麦冬皂苷D通过调控miR-519d-3p/EIF4E表达对肝癌细胞增殖、迁移、侵袭的实验研究

背景麦冬皂苷D(ophiopogonin D, OPD)是中药麦冬提取物中重要的单体成分且具有抗癌作用,但是否具有抗肝细胞癌(hepatocellular carcinoma, HCC)作用还未知.本研究假设OPD能够通过上调miR-519d-3p表达进而下调真核细胞翻译起始因子4E(eukaryotic translation initiation factor 4E, EIF4E)表达发挥抗HCC作用.目的探讨OPD对HCC细胞增殖、迁移和侵袭的影响及可能的作用机制.方法培养HCC细胞Hep G2和MHCC97,不同浓度(2.5μmol/L、5μmol/L、10μmol/L)的OPD作用48h后,四甲基噻唑蓝染色法(methylthiazoletrazolium, MTT)检测细胞增殖, Transwell检测细胞迁移和侵袭,实时荧光定量PCR(real-time quantitative PCR, RT-q PCR)检测细胞中miR-519d-3p和EIF4E m RNA表达, Western blot检测细胞周期蛋白D1(Cyclin D1)、p21、基质金属蛋白酶2(matrix metalloproteinase-2, MMP-2)、MMP-9和EIF4E蛋白表达.双荧光素酶报告基因实验验证miR-519d-3p和EIF4E之间关系.转染miR-519d-3p mimics、si-EIF4E构建miR-519d-3p过表达或EIF4E表达抑制的Hep G2和MHCC97细胞, RT-q PCR检测细胞中miR-519d-3p表达或Western blot检测EIF4E蛋白表达验证转染效率. MTT、Transwell、Western b l o t分别检测过表达m i R-519d-3p或抑制E I F4E表达对Hep G2和MHCC97细胞增殖、迁移和侵袭,及Cyclin D1、p21、MMP-2和MMP-9蛋白表达的影响.结果与对照组比,OPD组Hep G2细胞抑制率显著升高(P 0.05),迁移和侵袭数显著降低(P 0.05),Hep G2细胞中Cyclin D1、MMP-2和MMP-9蛋白表达显著降低(P 0.05),p21蛋白表达显著升高(P 0.05),miR-519d-3p表达显著升高(P 0.05),EIF4Em RNA和蛋白表达显著降低(P0.05),且呈浓度依赖性. miR-519d-3p在Hep G2细胞中靶向负调控EIF4E表达.miR-519d-3p过表达或抑制EIF4E表达均可抑制Hep G2细胞增殖、迁移和侵袭.抑制miR-519d-3p表达部分逆转了OPD对Hep G2细胞增殖、迁移和侵袭的抑制作用.结论OPD可能通过调控miR-519d-3p/EIF4E表达抑制HCC细胞的增殖、迁移和侵袭.     

长链非编码RNA SCARNA10对肝癌细胞增殖的影响及其机制

目的探讨长链非编码RNA SCARNA10对肝癌细胞增殖的影响及其机制。方法收集人肝癌细胞Hep G2、MH97H及人正常肝细胞L-7702,采用实时荧光定量PCR(q PCR)法检测细胞中的SCARNA10。将Hep G2和MH97H细胞各分为两部分,分别转染小干扰RNA(siRNA)和阴性对照RNA(NC) 36 h;收集细胞,采用q PCR法检测细胞中的增殖细胞核抗原(PCNA) mRNA,CCK-8法检测波长450 nm处的光密度(OD)值表示细胞增殖活性,克隆形成实验计数克隆形成数。核质分离提取实验观察SCARNA10在肝癌细胞胞核、胞质中的分布情况,RNA结合蛋白免疫沉淀(RIP)实验验证SCARNA10与SUZ12、EZH2的相互作用。结果 Hep G2、MH97H细胞中SCARNA10相对表达量均高于L-7702细胞(P均<0.05)。与转染NC比较,转染siRNA的Hep G2、MH97H细胞中PCNA mRNA表达量、细胞增殖OD值均降低,细胞克隆数均减少(P均<0.05)。核质分离提取实验显示,SCARNA10在Hep G2、MH97H细胞胞核内的表达...     

