     

上调人食管癌Eca109细胞Shh-Gli1信号通路对放射抗拒性及细胞周期的影响

目的:通过上调Sonic Hedgehog(Shh)信号通路关键因子Gli1,探究Shh信号通路与食管癌细胞放射抗拒性及细胞周期的关系。方法:用过表达Gli1质粒转染人食管癌Eca109细胞,记为Eca109-ox-Gli1组;转染空载质粒为阴性对照组;以不作处理的亲本细胞株为正常对照组。Real-time PCR与Western blot检测转染后细胞内Gli1的表达,集落形成实验检测细胞放射敏感性,流式细胞术检测转染前后细胞周期分布。结果:Real-time PCR与Western blot结果均显示Eca109-ox-Gli1组的Gli1表达显著高于阴性对照组和正常对照组(P0.05)。集落形成实验显示2 Gy射线照射后,Eca109-ox-Gli1组的存活分数较正常对照组明显升高(P0.05),转染后细胞对射线敏感性降低,放射抗拒性增加。Eca109-ox-Gli1组中S期细胞分布比例显著高于对照组(P0.01),再照射6Gy后,3组细胞均出现了G_2/M期阻滞,正常对照组相比于Eca109-ox-Gli1组G_2/M期细胞分布显著增高(P0.01)。结论 :上调Shh信号通路关键因子Gli1能够增强食管癌细胞的放射抗拒性,这一过程可能是通过调控细胞周期实现的。     

Sonic hedgehog信号通路与食管癌放射抗拒的相关性研究

目的:研究Sonic hedgehog(Shh)信号通路在食管癌放射抗拒中的作用及机制。方法:以人食管癌细胞Eca109为亲本株,通过X射线反复照射(累计照射剂量60 Gy)诱导形成放射抗拒细胞株Eca109R。分别采用集落形成实验检测细胞放射敏感性,CCK-8实验检测细胞活力的变化,来证实放射抗拒细胞株Eca109R的放射抗拒性。免疫荧光及Western blot检测Eca109R和亲本细胞Eca109内Gli1蛋白与Shh蛋白的表达。结果:集落形成实验显示2 Gy的X线照射后,Eca109和Eca109R细胞的存活分数(SF_2)分别为0.499±0.042和0.937±0.013;同时,CCK-8实验显示,Eca109R细胞的活力抑制率明显低于Eca109细胞(P0.05),证实Eca109R细胞有明显的放射抗拒性,诱导形成放射抗拒株成功。免疫荧光结果显示Eca109R细胞中Gli1表达明显高于Eca109细胞(P0.05)。Western blot实验结果显示Eca109R细胞中的Gli1与Shh蛋白表达明显高于Eca109细胞(P0.05)。结论:食管癌放射抗拒性的产生可能与Shh信号通路相关蛋白的过表达有关。     

miR-24-3p靶向KLF6基因调控IL-6/STAT3信号通路影响食管癌细胞的活力和凋亡

目的:探讨微小RNA-24-3p(miR-24-3p)对食管癌细胞活力和凋亡的影响及机制。方法:以人正常食管上皮细胞HEEC为对照,采用RT-qPCR检测食管癌细胞TE11、Eca109和EC9706中miR-24-3p和KLF6 mRNA的表达,Western blot检测KLF6蛋白的表达。用anti-miR-24-3p和KLF6 siRNA转染EC9706细胞,MTT检测细胞活力,流式细胞术检测细胞凋亡率,Western blot检测检测细胞中与增殖、凋亡相关的蛋白以及IL-6/STAT3信号通路相关蛋白的表达,ELISA法检测IL-6的表达。双萤光素酶报告基因实验验证miR-24-3p与KLF6靶向调控的关系。结果:食管癌癌细胞TE11、Eca109和EC9706中miR-24-3p表达上调(P<0.05),KLF6的mRNA和蛋白表达下调(P<0.05)。敲减EC9706细胞miR-24-3p表达可抑制其细胞活力,诱导其凋亡,并抑制细胞CDK4、cyclin D1、CDC25A、p-STAT3、IL-6及Bcl-2的表达,促进caspase-3和Bax的表达。结论...     

