circ-RAD23B通过miR-708-5p/CPNE1轴调控膀胱癌细胞增殖、细胞周期、凋亡的机制

目的 探讨circ-RAD23B对膀胱癌细胞增殖、细胞周期、凋亡的影响及分子机制。方法 选取49例膀胱癌患者癌组织及相应的癌旁组织;培养人正常膀胱上皮细胞SV-HUC-1和膀胱癌细胞系T24、RT4、UM-UC-3,将T24细胞分为NC组、si-NC组、si-circ-RAD23B组、miR-NC组、miR-708-5p组、si-钙离子依赖性磷脂结合蛋白(CPNE)1组、pcDNA-NC组、pcDNA-CPNE1组、si-circ-RAD23B+pcDNA-NC组、si-circ-RAD23B+pcDNA-CPNE1组。实时荧光定量聚合酶链反应(RT-qPCR)检测circ-RAD23B、miR-708-5p和CPNE1 mRNA表达水平;Western印迹检测蛋白表达;双荧光素酶报告实验验证circ-RAD23B和miR-708-5p及miR-708-5p和CPNE1之间的靶向关系;噻唑蓝(MTT)检测细胞增殖;流式细胞术检测细胞周期及凋亡情况。结果 与癌旁组织比较,膀胱癌组织中circ-RAD23B表达水平明显升高(P<0.05)。与SV-HUC-1细胞比较,膀胱癌细胞系T2...     

miR-17-5p、miR-17-3p和miR-20a-5p在胃间质瘤中表达

目的探讨miR-17-5p、miR-17-3p及miR-20a-5p在胃间质瘤(gastric stromal tumor,GST)中的差异表达及其与临床病理因素的关系。方法提取正常胃组织及GST组织共72例标本的总RNA,应用Real time RT-PCR方法检测miR-17-5p、miR-17-3p及miR-20a-5p的表达,用SPSS 19.0分析其与临床病理因素的关系及3个miRNA间的相关性。结果在GST中,miR-17-3p、miR-17-5p在肿瘤组织中表达较胃正常组织低(P0.001),但是在低危组和中高危组GST中表达差异无统计学意义(P0.05);miR-20a-5p表达在胃正常组织、低危组和中高危组之间均有差异表达,且随着恶性度的增加而下降(P0.001),3种miRNA的表达水平与肿瘤的侵袭、转移、年龄、肿瘤最大直径和核分裂象密切相关,而与瘤体是否破溃无关。结论 miR-17-5p、miR-17-3p、miR-20a-5p在GST中下调并相互作用可能是促进GST发生、发展因素之一。     

miR-483与结直肠癌关系的研究

背景:胰岛素样生长因子2(IGF2)基因在多种恶性肿瘤中呈高表达,在肿瘤发生中起重要作用。miR-483位于IGF2基因第7号内含子中,与宿主基因共表达,但其具体功能尚未明确。目的:检测miR-483-3p、miR-483-5p在结直肠癌中的表达情况,探讨其作为结直肠癌分子标记物的可能性。方法:收集75对结直肠癌组织和相应癌旁非癌组织样本,以real-time PCR检测miR-483-3p、miR-483-5p表达并分析两者间以及两者与肿瘤临床病理特征的关系,以ROC曲线分析两者对结直肠癌的诊断性能。结果:结直肠癌组织中的miR-483-3p、miR-483-5p相对表达量均显著高于相应癌旁非癌组织(P0.000 1),且两者在癌组织中的表达量呈显著正相关(rs=0.554 5,P0.000 1)。miR-483-3p和miR-483-5p诊断结直肠癌的最佳截点分别为9.22和11.61,相应诊断敏感性、特异性分别为78.67%、62.67%和50.67%、85.33%;如两者联合检测(并联试验),诊断敏感性可提高至89.48%。两者表达与结直肠癌患者的性别、年龄以及肿瘤大小、部位、分化程度和TNM分期均无相关性。结论:miR-483-3p、miR-483-5p在结直肠癌中呈高表达,可能与肿瘤发生有关。两者有望成为结直肠癌诊断潜在的分子标记物。     

miR-324-5 p通过靶向TRIP13基因调控宫颈癌细胞增殖、侵袭、迁移和凋亡

目的 探讨miR-324-5p对宫颈癌细胞增殖、侵袭、迁移和凋亡的影响及调控机制.方法 培养正常宫颈细胞Ectl/E6E7和宫颈癌细胞系Hela、C-33A、CaSki、SiHa,实时定量聚合酶链式反应(qRT-PCR)检测细胞中miR-324-5p和甲状腺激素受体因子(TRIP)13 mRNA表达,Western印迹...     

