过表达miR-140-5p对高脂饲养诱导的非酒精性脂肪性肝病大鼠的作用及机制

目的 探究过表达miR-140-5p对高脂饲养诱导的非酒精性脂肪性肝病(NAFLD)大鼠的作用及机制.方法 40只大鼠随机分为对照组、模型组、空载体组和过表达组,每组各10只.对照组给予普通饲料饲养,模型组给予高脂饲料饲养构建NAFLD大鼠模型,空载体组在模型组基础上于饲养第13周、第18周尾静脉注射含空载质粒的慢病毒...     

Lipotoxic hepatocyte-derived exosomal miR-1297 promotes hepatic stellate cell activation through the PTEN signaling pathway in metabolic-associated fatty liver disease

BACKGROUNDExosomes play an important role in metabolic-associated fatty liver disease (MAFLD), but the mechanism by which exosomes participate in MAFLD still remain unclear.AIMTo figure out the function of lipotoxic exosomal miR-1297 in MAFLD.METHODSMicroRNA sequencing was used to detect differentially expressed miRNAs (DE-miR) in lipotoxic exosomes derived from primary hepatocytes. Bioinformatic tools were applied to analyze the target genes and pathways regulated by the DE-miRs. Quantitative real-time PCR (qPCR) was conducted for the verification of DE-miRs. qPCR, western blot, immunofluorescence staining and ethynyl-20-deoxyuridine assay were used to evaluate the function of lipotoxic exosomal miR-1297 on hepatic stellate cells (LX2 cells). A luciferase reporter experiment was performed to confirm the relationship of miR-1297 and its target gene PTEN. RESULTSMicroRNA sequencing revealed that there were 61 exosomal DE-miRs (P < 0.05) with a fold-change > 2 from palmitic acid treated primary hepatocytes compared with the vehicle control group. miR-1297 was the most highly upregulated according to the microRNA sequencing. Bioinformatic tools showed a variety of target genes and pathways regulated by these DE-miRs were related to liver fibrosis. miR-1297 was overexpressed in exosomes derived from lipotoxic hepatocytes by qPCR. Fibrosis promoting genes (α-SMA, PCNA) were altered in LX2 cells after miR-1297 overexpression or miR-1297-rich lipotoxic exosome incubation via qPCR and western blot analysis. Immunofluorescence staining and ethynyl-20-deoxyuridine staining demonstrated that the activation and proliferation of LX2 cells were also promoted after the above treatment. PTEN was found to be the target gene of miR-1297 and knocking down PTEN contributed to the activation and proliferation of LX2 cells via modulating the PI3K/AKT signaling pathway.CONCLUSIONmiR-1297 was overexpressed in exosomes derived from lipotoxic hepatocytes. The lipotoxic hepatocyte-derived exosomal miR-1297 could promote the activation and proliferation of hepatic stellate cells through the PTEN/PI3K/AKT signaling pathway, accelerating the progression of MAFLD.     

Obesity-induced upregulation of miR-361-5p promotes hepatosteatosis through targeting Sirt1

ObjectiveObesity is associated with an increased risk of many metabolic disorders, including non-alcoholic fatty liver disease (NAFLD). However, the underlying mechanisms remain poorly understood. Recent studies have demonstrated that MicroRNA-mediated gene silencing plays an important role in hepatic triglyceride (TG) metabolism. In the present study, we aimed to investigate the pathological function of miR-361-5p in the development of NAFLD.MethodsExpression levels of miR-361-5p was determined by quantitative real-time PCR in livers of obese mice and NAFLD patients. Liver tissues from mice with miR-361-5p overexpression or inhibition were collected and analyzed by TG contents, gene expression profile.ResultsExpression of miR-361-5p was increased in the livers of two obese mouse models and NAFLD subjects. Overexpression of miR-361-5p in C57BL/6 mice led to hepatosteatosis, whereas inhibition of miR-361-5p expression in db/db mice improved TG accumulation and insulin sensitivity. Mechanistically, we identified Sirt1 as a direct target gene of miR-361-5p and re-introduction of Sirt1 largely abolished the metabolic action of miR-361-5p.ConclusionsOur results demonstrated the role of miR-361-5p in the regulation of hepatic TG homeostasis, which may provide potential therapeutic target for hepatosteatosis.     