P162对食管癌细胞株Eca109的放射增敏作用及其对p75NTR表达的影响

 目的：研究靶向Ras-GTP酶激活蛋白SH3功能区结合蛋白(G3BP)的新药P162对人食管癌细胞株Eca109的放射增敏作用及其对p75神经营养因子受体(p75NTR)表达的影响。方法：CCK-8法检测P162对食管癌细胞株Eca109增殖抑制的影响;集落形成实验检测P162对Eca109细胞的放射增敏效应,单击多靶模型拟合细胞存活曲线并计算放射增敏比;倒置显微镜观察细胞形态学改变;流式细胞术检测p75NTR的表达。结果：P162对食管癌细胞株Eca109有增殖抑制作用,且呈时间和剂量依赖性,2.5、5.0、10 μmol/L P162对Eca109细胞的放射增敏比分别为1.54、2.35和2.33。随着照射剂量的增加,食管癌细胞中p75NTR的表达增加,经5 μmol/L P162处理的实验组中p75NTR的表达明显低于未经处理的对照组。结论：P162对Eca109细胞有放射增敏作用,并且能抑制食管癌干细胞p75NTR的表达。P162的增敏作用可能与抑制食管癌干细胞有关。     

miR-21 inhibitor suppresses proliferation and migration of nasopharyngeal carcinoma cells through down-regulation of BCL2 expression

This study is to investigate the expression of miR-21 in nasopharyngeal carcinoma (NPC) cells, and the effect of miR-21 in the biological behavior and expression of B-cell lymphoma 2 (BCL2) in NPC cells. Paired NPC and adjacent non-tumor tissues were obtained from 53 patients who underwent primary surgical resection of NPC tissues. Luciferase reporter assay was performed to test whether BCL2 is a direct target of miR-21. Methylthiazolyl blue tetrazolium assay and colony assay were used to evaluate the effect of miR-21 on NPC cell proliferation. Transwell and wound-healing assays were carried out to test the effect of low expression of miR-21 on cancer cell migration and invasion. QRT-PCR and Western blotting were used to measure the levels of mRNA and protein expression, respectively. Tumor tissues showed a positive correlation between the levels of miR-21 and BCL2 protein expression. Cells transfected with miR-21 inhibitor healed slower compared the control (P < 0.05). In addition, cell migration was notably inhibited by the down-regulation of miR-21 in vitro (P < 0.05). The reduction in miR-21 expression showed a remarkable effect on the biological behavior of NPC cell clone formation (P < 0.05). Low expression of miR-21 by transfection with miRNA expression plasmid led to a decrease in BCL2 expression, which was accompanied by reduced migration and proliferation of the cancer cells. Our results demonstrated that miR-21 inhibitor down-regulated BCL2 expression level, suggesting that BCL2 might be a target gene for the initiation and development of NPC cells.     

Correlation and prognostic significance of MMP-2 and TFPI-2 differential expression in pancreatic carcinoma

Aberrant expression of matrix metalloproteinase (MMP)-2 and tissue factor pathway inhibitor (TFPI)-2 not only correlate with tumorigenesis, but also with tumor invasion and metastasis. This study aims to investigate the correlation and prognostic significance of MMP-2 and TFPI-2 differential expression in pancreatic carcinoma. Immunohistochemistry was used to evaluate MMP-2 and TFPI-2 expression in tumor tissues and corresponding non-tumor tissues from 122 patients with pancreatic carcinoma. The results showed that the expression of MMP-2 was significantly (P < 0.05) higher in tumor tissues (78.7%) than in adjacent non-tumor tissues (27.9%), whereas the expression of TFPI-2 was significantly (P < 0.001) lower in tumor tissues (27.9%) than in adjacent non-tumor tissues (79.5%). Spearman’s rank correlation test showed a negative correlation between MMP-2 and TFPI-2 expression (r = -0.346, P < 0.001). Kaplan-Meier survival analysis showed that high MMP-2 expression was significantly correlated with decreased disease-free survival (DFS) (P < 0.001) and overall survival (OS) (P < 0.001), while high TFPI-2 expression was significantly associated with increased DFS (P < 0.001) and OS (P < 0.001) of the patients. Multivariate analysis showed that high MMP-2 expression can act as an independent predictive factor for poor DFS (P = 0.01); and low TFPI-2 expression as an independent prognostic factor for poor DFS (P < 0.001) and OS (P < 0.001). In conclusion, our findings suggested that the differential expression of MMP-2 and TFPI-2 have a negative correlation in pancreatic carcinoma tissues; they may be considered as valuable biomarkers for prognosis of pancreatic carcinoma.     