miR-20a-5p在胰腺癌中的表达及作用机制研究

目的检测并分析胰腺癌组织和胰腺癌细胞株中miR-20a-5p的表达情况及对胰腺癌细胞发生、发展的影响。方法收集16对手术切除胰腺癌患者的癌组织及对应癌旁组织、5种胰腺癌细胞株及1株正常胰腺导管上皮细胞,通过实时荧光定量聚合酶链反应(quantitative realtime polymerase chain reaction,qRT-PCR)检测临床标本及胰腺癌细胞株中miR-20a-5p的表达水平;通过转染miR-20a-5p mimics及miR-20a-5p inhibitor分别上调及下调胰腺癌细胞(AsPC-1、BxPC-3)中miR-20a-5p的表达水平,采用CCK-8、EdU及流式凋亡实验检测过表达及敲低miR-20a-5p后对胰腺癌细胞活力、增殖及凋亡能力的影响。结果胰腺癌组织中miR-20a-5p的表达量显著高于癌旁组织(P0.01),5种胰腺癌细胞系中miR-20a-5p的表达量较正常胰腺细胞也明显升高(P0.05)。CCK-8及EdU实验结果显示,过表达miR-20a-5p促进胰腺癌细胞增殖能力,反之,干扰miR-20a-5p抑制胰腺癌细胞增殖。凋亡检测结果显示,过表达miR-20a-5p抑制胰腺癌细胞凋亡能力,反之,干扰miR-20a-5p促进胰腺癌细胞凋亡。结论胰腺癌组织和胰腺癌细胞系均高表达miR-20a-5p,上调miR-20a-5p能促进胰腺癌细胞增殖及抗凋亡能力。     

LncRNA CDKN2BAS通过调控miR-627-3p影响肺癌细胞增殖、凋亡和放射敏感性的机制

目的 探讨LncRNA CDKN2BAS对肺癌细胞NCI-H1299增殖、凋亡和放射敏感性的影响及其分子机制。方法 选取42例肺癌组织及相应癌旁组织;体外培养人正常肺支气管上皮细胞和肺癌细胞系;将NCI-H1299细胞分为NC组、si-NC组、si-LncRNA CDKN2BAS组、miR-NC组、miR-627-3p组、si-LncRNA CDKN2BAS+anti-miR-NC组、si-LncRNA CDKN2BAS+anti-miR-627-3p组;实时荧光定量-聚合酶链反应(RT-qPCR)检测LncRNA CDKN2BAS、miR-627-3p mRNA相对表达水平;噻唑蓝(MTT)检测细胞增殖;流式细胞术检测细胞凋亡;克隆形成实验检测放射敏感性;Western印迹检测相关蛋白的表达;双荧光素酶报告实验检测LncRNA CDKN2BAS和miR-627-3p的靶向关系。结果 与癌旁组织比较,肺癌组织中LncRNA CDKN2BAS mRNA表达明显升高,miR-627-3p mRNA表达水平明显降低(P<0.05);与BEAS-2B细胞比较,肺癌细胞NCI-H1299、...     

miR-7-5P在口腔鳞癌中表达及其调控CDK-10信号通路对细胞增殖、凋亡与周期的影响

目的 探索miR-7-5P在口腔鳞癌的表达及其调控CDK-10信号通路对口腔鳞癌细胞增殖、凋亡与周期的影响。方法 收集癌旁组织和癌组织样本,免疫组化染色和PCR检测CDK-10和miR-7-5P的表达。SCC-25细胞作为体外模型,检测miR-7-5P对SCC-25细胞增殖、LDH及CDK-10等的影响。结果 在腔鳞癌患者中miR-7-5P呈低表达,CDK-10高表达,miR-7-5P与CDK-10成负相关性。miR-7-5p过表达可降低口腔鳞癌CDK-10和Bcl2蛋白表达水平,提高Bax、LDH、caspase-3/8/9水平,促进细胞凋亡。抑制MiR-7-5p表达可提高CDK-10和Bcl2蛋白表达水平,降低Bax、LDH、caspase-3/8/9水平,抑制细胞凋亡。结论 miR-7-5p能够通过调控CDK-10表达抑制口腔鳞癌细胞增殖,促进凋亡,miR-7-5p对口腔鳞癌的诊断和治疗具有潜在的价值,提示miR-7-5p有希望成为口腔鳞癌分子标志物。     