Circulating MicroRNAs as Biomarkers of Accelerated Sarcopenia in Chronic Heart Failure

Background:Sarcopenia is a critical finding in patients with chronic heart failure (CHF). However, the search for a definitive biomarker to predict muscle and functional decline in CHF remains elusive.Objectives:We aimed to correlate the circulating levels of selected miRs with the indexes of sarcopenia during healthy aging and in patients with CHF.Methods:We analyzed the association of circulating microRNAs (miRs) levels including miR-21, miR-434-3p, miR424-5p, miR-133a, miR-455-3p and miR-181a with sarcopenia indexes in male, 61–73 years old healthy controls and patients with CHF (N = 89–92/group).Results:Patients with CHF had lower hand-grip strength (HGS), appendicular skeletal mass index (ASMI) and physical capacity than healthy controls. Circulating miR-21 levels were higher and miR-181a, miR-133a, miR-434-3p and miR-455-3p levels were lower in patients with CHF than healthy controls. Among the sarcopenia indexes, HGS showed the strongest correlation with miR-133a while ASMI showed the strongest correlations with miR-133a, miR-434-3p and miR-455-3p. Among the miRs, miR-434-3p showed the highest area under the curve in testing for sensitivity and specificity for CHF. These changes were associated with higher expressions of the markers of inflammation, oxidative stress and muscle damage in CHF patients.Conclusion:Taken together, our data show that circulating miRs can be useful markers of muscle health and physical capacity in the sarcopenic elderly with CHF.     

Repression of circRNA_000684 inhibits malignant phenotypes of pancreatic ductal adenocarcinoma cells via miR-145-mediated KLF5

BackgroundCircular RNAs (circRNAs) are aberrantly expressed in pancreatic ductal adenocarcinoma (PDAC). In the current study, we investigated how circRNA_000684 affected the progression of PDAC, and how it regulated kruppel-like factor 5 (KLF5) and microRNA (miR)-145.MethodsDifferentially expressed circRNAs, miRs and genes related to PDAC as well as their targeting relationship were predicted using bioinformatics analyses. Binding relationships among circRNA_000684, miR-145 and KLF5 were verified using dual-luciferase reporter gene assay, RIP and RNA pull-down assay, respectively. The effects of circRNA_000684, miR-145, KLF5 on the malignant phenotypes of PDAC cells and human umbilical vein endothelial cell (HUVEC) angiogenesis were assessed using loss- and gain-of function experiments by CCK-8 assay, scratch test, Transwell and tube formation assays. RT-qPCR and Western blot analysis were used to determine MCM2, MMP2 and MMP9 and VEGFA expression. In addition, the roles of circRNA_000684, miR-145, and KLF5 in tumor growth were validated through in vivo experiments.ResultsExpression of CircRNA_000684 and KLF5 was upregulated, whereas miR-145 expression was downregulated in PDAC tissues and cells. CircRNA_000684 repression or miR-145 elevation inhibited the proliferation, invasion and migration of PDAC cells and HUVEC angiogenesis, as evidenced by lower levels of MCM2, MMP2 and MMP9 and VEGFA. CircRNA_000684 negatively regulated miR-145 expression, while miR-145 negatively regulated KLF5. In-vivo, circRNA_000684 elevation or miR-145 repression promoted tumor growth.ConclusionTaken together, the present study provided evidence clarifying that circRNA_000684 could downregulate miR-145 expression and elevate KLF5 to promote the progression of PDAC.     

Deciphering the microRNA signature of pathological cardiac hypertrophy by engineered heart tissue- and sequencing-technology