IL-27基因修饰Eca109细胞的体外体内凋亡作用的研究

目的 研究IL-27基因转染人食管癌Eca109细胞株后在体外和体内对细胞凋亡的影响,从而探讨其抗肿瘤作用及其机制.方法 基因转染的方法 建立稳定表达IL-27基因的人食管癌细胞株(Eca109/IL-27),观察Eca109/IL-27细胞生长情况、移植瘤的生长情况及生存期,用流式细胞技术检测体外和体内的细胞凋亡率和Fas的表达,采用Western blot检测Survivin 的表达.结果 成功建立稳定转染的Eca109/IL-27细胞株,RT-PCR示Eca109/IL-27细胞中有mIL-27 p28和EBI3亚基基因表达,而Eca109/LXSN和Eca109细胞中未见表达(P＜0.01),IL-27基因转染不影响人食管癌细胞株的体外生长和细胞凋亡,Fas和Survivin的表达无变化(P＞0.05);但体内Eca109/IL-27移植瘤生长较Eca109和Eca109/LXSN滞后,生存时间延长(P＜0.05),肿瘤组织细胞凋亡率增高(P＜0.05),细胞表面Fas的表达增加(P＜0.05),Survivin表达降低(P＜0.05).结论 IL-27在体外不影响细胞凋亡,体内可能通过降低Survivin的表达,上调Fas的表达,诱导细胞凋亡产生抗肿瘤作用.     

小干扰RNA阻断信号转导子和转录激活子3信号对人食管鳞癌细胞株增殖的抑制作用

目的探讨信号转导子和转录激活子3（STAT3）小干扰RNA（siRNA）对食管鳞状细胞癌细胞株（EC9706和Eca109）中持续性激活STAT3信号的阻断情况及阻断STAT3信号对细胞增殖的影响。方法将化学合成的100nmol／L的STAT3 siRNA转染EC9706和Eca109细胞,逆转录聚合酶链反应检测转染前后STAT3mRNA的表达,WeStern blot检测转染前后STAT3及磷酸化STAT3（P—STAT3）蛋白的表达,凝胶电泳迁移率检测转染前后活化STAT3蛋白的核结合情况,四甲基偶氮唑蓝（MTT）检测转染前后细胞增殖能力的改变,流式细胞仪检测转染前后细胞周期的改变。结果STAT3 siRNA以时间依赖方式特异性地抑制STAT3 mRNA及STAT3、P-STAT3蛋白的表达,并且STAT3蛋白的核结合活性下降,使细胞周期阻滞于G0／G1期,细胞增殖受到明显的抑制。与对照组相比EC9706细胞转染后72hG0／G1期的细胞增加了16．1％,同时S期细胞减少11．1％;Eca109细胞转染后72hG0／G1期的细胞增加了11．8％,同时S期细胞也较对照组明显减少。结论STAT3 siRNA能够特异地阻断食管鳞癌细胞中STAT3信号的持续性激活并抑制肿瘤细胞的增殖。     

食管癌耐药皮下移植瘤裸鼠模型建立

 [摘要] 目的 建立食管癌耐药裸鼠模型及探讨食管癌耐药机制。方法 4周龄的BALB/c nu/nu裸小鼠36只随机分组分为6组,每组6只,左前肢肩胛下皮下分别接种食管癌细胞Eca109及食管癌耐药细胞Eca109/ABCG2,建立裸鼠皮下移植瘤模型。成瘤后腹腔注射阿霉素（Adriamycin, ADM）,1、4mg/kg,1次/3d 共注射7次,空白对照组使用生理盐水(normal saline, NS)代替ADM。RT-PCR方法检测移植瘤细胞中三磷酸腺苷结合转运蛋白G2（ATP-binding cassette transporter G2,ABCG2）mRNA 表达情况,流式细胞术(Flow cytometry, FCM)检测移植瘤细胞中ABCG2蛋白、凋亡及细胞中ADM含量。结果 成功建立裸鼠食管癌耐药细胞移植瘤模型,皮下接种细胞一周后成瘤,成瘤率100%。实验结束后,注射ADM药物的裸鼠,接种Eca109/ABCG2细胞的皮下移植瘤体积、重量和ABCG2 mRNA、蛋白表达量显著高于接种Eca109细胞移植瘤（P<0.05）,但细胞凋亡率及细胞内ADM含量显著降低（P<0.05）。结论 接种Eca109/ABCG2细胞的裸鼠皮下移植瘤模型是较好的食管癌耐药动物模型,具有ABCG2耐药表型,为研究ABCG2与食管癌耐药关系提供了较理想的动物模型。     