极性蛋白AF-6mRNA在肝细胞肝癌中的表达及其对侵袭的影响

目的:检测肝细胞肝癌(hepatocellular carcinoma,HCC)癌组织、癌旁组织(adjacent normal liver tissue,ANLT)及不同侵袭能力细胞系中极性蛋白AF-6 m RNA的表达情况,分析其在不同组织及不同细胞系中的表达差异及意义.方法:利用实时定量PCR检测(real-time quantitative,q RT-PCR)检测AF-6 m RNA在3 0对癌组织、A N LT和4种细胞系(L 0 2、Hep G2、MHCC97-H和HCCLM3)中的表达情况.结果:AF-6 m RNA在93.3%(28/30)的HCC中呈低表达;正常肝细胞株L02中AF-6 m RNA含量明显高于肝癌细胞株(P0.05);高侵袭转移能力的细胞系MHCC97-H及HCCLM3只有极低的AF-6 m RNA表达,且明显低于低侵袭转移能力的细胞系Hep G2(P0.05).结论:AF-6 m RNA在肝癌中的低表达可能与高侵袭能力相关,提示AF-6 m RNA在将来可能会成为治疗侵袭性HCC的潜在靶点.     

上皮细胞黏附分子在肝细胞癌诊疗中的作用

上皮细胞黏附分子(Ep CAM)为一种跨膜糖蛋白,表达于上皮组织和多数上皮源性恶性肿瘤中,与细胞的黏附、迁移、增殖、分化以及肿瘤的发生、进展等有关。近年来,Ep CAM被认为是肝细胞癌(HCC)干细胞标志物,阐述了其在HCC诊断、治疗及预后判定中的作用,认为其可能为未来的分子靶向治疗提供线索。     

B7-H1在肝癌中的表达及其对肝癌细胞增殖和凋亡的影响

目的探讨B7-H1在人肝癌组织中的表达情况及其对肝癌Hep G2细胞增殖能力和凋亡水平的影响。方法采用组织化学染色方法观察肝癌组织和癌旁正常组织中B7-H1的表达情况。采用Lonza电转染的方法转染si-B7-H1-1和si-B7-H1-2进入肝癌Hep G2细胞,并通过RTPCR和Weatern印迹方法检测肝癌Hep G2细胞中B7-H1的表达情况。敲低肝癌Hep G2细胞中B7-H1的表达后,采用MTT方法检测肝癌Hep G2细胞的增殖情况,并采用Annexin V/7-AAD双染的方法检测肝癌Hep G2细胞的凋亡水平。结果与癌旁正常组织相比,肝癌组织中B7-H1的表达水平显著升高。采用Lonza电转染的方法转染si-B7-H1-1和si-B7-H1-2进入肝癌Hep G2细胞后,肝癌Hep G2细胞中-B7-H1的表达水平均显著降低。转染si-B7-H1-1和si-B7-H1-2敲低肝癌Hep G2细胞中B7-H1表达后,肝癌Hep G2细胞的增殖能力均显著降低,与对照组相比差异显著(P0.01)。转染si-B7-H1-1和si-B7-H1-2敲低肝癌Hep G2细胞中B7-H1表达后,肝癌Hep G2细胞的凋亡均显著升高,与对照组相比差异显著(P0.01)。结论肝癌组织中B7-H1的表达水平显著升高,且B7-H1可促进肝癌Hep G2细胞的增殖能力,并抑制肝癌Hep G2细胞的凋亡水平,提示肝癌组织中高表达的B7-H1与肝癌的发生和发展密切相关。     