Pathological cardiac hypertrophy and fibrosis are modulated by a set of microRNAs, most of which have been detected in biologically complex animal models of hypertrophy by arrays with moderate sensitivity and disregard of passenger strand (previously “star”) microRNAs. Here, we aimed at precisely analyzing the microRNA signature of cardiac hypertrophy and fibrosis by RNA sequencing in a standardized in vitro hypertrophy model based on engineered heart tissue (EHT). Spontaneously beating, force-generating fibrin EHTs from neonatal rat heart cells were subjected to afterload enhancement for 7 days (AE-EHT), and EHTs without intervention served as controls. AE resulted in reduced contractile force and relaxation velocity, fibrotic changes and reactivation of the fetal gene program. Small RNAs were extracted from control and AE-EHTs and sequencing yielded almost 750 different mature microRNAs, many of which have never been described before in rats. The detection of both arms of the precursor stem–loop (pre-miRNA), namely -3p and -5p miRs, was frequent. 22 abundantly sequenced microRNAs were > 1.3 × upregulated and 15 abundantly sequenced microRNAs downregulated to < 0.77 ×. Among the upregulated microRNAs were 3 pairs of guide and passenger strand microRNAs (miR-21-5p/-3p, miR-322-5p/-3p, miR-210-3p/-5p) and one single passenger strand microRNA (miR-140-3p). Among downregulated microRNAs were 3 pairs (miR-133a-3p/-5p, miR-30e-5p/3p, miR-30c-5p/-3p). Preincubating EHTs with anti-miR-21-5p markedly attenuated the AE-induced contractile failure, cardiomyocyte hypertrophy and fibrotic response, recapitulating prior results in whole animals. Taken together, AE-induced pathological hypertrophy in EHTs is associated with 37 differentially regulated microRNAs, including many passenger strands. Antagonizing miR-21-5p ameliorates dysfunction in this model.     

Long noncoding RNA GAS5 inhibits LX-2 cells activation by suppressing NF-κB signalling through regulation of the miR-433–3p/TLR10 axis

BackgroundLiver fibrosis is a common disease that can lead to hepatic failure.AimsOur aims were to reveal the role of GAS5 in the regulation of liver fibrosis.MethodsLX-2 human hepatic satellite cells (HSCs) were cultured and activated using TGF-β1 treatment. A CCK-8 assay was performed to assess cell viability. A luciferase assay was employed to monitor the interactions between miR-433–3p and GAS5 or toll-like receptor 10 (TLR10). Western blotting and real-time quantitative PCR (RT-qPCR) were applied to detect the expression levels of α-SMA, Col. I, PCNA-, MMP2-, MMP9-, TLR10-, and NF-κB-related molecules at the protein and RNA levels.ResultsGAS5 and TLR10 were decreased while miR-433–3p was upregulated in TGF-β1-activated LX-2 cells. Upregulation of GAS5 or downregulation of miR-433–3p suppressed HSC activation, and luciferase assays indicated that miR-433–3p binds with GAS5 and the 3′-UTR of TLR10. MiR-433–3p upregulation and TLR10 downregulation rescued the impacts of GAS5 overexpression or miR-433–3p knockdown on LX-2 cells. Upregulation of GAS5 also suppressed the phosphorylation of NF-κB through the miR-433–3p/TLR10 axis.ConclusionLncRNA GAS5 exerts an inhibitory effect on HSC activation by suppressing NF-κB signalling through regulation of the miR-433–3p/TLR10 axis.     

Neuroprotective effects of coenzyme Q10 in Parkinson's model via a novel Q10/miR-149-5p/MMPs pathway

Parkinson's disease (PD) is a complex neurodegenerative disease in which the understanding of the underlying molecular mechanisms can be constructive in the diagnosis and treatment. Matrix metalloproteinase (MMPs) elevation and damage to the blood–brain barrier (BBB) are critical mechanisms involved in the PD separation. Studies have revealed that changes in miR-149-5p and CoQ10 are associated with BBB damage, and CoQ10 can affect the levels of some miRs. Hence, in the present study, we aimed to evaluate CoQ10 and miR-149-5p mimic on miR-149-5p, MMPs and TH expression, and behavioral functions of the PD models. PD was induced by injection of 6-OHDA into the rats' Medial Forbrain Bundle (MFB). The behavioral tests, including the Rotation test, Rotarod test, and Open field test, have been directed two weeks after PD induction. Next, the MiR-149-5p mimic (miR-mimic) and CoQ10 have been administered to rats. The same behavioral tests have been evaluated two weeks after administration to investigate the effect of miR-149-5p mimic and CoQ10. The rats were followed extra four weeks, and the behavioral tests have performed again. Finally, the expression of MMPs and miR-149-5p genes was measured using RT-qPCR, and tyrosine hydroxylase (TH) was assessed through immunohistochemistry analysis. According to the obtained results, the level of miR-149-5p has decreased, followed by PD induction in rats. RT-qPCR analysis has represented upregulation and downregulation of miR-149-5p and MMP-2,9, respectively, after miR-mimic and CoQ10 treatment. The treated rats have also represented improved motor function and increased TH?+ ?cells in the striatum according to the behavioral tests and immunohistochemistry assay. Taking together miR-149 and CoQ10 has shown to have an impressive potential to prevent damage to dopaminergic neurons caused by 6-OHDA injection through reducing MMP-2,9, increased TH expression, and improved motor function.

