miR-204 inhibits proliferation of Hodgkin lymphoma cells by targeting Sirt1/p53 signaling pathway

AIM: To investigate the effect of microRNA-204 (miR-204) on the proliferation of Hodgkin lymphoma cells and the underlying mechanism. METHODS: The expression of miR-204 and Sirt1 mRNA in Hodgkin lymphoma tissues was detected by RT-qPCR. After transfection with miR-204 mimic, Sirt1 siRNA and miR-204 mimic+pcDNA3.1-Sirt1 into the L428 cells, the cell viability and BrdU incorporation were measured by CCK-8 assay and BrdU assay, respectively. The protein levels of Sirt1 and acetylated p53 (ac-p53) were determined by Western blot.The targeting relationship between miR-204 and Sirt1 was verified by double luciferase reporter assay. RESULTS: The low expression of miR-204 and the high mRNA expression of Sirt1 were found in the Hodgkin lymphoma tissues. Compared with control group, the cell viability, BrdU incorporation and the protein levels of Sirt1 and ac-p53 were significantly decreased after L428 cells were transfected with miR-204 mimic or Sirt1 siRNA (P<0.05). Compared with miR-204 mimic alone group, the cell viability, BrdU incorporation and the protein levels of Sirt1 and ac-p53 were increased after L428 cells were co-transfected with miR-204 mimic and pcDNA3.1-Sirt1 (P<0.05). The results of double luciferase reporter assay confiermed that Sirt1 was the target gene of miR-204. CONCLUSION: The inhibitory effect of miR-204 on the proliferation of L428 cells may be achieved by inhibiting the expression of Sirt1 and promoting the up-regulation of ac-p53.     

miRNA-7-mediated Bax/Bcl-2 expression promotes apoptosis of human nasopharyngeal carcinoma CNE-1 cells

AIM: To investigate the relationship of microRNA-7 (miRNA-7) over-expression and Bax/Bcl-2 expression in human nasopharyngeal carcinoma CNE-1 cells.METHODS: The CNE-1 cells were transfected with miRNA-7 mimics using Lipofectamine 2000. The expression of miRNA-7 was detected by real-time PCR. CCK-8 assay and Hoechst 33258 staining were used to detect the cell activity and apoptosis. The expression of Bax/Bcl-2 at mRNA and protein levels was determined by real-time PCR and Western blot. RESULTS: The expression of miRNA-7 was increased significantly in the CNE-1 cells compared with negative control group and mock group (P<0.01). The activity of CNE-1 cells were extremely decreased after tansfected with miRNA-7 mimics (P<0.01). The typical apoptotic nuclear morphological changes were observed in the CNE-1 cells under the fluorescence microscope with Hoechst 33258 staining. The expression of Bax at mRNA and protein levels was significantly increased compared with the other 2 groups (P<0.01), while the Bcl-2 expression at mRNA and protein levels was significantly down-regulated (P<0.01).CONCLUSION: Over-expression of miRNA-7 significantly inhibits the growth and promotes the apoptosis of nasopharyngeal carcinoma CNE-1 cells by increasing the expression of Bax and down-regulating Bcl-2.     

Effects of resveratrol on viability,invasion and autophagy of osteosarcoma MG-63 cells by up-regulating miR-34a

AIM: To investigate the effects of resveratrol on the viability, invasion and autophagy of osteosarcoma MG-63 cells and the regulatory effect of microRNA-34a (miR-34a). METHODS: MG-63 cells were divided into 6 groups:control group and resveratrol treatment groups at doses of 10, 20, 40, 60 and 80 μmol/L. MTT assay, Transwell chamber method and Western blot were used to detect the effects of resveratrol on the viability, invasion ability and expression of autophagy-related proteins in the osteosarcoma cells. The effect of resveratrol at different concentrations on the expression of miR-34a in the osteosarcoma cells was detected by RT-qPCR. The effects of miR-34a mimic and miR-34a mimic negative control (miR-34a NC) transfection on the viability and invasion ability of osteosarcoma cells after treated with resveratrol at different concentrations were analyzed. The effects of miR-34a mimic transfection on autophagy-related proteins LC3-I, LC3-Ⅱ and beclin-1 were determined by Western blot. RESULTS: Compared with control group, resveratrol inhibited the viability and invasion ability of the MG-63 cells and promoted autophagy (P<0.05). Resveratrol up-regulated the expression of miR-34a in the MG-63 cells in a dose-dependent manner (P<0.05). In addition, the ratio of LC3-Ⅱ/LC3-I was increased, and beclin-1 was up-regulated (P<0.05). Co-treatment with miR-34a mimic and resveratrol increased inhibitory effects of resveratrol on the viability and invasion ability and invasion of the MG-63 cells and also promoted autophagy. CONCLUSION: Resveratrol inhibits the viability and invasion of osteosarcoma MG-63 cells and promotes auto-phagy by up-regulating miR-34a expression.     