真核起始因子3e亚基与原发性肝细胞癌的发生与发展正相关

背景真核起始因子3 (eukaryotic initiation factor 3, e IF3)是哺乳动物细胞中最复杂的翻译起始因子,真核起始因子3e亚基(eukaryotic initiation factor 3e subunit,e IF3e)是e IF313个亚基中的一个,其表达水平的失调与癌症的发生和发展密切相关.然而, e IF3e在不同类型的恶性肿瘤中的报道相互矛盾.迄今为止, e IF3e在原发性肝细胞癌(primary hepatocellular carcinoma,HCC)中的作用不明.目的研究e IF3e在HCC发生和发展中的作用.方法从临床上随机获取5例HCC病人手术后的新鲜肝癌组织及癌旁组织标本,用q RT-PCR和Western Blot分别定量检测肝癌组织和癌旁组织内e IF3e的m RNA转录水平和蛋白表达水平.通过转染e IF3e过表达质粒或e IF3e干扰质粒进入Hep G2,用q RT-PCR及Western Blot分别定量检测细胞内e IF3e转录和翻译表达水平,证实e IF3E过表达上调和干扰后的下调.用Kit-8细胞计数法(Cell Counting Kit-8, CCK-8)评价细胞增殖行为;用划痕实验观察细胞迁移行为;用流氏分析法调查细胞凋亡行为;运用裸鼠成瘤实验评价e IF3e对肿瘤生长的影响.结果和癌旁组织比较,发现肝癌组织中e IF3e上调.细胞实验证实,肝癌细胞系Hep G2及Huh7中e IF3e m RNA转录水平均高于正常肝细胞系HL7702.过表达质粒和干扰质粒分别瞬时转染Hep G2,发现e IF3e上调后增强了Hep G2增殖和迁移行为,但对细胞凋亡无影响;而e IF3e下调后,减弱了Hep G2增殖和迁移行为,促进凋亡;裸鼠实验结果证实e IF3e促进肿瘤生长.结论e IF3e的过表达与原发性肝细胞癌的发生和发展正相关,有潜力成为HCC治疗新靶点.     

下调GPC-3基因转录对肝癌细胞侵袭及血管新生的抑制作用

目的:观察以短发夹RNA(short hairpin RNA,shRNA)下调磷脂酰肌醇蛋白多糖-3(glypican-3,GPC-3)基因转录,对抑制肝癌MHCC-97H细胞侵袭和血管新生的作用与机制.方法:将对GPC-3特异性shRNA转染肝癌MHCC-97H细胞,以荧光定量PCR和Western blot分析GPC-3 mRNA及蛋白表达;以5-ethynyl-2'-deoxyuridine(EdU)和Transwell法等评估细胞增殖、迁移和侵袭能力.结果:shRNA1转染MHCC-97H细胞,GPC-3在mRNA水平下降75.6%(t=15.473,P0.001),蛋白表达同步下调;干预GPC-3基因转录,可抑制肝癌细胞增殖,细胞迁移与侵袭能力减低,与抗癌药物具协同作用;Wnt/β-catenin中β-catenin表达下调67.7%;Hedgehogs通路中脑胶质瘤相关癌基因1(glioma-associated oncogene 1,Gli1)表达上调53.3%;shRNA1转染72 h细胞血管内皮生长因子(vascular endothelial growth factor,VEGF)表达下调54.2%(t=46.746,P0.001).结论:shRNA下调GPC-3转录,经Wnt/β-catenin和Hh信号通路抑制癌细胞迁移、侵袭和血管新生,为肝癌基因治疗潜在的分子靶目标.     

miR-138在肝细胞癌中的表达及其对MHCC97H细胞侵袭、迁移能力的影响

目的 观察miR-138在肝细胞癌(HCC)组织、细胞中的表达变化,并探讨miR-138对MHCC97H细胞侵袭、迁移能力及上皮间质转化(EMT)的影响.方法 采用qRT-PCR检测HCC组织及癌旁组织、MHCC97H、MHCC97L、HepG2及正常肝细胞系L02细胞中的miR-138.转染miR-138 mimic...     

Tumor cells derived-extracellular vesicles transfer miR-3129 to promote hepatocellular carcinoma metastasis by targeting TXNIP

BackgroundHepatocellular carcinoma (HCC) is the most predominant primary liver cancer. Extracellular vesicles (EV)-mediated microRNA (miRNA) delivery is critical in cancer metastasis. We aimed to identify the mechanism of HCC cell-derived EVs-mediated miR-3129 in HCC.MethodsAfter EVs isolation and identification, miR-3129 expression in plasma EVs was evaluated and its diagnostic efficiency was analyzed. miR-3129 inhibitor was transfected into HepG2 and SMMC7721 cells, and cell malignant episodes were assessed. HCC cells were incubated with EVs from MHCC-97H cells and transfected with miR-3129 inhibitor and/or TXNIP. The nude mice were injected with MHCC-97H cells-EV or MHCC-97H cells-EV/miR-3129 inhibitor, and HCC growth and metastasis were assessed.ResultsmiR-3129 was highly expressed in plasma EVs from HCC patients, which was the essential diagnostic biomarker for HCC. miR-3129 downregulation inhibited the malignant episodes of HCC cells. MHCC-97H cell-EVs were absorbed by HCC cells and transferred miR-3129 to HCC cells. EVs-carried miR-3129 promoted malignant episodes of HCC cells, which were weakened by miR-3129 inhibition in EVs. miR-3129 targeted TXNIP. TXNIP overexpression averted the effect of EVs-carried miR-3129 in HCC. In vivo, MHCC-97H cell-EVs transferred miR-3129 to facilitate HCC growth and metastasis.ConclusionMHCC-97H cell-EVs transferred miR-3129 to promote HCC metastasis by targeting TXNIP.     