     

MicroRNA profile indicates downregulation of the TGFβ pathway in sporadic non-functioning pituitary adenomas

MicroRNAs (miRs) are small, 16–29 nucleotide long, non-coding RNA molecules which regulate the stability or translational efficiency of targeted mRNAs via RNA interference. MiRs participate in the control of cell proliferation, cell differentiation, signal transduction, cell death, and they play a role in carcinogenesis. The aims of our study were to analyse the expression profile of miRs in sporadic clinically non-functioning pituitary adenomas (NFPA) and in normal pituitary tissues, and to identify biological pathways altered in these pituitary tumors. MiR expression profiles of 12 pituitary tissue specimens (8 NFPA and 4 normal pituitary tissues) were determined using miR array based on quantitative real-time PCR with 678 different primers. Five overexpressed miRs and mRNA expression of Smads (Smad1-9), MEG and DLK1 genes were evaluated with individual Taqman assays in 10 NFPA and 10 normal pituitary tissues. Pathway analysis was performed by the DIANA-mirPath tool. Complex bioinformatical analysis by multiple algorithms and association studies between miRs, Smad3 and tumor size was performed. Of the 457 miRs expressed in both NFPA and normal tissues, 162 were significantly under- or overexpressed in NFPA compared to normal pituitary tissues Expression of Smad3, Smad6, Smad9, MEG and DLK1 was significantly lower in NFPA than in normal tissues. Pathway analysis together with in silico target prediction analysis indicated possible downregulation of the TGFβ signaling pathway in NFPA by a specific subset of miRs. Five miRs predicted to target Smad3 (miR-135a, miR-140-5p, miR-582-3p, miR-582-5p and miR-938) were overexpressed. Correlation was observed between the expression of seven overexpressed miRs and tumor size. Downregulation of the TGFβ signaling through Smad3 via miRs may have a possible role in the complex regulation of signaling pathways involved in the tumorigenesis process of NFPA.     

Tumor-derived extracellular vesicles containing long noncoding RNA PART1 exert oncogenic effect in hepatocellular carcinoma by polarizing macrophages into M2

AimWe explored whether tumor-derived extracellular vesicles (EVs) could deliver long noncoding RNA (lncRNA) PART1 into macrophage to orchestrate macrophage polarization in the progression of hepatocellular carcinoma (HCC).MethodThe expression patterns of PART1, microRNA (miR)-372-3p and TLR4 were detected by RT-qPCR in the HCC tissues and HCC cells. PART1 was silenced or overexpressed in HCC cells to assess its effects on the HCC cell process. EVs were isolated from PART1-overexpressed HCC cells, and co-cultured with macrophages, and gain- and loss-of-function assays were implemented in macrophages to evaluate their role in macrophage polarization. Relationship among PART1, miR-372-3p, and TLR4 was evaluated. Effect of EV-PART1 on tumorigenicity in vivo was detected by subcutaneous tumorigenicity test in nude mice.ResultPART1 and TLR4 were upregulated while miR-372-3p was downregulated in HCC tissues and cells. PART1 increased HCC cell proliferation, migration, invasion, and EMT. Mechanistically, PART1 bound to miR-372-3p to downregulate its expression, whereas TLR4 was negatively targeted by miR-372-3p in the macrophages. EVs containing PART1, TLR4 overexpression, or miR-372-3p inhibition induced M2 polarization of macrophages. Also, EVs containing PART1 promoted M2 polarization of macrophages and the occurrence of HCC by affecting miR-372-3p/TLR4 axis.ConclusionHCC cell-derived EVs might up-regulate TLR4 by inhibiting miR-372-3p via PART1 delivery to promote macrophage M2 polarization in HCC.     