miR-574-3p在结直肠癌中的表达和作用机制研究

目的 检测并分析结直肠癌组织和细胞系中miR-574-3p的表达情况及其对结直肠癌细胞发生、发展的影响.方法 收集武汉市第三医院11对手术切除结直肠癌患者的癌组织和对应癌旁组织,3种结直肠癌细胞系和1种正常结直肠上皮细胞,通过实时荧光定量聚合酶链反应(qRT-PCR)检测临床样本及结直肠癌细胞系中miR-574-3p的...     

右美托咪定通过调控LncRNA HOXA11-AS/miR-515-5p抑制膀胱癌细胞增殖并诱导细胞凋亡

目的 探讨右美托咪定(Dex)通过调控长链非编码RNA HOXA11-AS(LncRNA HOXA11-AS)/微小RNA-515-5p(miR-515-5p)对膀胱癌细胞增殖、凋亡的影响及作用机制。方法 采用不同浓度(25、50、100、200 ng/ml)的Dex处理膀胱癌T24细胞,四甲基偶氮唑蓝(MTT)比色法检测细胞存活率;流式细胞术检测Dex对T24细胞凋亡率的影响;实时荧光定量聚合酶链反应(qRT-PCR)检测Dex对HOXA11-AS、miR-515-5p表达水平的影响。利用脂质体方法分别将si-HOXA11-AS及阴性对照(si-NC)、miR-515-5p模拟物(mimics)及阴性对照(miR-NC)转染至T24细胞,通过MTT、流式细胞术检测细胞增殖与凋亡能力变化。双荧光素酶报告实验确定HOXA11-AS与miR-515-5p的靶向关系。Western印迹检测细胞周期蛋白(Cyclin)D1、活化的含半胱氨酸的天冬氨酸蛋白水解酶(C-caspase)-3表达量。结果 Dex可明显提高细胞凋亡率及C-caspase-3、miR-515-5p的表达水平(P<0...     

miR-145-3p在肝癌中的表达及其对肝癌细胞生长的调控作用

背景miR-145-3p在头颈癌、肺癌和胃癌等肿瘤可发挥抑癌的作用,而其在肝癌中的表达和作用并不清楚.目的探讨miR-145-3p在肝癌中的表达及其对肝癌细胞的增殖与凋亡的调控作用.方法用RT-q PCR法检测肝癌组织、癌旁组织、肝细胞株(Hep3B、Huh-7、Hep G2和SMMC-7721)与正常肝细胞株L-02中miR-145-3p的表达水平;将miR-145-3pmimic或miR-145-3pinhibitor转入Hep3B细胞,用CCK-8法、流式细胞术、TUNEL法和Westernblot法分别检测细胞活力、细胞周期、细胞凋亡和4型黏蛋白(mucin4, MUC4)表达.用荧光素酶报告基因实验鉴定miR-145-3p的靶基因.将pc DNA-MUC4转入已转染miR-145-3p mimic的细胞,用CCK-8法和TUNEL法分别检测细胞活力与细胞凋亡.结果miR-145-3p在肝癌组织和细胞中呈低表达.过表达miR-145-3p能抑制细胞增值和G0/G1期到S期转换,促进凋亡和降低MUC4表达;而敲减miR-145-3p则作用相反. MUC4是miR-145-3p的靶基因.过表达MUC4能逆转miR-145-3p mimic对细胞存活的抑制作用.结论miR-145-3p在肝癌低表达,且其表达与T分期呈负相关.过表达miR-145-3p可抑制肝癌细胞存活与生长,而敲减miR-145-3p能促进肝癌细胞存活与生长.     