不同转移潜能肝癌细胞株中CD标志物的表达差异及意义

目的探讨不同转移潜能的肝癌细胞株中几种CD标记物的表达差异及其意义,为进一步利用CD分子标志物分离多潜能肝癌干细胞奠定基础。方法常规培养三种不同转移潜能的肝癌细胞株HepG2、MHCC-97H、SK-HEP-1,胰酶消化获得单细胞悬液后,经流式抗体染色,通过流式细胞仪分析三种肝癌细胞株中CD133、CD90、CD44、CD34、CD24的表达差异及意义。结果 CD133+细胞在HepG2细胞株仅占0.1%,而在MHCC-97H、SK-HEP-1细胞中表达也较低;CD90+、CD44+、CD90+CD44+表达水平随细胞转移潜能的增加呈递增趋势(P<0.05)。CD44+CD24+在HepG2、MHCC-97H、SK-HEP-1细胞中的阳性表达率分别为0.05%、10.3%和0.3%(P<0.05);三者中均无CD34+和CD133+CD90+细胞表达。结论 CD90和CD44与肝癌细胞的转移潜能有一定的相关性,可能成为潜在的肝癌肿瘤干细胞标记物。     

The response of Golgi protein 73 to transcatheter arterial chemoembolization in patients with hepatocellular carcinoma may relate to the influence of certain chemotherapeutics

BACKGROUND: Golgi protein 73(GP73) is a promising biomarker of hepatocellular carcinoma(HCC). It decreases after surgical resection, and resumes upon recurrence, indicating a potential indicator for the effectiveness of the treatment. But changes of GP73 after transcatheter arterial chemoembolization(TACE) have not been reported so far. This study was to investigate the dynamic changes of GP73 in HCC patients after TACE treatment, and the possible underlying mechanisms in the cell cultures.METHODS: Blood samples were collected from 72 HCC patients, before TACE, at day 1 and day 30 after TACE. GP73 levels were measured by Western blotting. The dynamic changes of GP73 were analyzed and compared with image changes and clinical data. The effects of chemotherapeutic agents(5-FU and pirarubicin) on GP73 expression were tested in three HCC cell lines(Hep G2, HCCLM3 and MHCC97H).RESULTS: The GP73 level was significantly elevated at day 1and day 30 after TACE in HCC patients compared with that before the procedure(P0.05). There was no statistical difference between the two time points after TACE, nor correlationbetween GP73 levels and clinicopathological features, tumor metastasis, and patient survival. Pirarubicin, not 5-FU, significantly increased GP73 expression in three cell lines. CONCLUSIONS: Unlike surgical resection which decreases the GP73 level, TACE significantly increased GP73 expression in patients with HCC. No correlations were observed among GP73 levels, tumor characteristics and prognosis of patients with HCC.     

siRNA干扰纤维蛋白原α链基因对人肝癌细胞增殖和凋亡的影响

背景：纤维蛋白原（FG）是由肝细胞合成、分泌的糖蛋白。除凝血和纤溶外,FG在细胞增殖、血管发生、肿瘤的发生、进展和转移中亦发挥重要作用。肝细胞癌患者血浆FG水平显著高于健康人。目的：观察以RNA干扰技术抑制FG仅链（FGA）基因对人肝癌细胞增殖和凋亡的影响。方法：构建FGAsiRNA干扰质粒,将重组质粒pU6．FGAsiRNA稳定转染入人肝癌细胞株HepG2,同时设置空质粒载体pU6转染组作为对照。以RT－PCR、蛋白质印迹法在mRNA和蛋白质水平验证干扰效果,以CCK－8实验和流式细胞术检测各组HepG2细胞的增殖和凋亡情况。结果：FGAsiRNA转染组HepG2细胞FGAmRNA和蛋白表达明显低于空载体转染组,细胞增殖显著受抑（P〈0．001）,细胞凋亡显著增加（P〈0．001）。结论：RNA干扰技术能有效下调人肝癌细胞的FGA表达,抑制肿瘤细胞生长增殖并促进其凋亡。FGA可能成为肝细胞癌治疗的潜在靶点之一。     