miR-222 targets ACOX1, promotes triglyceride accumulation in hepatocytes

BackgroundNon-alcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver diseases. However, the exact pathogenesis of NAFLD remains to be elucidated. Despite the association with tumors and cardiovascular diseases, the role of miR-222 in NAFLD remains unclear. The present study was to investigate the role of miR-222 in NAFLD.MethodsWild-type C57BL/6 mice were fed a high-fat diet for 12 weeks to induce NAFLD. Normal human liver cell line (L02) was cultured with free fatty acid (FFA)-containing medium to stimulate cell steatosis. The mRNA levels of miR-222 and acyl Coenzyme A xidase 1 (ACOX1) were detected by quantitative-PCR (Q-PCR). The prediction of ACOX1 as the target gene for miR-222 was conducted via TargetScan. The overexpression or inhibition of miR-222 was mediated by miR-222 mimics or antagomir, and intracellular triglyceride levels were measured using a triglyceride kit. Luciferase reporter assays verified ACOX1 as the target gene for miR-222.ResultsmiR-222 was significantly elevated in both the in vivo and in vitro NAFLD models. Overexpression of miR-222 significantly increased triglyceride content in the L02 cells, while inhibition of miR-222 expression restricted the accumulation of triglyceride. Overexpression of miR-222 significantly inhibited ACOX1 expression. Transient transfection assays verified that ACOX1 3′-UTR luciferase reporter activity could be inhibited by miR-222 overexpression.ConclusionsThe present study suggested that miR-222 promotes the accumulation of triglycerides by inhibiting ACOX1.     

MiR-628–5p Inhibits Cervical Carcinoma Proliferation and Promotes Apoptosis by Targeting VEGF

BackgroundIt has been reported that the dysregulation of microRNAs (miRNAs) is implicated in the biological processes of diverse diseases, including the tumorigenesis of human cancers. MicroRNA-628–5p (miR-628–5p) is differentially expressed and plays a critical role in several cancers, but the role of miR-628–5p in cervical cancer has not been well studied.MethodsThe TCGA database and RT-qPCR were used to evaluate the expression profile of miR-628–5p in cervical cancer tissues. Transfection efficiency of synthetic miRNAs was detected using RT-qPCR. The biological effects of miR-628–5p on cervical cancer cells were assessed by the CCK-8 assay, flow cytometry, western blot analysis, and the tube formation assay. The expression levels of key proteins involved in cell apoptosis, the cell cycle and the PI3K pathway were analyzed by western blot analysis. Bioinformatic analysis and the luciferase reporter assay were performed to investigate the targeted relationship between miR-628–5p and vascular endothelial growth factor (VEGF).ResultsMiR-628–5p was downregulated and negatively correlated with Ki-67 expression in cervical cancer tissues, and its low level predicted poor survival of patients. Functional assays indicated that miR-628–5p inhibited cell proliferation and promoted cell apoptosis. Mechanically, VEGF was verified to be a downstream target of miR-628–5p. Moreover, overexpression of VEGF could reverse the effects of miR-628–5p on VEGF/PI3K/AKT signaling, cell proliferation, apoptosis, the cell cycle and angiogenesis in cervical cancer.ConclusionsMiR-628–5p inhibited cervical cancer cell proliferation and promoted apoptosis by targeting VEGF.     

Identification of microRNA biomarkers in serum of patients at different stages of atrial fibrillation

BackgroundAtrial fibrillation (AF) is a type of cardiac arrhythmia which is caused by irregular electrical activities in the atria.ObjectiveTo identify serum microRNA (miRNA) biomarkers at three durations (duration since diagnosis of AF) of AF.MethodsThis study included 14 patients with AF and 8 healthy subjects. The blood sample was collected from each patient at baseline (time of diagnosis) and 12-month and 24-month follow-up periods. The serum was used for miRNA sequencing. The differentially expressed miRNAs (DEMs) between the 3 AF and control groups were independently compared. The predicted target genes of DEMs were subjected to functional enrichment and protein-protein interaction network analyses. Additionally, the miRNA-target gene networks were constructed for the 3 AF groups and miRNA time series analysis was performed. The expression of several key miRNAs was verified by real-time quantitative polymerase chain reaction (qRT-PCR).ResultsIn total, 28, 22, and 24 DEMs were identified in the baseline, 12-month, and 24-month groups, respectively. miR-483-5p was the common DEM in the 3 AF groups. In the baseline and 12-month groups, the miR-200b-3p and miR-125b-5p target genes were significantly enriched in the Wnt signaling and several cancer-related pathways, respectively. In the 12-month group, the miR-34a-5p target genes were enriched in the cancer-related pathways. In the miRNA-target gene network, miR-34a-5p regulated the highest number of target genes. The time series analysis revealed that 7 miRNAs, which were downregulated in the control group, were upregulated in the AF groups. The qRT-PCR analysis revealed that the 24-month group exhibited a significant upregulation of miR-483-5p (p < 0.05), whereas the baseline group exhibited significant a downregulation of miR-125b-5p (p < 0.05).ConclusionIn patients with AF, miR-125b-5p and miR-483-5p can be potential biomarkers of the baseline and 24-month periods, respectively.     