Extracellular Polysaccharide from Rhizopus nigricans Inhibits Hepatocellular Carcinoma via miR-494-3p/TRIM36 Axis and Cyclin E Ubiquitination

Background and AimsThis study was designed to uncover the mechanism for extracellular polysaccharide (EPS1-1)-mediated effects on hepatocellular carcinoma (HCC) development.MethodsHCC cells were treated with EPS1-1, miR-494-3p mimic, sh-TRIM36, and pcDNA3.1-TRIM36. The levels of miR-494-3p and TRIM36 were measured in normal hepatocytes, THLE-2, and HepG2 and HuH7HCC cell lines, along with the protein expression of cyclin D/E and p21. The proliferation, cell cycle, and apoptosis of HCC cells were assayed. The interactions between miR-494-3p and TRIM36, and between TRIM36 and cyclin E were assessed. Finally, the expression and localization of TRIM36 and cyclin E were monitored, and tumor apoptosis was detected, in tumor xenograft model.ResultsEPS1-1 suppressed HCC cell proliferation and cyclin D/E expression and promoted apoptosis and p21 expression. miR-494-3p was upregulated and TRIM36 was downregulated in HCC cells. Transfection with miR-494-3p mimic or sh-TRIM36 facilitated HCC cell proliferation and the expression of cyclin D/E protein but they inhibited apoptosis and p21 expression in the presence of EPS1-1. Overexpression of TRIM36 further consolidated EPS1-1-mediated inhibition of HCC proliferation, cyclin D/E, and the promotion of apoptosis and p21 expression. Those effects were reversed by miR-494-3p overexpression. TRIM36 was a target gene of miR-494-3p, and TRIM36 induced cyclin E ubiquitination. EPS1-1 suppressed cyclin E expression, promoted TRIM36 expression and tumor apoptosis, all of which were abrogated by increasing the expression of miR-494-3p in vivo.ConclusionsEPS1-1 protected against HCC by limiting its proliferation and survival through the miR-494-3p/TRIM36 axis and by inducing cyclin E ubiquitination.     

miR-106b-25/miR-17-92 clusters: Polycistrons with oncogenic roles in hepatocellular carcinoma

MicroRNAs are small endogenously expressed RNA molecules which are involved in the process of silencing gene expression through translational regulation. The polycistronic miR-17-92 cluster is the first microRNA cluster shown to play a role in tumorigenesis. It has two other paralogs in the human genome, the miR-106b-25 cluster and the miR-106a-363 cluster. Collectively, the microRNAs encoded by these clusters can be further grouped based on the seed sequences into four families, namely the miR-17, the miR-92, the miR-18 and the miR-19 families. Over-expression of the miR-106b-25 and miR-17-92 clusters has been reported not only during the development of cirrhosis but also subsequently during the development of hepatocellular carcinoma. Members of these clusters have also been shown to affect the replication of hepatitis B and hepatitis C viruses. Various targets of these microRNAs have been identified, and these targets are involved in tumor growth, cell survival and metastasis. In this review, we first describe the regulation of these clusters by c-Myc and E2F1, and how the members of these clusters in turn regulate E2F1 expression forming an auto-regulatory loop. In addition, the roles of the various members of the clusters in affecting relevant target gene expression in the pathogenesis of hepatocellular carcinoma will also be discussed.     

Hsa_circ_0074491 regulates the malignance of cholesteatoma keratinocytes by modulating the PI3K/Akt pathway by binding to miR-22-3p and miR-125a-5p: An observational study

Cholesteatoma is a benign cystic lesion that can continue to grow like a tumor. Circular ribonucleic acid (RNA) hsa_circ_0074491 (circ_0074491) has been reported to be down-regulated in cholesteatoma tissues. However, the role and regulatory mechanism of circ_0074491 in the growth of cholesteatoma are unclear.The expression of circ_0074491, microRNA (miR)-22-3p, and miR-125a-5p in cholesteatoma tissues was detected by quantitative real-time polymerase chain reaction. The proliferation, cell cycle, apoptosis, migration, and invasion of cholesteatoma keratinocytes were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, plate clone, flow cytometry, or transwell assays. Several protein levels were examined by western blotting. The targeting relationship between miR-22-3p or miR-125a-5p and circ_0074491 was verified via dual-luciferase reporter and RNA pull-down assays.We observed the downregulation of circ_0074491 in cholesteatoma tissues. Furthermore, circ_0074491 knockdown facilitated cell proliferation, migration, invasion, and repressed cell apoptosis in cholesteatoma keratinocytes. Circ_0074491 was verified as a decoy for miR-22-3p and miR-125a-5p in cholesteatoma keratinocytes. Both miR-22-3p and miR-125a-5p silencing reversed the impacts of circ_0074491 silencing on proliferation, apoptosis, migration, and invasion of cholesteatoma keratinocytes. Also, circ_0074491 knockdown activated the PI3K/Akt pathway in cholesteatoma keratinocytes via miR-22-3p and miR-125a-5p.Circ_0074491 played a suppressive role in cholesteatoma through inactivating the PI3K/Akt pathway via binding to miR-22-3p and miR-125a-5p, which provided a novel evidence for the involvement of circRNA in the development of cholesteatoma.     