EpCAM,a new marker for cancer stem cells in hepatocellular carcinoma

Background & Aims: Cancer progression/metastases and embryonic development share many properties including cellular plasticity, dynamic cell motility, and integral interaction with the microenvironment. We hypothesized that the heterogeneous nature of hepatocellular carcinoma (HCC), in part, may be owing to the presence of hepatic cancer cells with stem/progenitor features. Methods: Gene expression profiling and immunohistochemistry analyses were used to analyze 235 tumor specimens derived from 2 recently identified HCC subtypes (EpCAM(+) alpha-fetoprotein [AFP(+)] HCC and EpCAM(-) AFP(-) HCC). These subtypes differed in their expression of AFP, a molecule produced in the developing embryo, and EpCAM, a cell surface hepatic stem cell marker. Fluorescence-activated cell sorting was used to isolate EpCAM(+) HCC cells, which were tested for hepatic stem/progenitor cell properties. Results: Gene expression and pathway analyses revealed that the EpCAM(+) AFP(+) HCC subtype had features of hepatic stem/progenitor cells. Indeed, the fluorescence-activated cell sorting-isolated EpCAM(+) HCC cells displayed hepatic cancer stem cell-like traits including the abilities to self-renew and differentiate. Moreover, these cells were capable of initiating highly invasive HCC in nonobese diabetic, severe combined immunodeficient mice. Activation of Wnt/beta-catenin signaling enriched the EpCAM(+) cell population, whereas RNA interference-based blockage of EpCAM, a Wnt/beta-catenin signaling target, attenuated the activities of these cells. Conclusions: Taken together, our results suggest that HCC growth and invasiveness is dictated by a subset of EpCAM(+) cells, opening a new avenue for HCC cancer cell eradication by targeting Wnt/beta-catenin signaling components such as EpCAM.     

The membrane-cytoskeleton organizer ezrin is necessary for hepatocellular carcinoma cell growth and invasiveness

Purpose The change of cell mobility is one of the preconditions of tumor metastasis. Cell skeleton alteration and rearrangement of F-actin was closely related to cell mobility. Ezrin is a membrane-cytoskeleton organizer that can mediate the rearrangement and the function of F-actin. In this paper, we investigated the effect of ezrin on hepatocellullar carcinoma cell growth and invasiveness.Methods Hepatocellular carcinoma cell lines such as MHCC-1, MHCC97-H, SF7721, SMMC7721, Hep3B, and HepG2 were chosen in this study. We first examined the expression and the distribution of ezrin and F-actin in these cell lines using immunofluorescence, RT–PCR, and the western blot. Next we used small interfering RNA (siRNA) to down-regulate ezrin expression in MHCC-1, MHCC97-H, SF7721, and HepG2 to investigate the role of ezrin in tumor cell growth and invasiveness.Results Our preliminary results showed that the expression of ezrin and γ-actin in MHCC-1, MHCC97-H, and SF7721 with higher metastatic potential were obviously up-regulated than those in SMMC7721, Hep3B, and HepG2 with lower potential. No different expression of β-actin was found in the above tumor cell lines. The outcome of RNAi indicated that decreasing ezrin expression can notably inhibit the proliferation of the four hepatocellular carcinoma cell lines (p < 0.01, n = 10). The proportion of cells in G2-M phase also decreased after RNAi. The number of pseudopods decreased as well after RNAi treatment (p < 0.01, n = 5). The mobility and invasiveness of cancer cells decreased with decreasing ezrin expression tested by transwell assay (p < 0.01, n = 8).Conclusion Ezrin plays an important role in the process of hepatocellular carcinoma cell proliferation, migration, and invasiveness.     