miR-217调控lncRNAMALAT1影响食管鳞癌细胞的生物学行为

目的　探讨miR-217通过调控lncRNA MALAT1抑制食管鳞状细胞癌细胞的增殖,迁移和侵袭行为及其机制。 方法　qPCR检测miR-217在食管鳞状细胞癌组织和不同细胞株中的表达情况;双荧光素酶报告基因检测miR-217与MALAT1之间的相互作用;MTT增殖实验检测抑制miR-217后食管鳞状细胞癌细胞的增殖能力的变化情况;划痕愈合试验和Transwell侵袭实验检测抑制miR-217后食管鳞状细胞癌细胞的迁移和侵袭行为的变化情况;Western blotting实验检测miR-217对MALAT1下游相关蛋白表达情况的影响。 结果　与正常食管组织相比,食管鳞状细胞癌组织中miR-217的表达水平相对上调,与其他细胞株相比,Ec109细胞中miR-217表达最高;双荧光素酶实验证实miR-217能与MALAT1的3’ UTR特异性结合,可以调控MALAT1的表达与活性;抑制miR-217的表达后可以抑制食管鳞状细胞癌细胞的增殖、迁移和侵袭能力;抑制miR-217后MALAT1下游MIA2,ROBO1表达明显下调。 结论　miR-217可以调控MALAT1的表达影响食管鳞状细胞癌细胞的生物学行为。     

神经生长因子在食管鳞癌细胞中的表达及分泌

目的 探讨神经生长因子（NGF)与食管鳞癌细胞分化的相关性。方法 采用有限稀释法分选出圆形和梭形单细胞克隆,采用无血清悬浮培养获得细胞球细胞, 贴壁的Eca109细胞分别在含血清和不含血清培养基中培养48h;分别采用反转录-聚合酶链式反应（RT-PCR)技术和免疫印迹法,检测NGF在食管鳞癌细胞中mRNA水平和蛋白水平的表达;免疫荧光技术检测NGF在食管鳞癌细胞中的表达定位;免疫组织化学法检测食管鳞癌组织中NGF的表达定位;用酶联免疫吸附法（ELISA）检测NGF在Eca109细胞培养基中的分泌情况。结果 在Eca109细胞中能检测到NGF的mRNA水平和蛋白水平的表达,其中NGF在细胞球细胞中的mRNA水平和蛋白水平的表达量最高。食管癌组织中检测到NGF表达于细胞质。Eca109细胞在无血清培养条件下能够分泌NGF,且明显高于含血清培养基中的含量。结论 食管癌细胞系Eca109表达并分泌NGF,并且食管癌组织中表达NGF,NGF可能在维持食管鳞状细胞癌的干细胞特性发挥了重要作用。     

Up-regulation of long non-coding RNA Sox2ot promotes hepatocellular carcinoma cell metastasis and correlates with poor prognosis

Background: Long non-coding RNAs (lncRNAs) have been shown to have important regulatory roles in cancer biology, and the lncRNA Sox2ot is up-regulated in some tumors. However, the contributions of Sox2ot to hepatocellular carcinoma (HCC) remain largely unknown. Methods: In the present study, expression of lncRNA Sox2ot was evaluated by quantitative real-time PCR in tumor tissues and adjacent non-tumor tissues in 84 HCC patients. The association of lncRNA Sox2ot expression with clinicopathological features and the prognosis of HCC patients were also analyzed. Survival analysis was performed using the Kaplan-Meier method and Cox’s proportional hazards model. Small interfering RNA assay was used to explore the function of lncRNA Sox2ot on HCC cell migration and invasion. Results: lncRNA Sox2ot expression level was significantly higher in HCC tissues compared with adjacent non-tumor tissues (P<0.05). High expression of lncRNA Sox2ot was associated with histological grade, TNM stage, and vein invasion. The 5-year overall survival of high lncRNA Sox2ot expression group was significantly shorter than that of low lncRNA Sox2ot expression group (P<0.05). The multivariate Cox regression analysis indicated that lncRNA Sox2ot expression was an independent prognostic factor for overall survival. In addition, the metastasis ability of HCC cells was significantly decreased by knocking down lncRNA Sox2ot expression. Conclusions: The results suggested that lncRNA Sox2ot played crucial roles in promoting HCC cell migration and invasion, and might represent a novel prognostic biomarker for HCC.