miR-34a induces senescence of bone marrow-derived mesenchymal stem cells under high glucose condition by SIRT1

AIM:To detect the effect and potential mechanism of microRNA-34a (miR-34a) on the senescence of bone marrow-derived mesenchymal stem cells (BMSCs) under high glucose condition. METHODS:BMSCs were isolated and cultured from 60~80 g male SD rats. The BMSCs were divided into 5 groups:normal glucose(NG) group, high glucose(HG) group, HG+miR-34a mimic group, HG+miR-34a NC group and HG+miR-34a inhibitor group. In order to confirm whether miR-34a regulated the senescence of BMSCs under high glucose condition by regulating the expression of silent information regulator 1(SIRT1), in addition to the above groups, HG+siRNA-SIRT1 group, HG+siRNA-NT group and HG+miR-34a inhibitor+siRNA-SIRT1 group were added. The expression of miR-34a and SIRT1 mRNA was detected by RT-qPCR. CCK-8 assay and senescence-associated β-galactosidase assay were used to detect cell viability and senescence, respectively. The protein expression of SIRT1, forkhead box O3a (FOXO3a) and P21 in the BMSCs was analyzed by Western blot. RESULTS:The expression of miR-34a in HG group was increased significantly compared with NG group (P<0.01), and long-term exposure of the BMSCs to high glucose lead to decreased cell viability and increased senescence (P<0.05). Compared with HG+miR-34a NC group, the cell viability in HG+miR-34a mimic group was decreased significantly (P<0.01), the senescence of BMSCs was increased significantly (P<0.01), the protein expression of SIRT1 was decreased significantly (P<0.01) and the protein expression of FOXO3a was increased significantly (P<0.01). However, inhibition of miR-34a expression showed the opposite effect to miR-34a mimic. Similar to the HG+miR-34a mimic group, the protein expression of P21 and FOXO3a in HG+siRNA-SIRT1 group were significantly higher than that in HG group (P<0.01). After adding siRNA-SIRT1 into HG+miR-34a inhibitor group, the inhibitory effect of the miR-34a inhibitor on the expression of P21 and FOXO3a in BMSCs were partly weakened (P<0.05). CONCLUSION:miR-34a regulate the senescence of BMSCs under high glucose condition by regulating the expression of SIRT1.     

Effects of extract of Oratosquilla on expression of P53, COX-2 and VEGF in human nasopharyngeal carcinoma cell line

AIM: To study the inhibitory effect of the extract of Oratosquilla(EOS) on the expression of P53, cyclooxygenase-2(COX-2) and vascular endothelial growth factor(VEGF) in nasopharyngeal carcinoma cell line CNE-2Z.METHODS: CNE-2Z cells were treated with different concentrations of EOS for 24 h. The methods of RT-PCR and immunocytochemistry were used to detect the expression of COX-2 and VEGF at mRNA and protein levels, respectively. The protein expression of P53 was determined by Western blotting.RESULTS: After treated with EOS, the protein expression of P53 in CNE-2Z cells was decreased(P<0.01), and the expression of COX-2 and VEGF at mRNA and protein levels was also significantly decreased in a dose-dependent manner(P<0.01). The expression of COX-2 was positively correlated with that of VEGF(P<0.05), and a positive correlation between the expression of COX-2 and P53 protein(P<0.05) was also observed.CONCLUSION: EOS may play its antitumor effect by inhibiting the expression of P53, COX-2 and VEGF in nasopharyngeal carcinoma cell line CNE-2Z.     

siRNA targeting TRIM29 gene induces apoptosis of nasopharyngeal carcinoma cells by inhibiting PI3K/AKT signaling pathway