Effect of adipose-derived mesenchymal stem cells on hepatocellular carcinoma: In vitro inhibition of carcinogenesis

AIM To investigate the effect of adipose-derived mesenchymal stem cells(ADMSCs)and their conditioned media(CM) on hepatocellular carcinoma(HCC) cell tumorigenesis.METHODS The proliferation rate of HepG2 and PLC-PRF-5 HCC cancer cells was measured using the trypan blue exclusion method and confirmed using the cell-counting kit8(commonly known as CCK-8) assay. Apoptosis was detected by flow cytometry using annexin V-FITC. Protein and mRNA expression was quantified by ELISA and real time PCR, respectively. Migration and invasion rates were performed by Transwell migration and invasion assays. Wound healing was examined to confirm the data obtained from the migration assays.RESULTS Our data demonstrated that when co-culturing HCC cell lines with ADMSCs or treating them with ADMSC CM, the HCC cell proliferation rate was significantly inhibited and the apoptosis rate increased. The decreased proliferation rate was accompanied by an upregulation of P53 and Retinoblastoma mRNA and a downregulation of c-Myc and hTERT mRNA levels. More notably, ADMSCs and their CM suppressed the expression of the two important markers of HCC carcinogenicity, alpha-fetoprotein and Des-gamma-carboxyprothrombin. In addition, the migration and invasion levels of HepG2 and PLC-PRF-5 cells significantly decreased, potentially through increased expression of the tissue inhibitor metalloproteinases TIMP-1, TIMP-2 and TIMP-3.CONCLUSION These findings shed new light on a protective and therapeutic role for ADMSCs and their CM in controlling HCC invasiveness and carcinogenesis.     

ASRGL1 downregulation suppresses hepatocellular carcinoma tumorigenesis in a CDK1-dependent manner

The asparaginase-like protein 1 (ASRGL1) catalyzes the hydrolysis of L-asparagine to L-aspartic acid and ammonia. Emerging evidences have shown a strong correlation between ASRGL1 expression and tumorigenesis. However, the expression and biological function of ASRGL1 in hepatocellular carcinoma (HCC) are still unclear. Here, we explored anti-tumor activity and fundamental mechanisms of ASRGL1 blockade in the HCC progression. Expression levels of ASRGL1 in patients with HCC were higher than those in the adjacent normal tissue. In addition, increased expression of ASRGL1 in HCC patients was correlated with poor overall survival. Knockdown of ASRGL1 gene in HepG2 and Li-7 cell lines inhibited cell proliferation, migration and invasion, but promoted apoptosis in vitro. ASRGL1 knockdown suppressed tumor growth in vivo. Conversely, ASRGL1 overexpression promoted cell proliferation, migration and invasion in HepG2 cells. Through bioinformatics analysis, we found that ASRGL1 might participate in the regulation of the cell cycle. Flow cytometry analysis conformed that ASRGL1 knockdown captured the cell cycle during the G2/M phase. ASRGL1 blockade promoted P53 protein expression and reduced expression of cyclin B and CDK1 proteins, as well as failed to binding. Moreover, CDK1 overexpression was able to reverse the decreased proliferation, migration and invasion of HepG2 cells induced by ASRGL1 knockdown. Collectively, our studies indicate that ASRGL1 blockade functions to inhibit cyclin B/CDK1-dependent cell cycle, leading to G2-to-M phase transition failure and tumor suppression in HCC.     

Decaprenyl diphosphate synthase subunit 2 as a prognosis factor in hepatocellular carcinoma

AIM:To investigate the involvement of decaprenyl diphosphate synthase subunit 2(PDSS2) in development and progression of human hepatocellular carcinoma(HCC).METHODS:PDSS2 protein expression was examined in well-and poorly differentiated HCC tumor samples.The levels of PDSS2 expression were compared with clinical features and prognosis of HCC patients.The effects of PDSS2 on cell proliferation,cell cycle,apoptosis,cell migration,and invasion in HCC Hep G2 cells were also investigated.RESULTS:PDSS2 was downregulated in poorly differentiated cancer samples compared with welldifferentiated tumor samples,and the expression level was markedly lower in HCC tissues than in histologically normal tissue adjacent to the cancer.Reduced protein expression was negatively associated with the status of HCC progression.In addition,overexpression of PDSS2dramatically suppressed cell proliferation and colony formation,and induced apoptosis in Hep G2 cells by inducing G1-phase cell-cycle arrest.The migration and invasion capabilities of Hep G2 cells were significantly decreased following PDSS2 overexpression.CONCLUSION:Decreased PDSS2 expression is an unfavorable prognostic factor for HCC,and PDSS2 has potent anticancer activity in HCC tissues and Hep G2cells.