Effects of a low-fat diet on the hepatic expression of adiponectin and its receptors in rats with NAFLD

Background. Non-alcoholic fatty liver disease (NAFLD) is correlated with obesity, but specific therapeutic interventions are lacking. Adiponectin is an adipokine with anti-inflammatory activity and is considered a hepatic protector. We aimed to investigate effects of a low-fat diet on the hepatic expression of adiponectin and its receptors in rats with NAFLD.Materials and methods. Sixteen male SD rats were fed a high-fat diet for 8 weeks (HFD1 group) or 16 weeks (HFD2 group) to induce NAFLD, and these rats were compared with rats on a normal diet for 8 weeks (NC1 group) or 16 weeks (NC2 group). Another group of 8 rats was fed an HFD for 8 weeks and then switched to a low-fat diet (DIET group) until the 16th week. The expression of hepatic adiponectin and its receptors was detected by western blotting, immunohistochemistry and RT-qPCR.Results. The NAFLD activity score (NAS) in the HFD groups increased from 3.2 ± 0.45 (8th week) to 6.2 ± 0.84 (16th week) (P < 0.001), reflecting the progression in the NAFLD histology. In contrast to the HFD2 group, the low-fat diet ameliorated the steatosis, ballooning degeneration and inflammation. Dietary intervention augmented the expression of adiponectin and its receptors, which was down-regulated in the HFD2 group.Conclusions. The NAFLD rat model was successfully developed by feeding the animals a high-fat diet. Adiponectin may play a role in the pathogenesis of NAFLD, especially in the progression from steatosis to NASH. The low-fat diet alleviated the histological lesions associated with NAFLD by up-regulating the expression of adiponectin and its receptors.     

Circ_0078710 promotes the development of liver cancer by upregulating TXNDC5 via miR-431-5p

Introduction and objectivesLiver cancer, with high recurrence and metastasis rate, is a common malignant tumor. Circular RNA_0078710 (circ_0078710) has been shown to be take part in the advance of hepatocellular carcinoma. However, the interaction between circ_0091579 and microRNA-431-5p (miR-431-5p) in liver cancer has not been studied.Materials and methodsThe expressions of circ_0078710, miR-431-5p and Thioredoxin domain-containing 5 (TXNDC5) in liver cancer tissues and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The effect of cric_0078710 in liver cancer cells was assessed by Cell Counting Kit-8 (CCK-8) assay, Transwell, flow cytometry and Dual-luciferase reporter assay. Glycolysis metabolism was examined by lactate production, glucose uptake and ATP level. The protein levels of ki-67, bax and TXNEC5 were tested by western blot. The role of circ_0078710 in vivo was determined by animal study.ResultsCirc_0078710 and TXNDC5 were notably expressed in liver cancer tissues and cells. Circ_0078710 knockdown diminished proliferation, migration, invasion and glycolytic metabolism of huh7 and Hep3B cells, and accelerated cell apoptosis. MiR-431-5p is the target of circ_0078710, and silence circ_0078710 can inhibit the malignant behavior and glycolysis of hepatocellular carcinoma (HCC) cells by releasing miR-431-5p. In addition, TXNDC5 was a target of miR-431-5p, and overexpression of TXNDC5 restored cell proliferation and glycolysis inhibition due to miR-431-5p. Animal experiments made clear the anti-tumor effect of circ_0078710 knockdown.ConclusionCirc_0078710 promotes the progression of liver cancer by regulating TXNDC5 expression by targeting miR-431-5p. These results demonstrate that circ_0078710 could be a remedy target for liver cancer.