血清miR-92a-1-5p及miR-92a-2-5p表达水平与老年卒中后抑郁的关系

目的 分析血清微小核糖核酸-92a-1-5p ( miR-92a-1-5p)、 miR-92a-2-5p 表达水平与老年卒中后抑郁的关系.方法 选取2018年2月至2020年10月胶州中心医院收治的129例老年卒中患者为研究组,另选取110名同期健康体检者为对照组,均检测血清miR-92a-1-5p、miR-92a-2...     

非酒精性脂肪性肝病合并2型糖尿病患者外周血miR-17、miR-20a和miR-20b变化及其临床意义*

目的 探讨非酒精性脂肪性肝病(NAFLD)合并2型糖尿病(T2DM)患者外周血miR-17、miR-20a和miR-20b变化及其临床意义。方法 2018年12月～2020年6月我院收治的T2DM患者46例和NAFLD合并T2DM患者50例(轻度19例、中度17例和重度14例)。采用实时荧光定量RT-PCR法检测血清miR-17、miR-20a和miR-20b mRNA水平。采用多因素Logistic回归分析NAFLD合并T2DM发生的独立危险因素,应用受试者工作特征曲线(ROC)下面积(AUC)分析各指标诊断严重NAFLD的效能。结果 NAFLD合并T2DM患者外周血miR-17、miR-20a和miR-20b mRNA水平分别为(5.6±1.3)、(3.8±0.9)和(1.8±0.5),显著高于T2DM患者【分别为(4.4±1.1)、(3.1±0.6)和(1.4±0.4),P<0.05】;重度NAFLD组血清miR-17、miR-20a和miR-20b mRNA水平分别为(6.0±1.1)、(4.0±0.8)和(1.9±0.5),显著高于中度患者【分别为(4.4±1.0)、(3.4±0.6)和(1.5±0.4),P<0.05】或轻度患者【分别为(4.1±0.6)、(2.8±0.8)和(1.2±0.3),P<0.05】;多因素Logistic回归分析显示,BMI、血清LDL-C、miR-17、miR-20a和miR-20b是NAFLD合并T2DM发生的独立危险因素(P<0.05);ROC分析结果显示,血清miR-17、miR-20a和miR-20b诊断严重NAFLD的AUC分别为0.75、0.74和0.70。结论 NAFLD合并T2DM患者外周血miR-17、miR-20a和miR-20b水平显著升高,可能参与了NAFLD的发病过程,对判断NAFLD的严重程度具有一定的意义。     

LncRNA CYTOR promotes pancreatic cancer cell proliferation and migration by sponging miR-205-5p

Background/aimsStudies have found that LncRNA CYTOR is an important regulator of cancer. However, the function of lncRNA CYTOR in pancreatic cancer (PC) is unclear. This study amid to explore the regulation of lncRNA CYTOR in PC.MethodsThe expression of CYTOR and miR-205-5p in PC was detected by RT-qPCR. CCK-8 assay, colony formation assay and scratch test were conducted to detect the effects of CYTOR and miR-205-5p on proliferation and migration of PC cells. Target gene prediction and screening and luciferase reporter assays were used to verify downstream target genes of CYTOR and miR-205-5p. The expression of Cyclin-dependent protein kinase 6 (CDK6) was detected by Western blotting. The tumor growth in mice was detected by in vivo experiments in nude mice.ResultsThe expression of LncRNA CYTOR was significantly elevated in PC. Knockdown of CYTOR significantly inhibited cell proliferation and migration of PC cells. In vivo animal studies showed that CYTOR promoted tumor growth. MiR-205-5p was a direct target of CYTOR, and the expression levels of miR-205-5p were significantly reduced in PC cell lines. Furthermore, co-transfection of shCYTOR with miR-205-5p inhibitor partially abolished the effect of shCYTOR on cell proliferation and migration. In addition, CYTOR was negatively correlated with the expression of miR-205-5p. CDK6 was a direct target of miR-205-5p, and miR-205-5p mimic and sh CYTOR significantly reduced the expression levels of CDK6.ConclusionCYTOR can promote PC progression by modulating the miR-205-5p/CDK6 axis, which may be a potential therapeutic target for PC.     

结直肠癌组织中miR-338-3p、SMO的表达变化及意义

目的观察结直肠癌组织中微小RNA(miRNA)-338-3p(miR-338-3p)与Smoothened(SMO)的表达变化,并探讨其意义。方法 30例结直肠癌患者,手术时留取癌组织及癌旁组织,抽提其中的总RNA及蛋白质,采用实时荧光定量PCR检测标本中的miR-338-3p,用半定量RT-PCR检测SMO mRNA,Western blot检测SMO蛋白。结果结直肠癌组织中miR-338-3p的表达量(2-ΔΔCt)为0.153 7±0.126 4,SMO mRNA的相对表达量为0.371±0.116,SMO蛋白的灰度值为3.195±1.623,癌旁组织分别为0.901 5±0.426 3、0.366±0.117、0.733±0.305,两种组织中的miR-338-3p、SMO蛋白表达量相比,P均<0.01;miR-338-3p与SMO蛋白的表达呈负相关(r=-0.877,P<0.01)。结论结直肠癌组织中miR-338-3p表达明显下调,SMO蛋白表达明显上升;miR-338-3p可能通过转录后基因沉默机制使SMO蛋白表达下降,从而抑制结直肠癌的发生发展。     

藤梨根提取物通过调控miR-192-5p/ARPP19轴影响结直肠癌细胞的增殖和凋亡

背景 藤梨根提取物(rattan root extract,RRE)可抑制胃癌、肺癌等肿瘤细胞增殖,具有一定抗肿瘤作用,但其是否影响结直肠癌细胞的恶性表型还未知.miR-192-5p在结直肠癌组织中表达降低,且其低表达与肿瘤大小等临床病理特征相关,可作为结直肠癌诊治的潜在生物学标志物.StarBase生物信息学软件预测...     

miR-152-3 p靶蛋白差异表达及调控机制在肝癌复发中的作用

目的比较肝癌复发与预后良好患者癌组织的蛋白表达,分析miR-152-3p相关的靶蛋白差异及调控机制,探讨miR-152-3p在肝癌复发中的作用。方法应用TMT标记全蛋白质组学测序方法和RT-PCR分别检测肝癌切除术后2年复发(n=6)与5年预后良好(n=6)患者肝癌组织的蛋白质表达和miR-152-3p的表达水平;联合六大数据库检索分析miR-152-3p靶基因,并运用Gene Ontology、DAVID和REACTOME数据库进行靶基因筛选、富集注释和信号转导通路富集分析;将筛选的miR-152-3p靶基因进行基因突变频率和生存曲线分析,验证miR-152-3p靶基因在肝癌复发中的作用。计量资料2组间比较采用独立样本t检验。肝脏组织有关基因生存率分析采用Kaplan-Meier分析。结果肝癌切除术后预后良好患者癌组织的miR-152-3p转录表达水平显著高于复发患者癌组织的水平(P<0.05)。蛋白测序结果显示,预后良好患者与复发患者的癌组织存在365个差异表达蛋白,联合肝癌复发数据库分析显示,其中有17个蛋白受miR-152-3p调控。进一步的信号通路分析发现,17个受miR-152-3p调控的靶基因其功能集中于线粒体核糖体翻译调控;多重富集发现靶基因与线粒体呼吸链复合体密切关系的蛋白6个,分别为AKAP1、FOXRED1、MRPL28、MRPL50、SHC1、STAU1。基因突变频率及生存曲线分析发现,线粒体呼吸链相关靶蛋白的功能缺失或减弱会严重影响患者的生存率。结论miR-152-3p在HCC切除术后预后良好和复发患者的癌组织表达差异显著,miR-152-3p在肝癌复发中作用机制可能是通过调控靶基因AKAP1、FOXRED1、MRPL28、MRPL50、SHC1、STAU1作用于线粒体呼吸链,影响细胞氧化呼吸功能导致肝癌复发。