AIM:To investigate the effect of TRIM29 gene expression silencing on the apoptosis and PI3K/AKT signaling pathway in human nasopharyngeal carcinoma 5-8F cells. METHODS:The 5-8F cells were divided into blank group, negative control (NC) group (transfected negative control siRNA) and si-TRIM29 group (transfected TRIM29 specific siRNA). The viability of the 5-8F cells transfected with si-TRIM29 for 0~96 h was measured by CCK-8 assay. The apoptotic rate and the protein levels of TRIM29, cleaved caspase-3, cleaved caspase-9, Bcl-2, Bax, t-AKT and p-AKT in the 5-8F cells transfected with si-TRIM29 for 48 h were determined by flow cytometry and Western blot, respectively. PI3K/AKT signal specific inhibitor LY294002 at 10 μmol/L and si-TRIM29 alone or in combination were treated with the 5-8F cells, and the cells were divided into blank group, LY294002 group and LY294002+si-TRIM29 group. The apoptotic rates in the 3 groups were detected by flow cytometry. RESULTS:The protein expression of TRIM29 in the 5-8F cells transfected with TRIM29 siRNA was significantly lower than that in blank group (P<0.05). Compared with blank group, the cell viability was significantly decreased, the apoptotic rate was significantly increased, the protein levels of cleaved caspase-3, cleaved caspase-9 and Bax were significantly increased, and the protein levels of Bcl-2 and p-AKT were significantly decreased in si-TRIM29 group (P<0.05). The apoptotic rate in LY294002 group was higher than that in blank group, while that in LY294002+si-TRIM29 group was even higher than that in LY294002 group (P<0.05). CONCLUSION:Silencing of TRIM29 gene expression induces apoptosis of nasopharyngeal carcinoma 5-8F cells by inhibiting PI3K/AKT signaling pathway.     

Effect of miR-34a expression on transplantation of adipose-derived stem cells for treatment of Achilles tendonitis

AIM: To elucidate the role of microRNA-34a (miR-34a) in transplantation of human adipose-derived stem cells (hADSCs) for treatment of Achilles tendonitis. METHODS: The viability of hADSCs transfected with miR-34a mimic and miR-34a inhibitor for 24 h, 48 h, 72 h and 96 h was measured by CCK-8 assay. A rat model of collagenase-induced Achilles tendonitis was established. The rats with Achilles tendonitis were divided into 5 groups:PBS group, hADSCs group, hADSCs+NC group, hADSCs+miR-34a group and hADSCs+anti-miR-34a group. The tendon tissues were isolated to detect stiffness, stress and maximum loading tension by biomechanical evaluation and to assess miR-34a expression level as well as the expression of collagen I, scleraxis (Scx) and tenascin C (TNC) at mRNA and protein levels by RT-qPCR and Western blot. RESULTS: miR-34a over-expression and knockdown suppressed and enhanced the viability of hADSCs in a time-dependent manner, respectively. Moreover, stiffness, stress and maximum loading tension in hADSCs group were increased compared with PBS group, while these biomechanical indexes in hADSCs+miR-34a group and hADSCs+anti-miR-34a group were improved and reduced as compared with hADSCs+NC group, respectively. Furthermore, up-regulation of collagen I, Scx and TNC expression at mRNA and protein levels was observed in hADSCs group as compared with PBS group. Meanwhile, miR-34a expression was increased but the expression of collagen I, Scx and TNC at mRNA and protein levels declined in hADSCs+miR-34a group. In contrast, reversed effects on the trends mentioned above were observed in hADSCs+anti-miR-34a group.CONCLUSION: miR-34a affects therapeutic outcome for Achilles tendonitis by regulating the viability and differentiation of hADSCs.     

Effect of transketolase-like protein 1 on proliferation of human nasopharyngeal carcinoma cells

AIM: To investigate the effect of transketolase-like protein 1 (TKTL1) on proliferation of human nasopharyngeal carcinoma cells in vitro. METHODS: The siRNA against TKTL1 mRNA was constructed and transfected into human nasopharyngeal carcinoma cells (CNE cell line). The activity of transketolase was detected before and after RNA interference.Real-time PCR was used to determine the mRNA expression of transketolase (TKT) gene family in the CNE cells.Flow cytometry and MTT test were used to detect the effect of anti-TKTL1 siRNA on cell proliferation and cell cycle in the CNE cells. RESULTS: The total transketolase activity was significantly decreased in the CNE cells transfected with siRNA TKTL1 construct compared with the cells transfected with control vector or untransfected CNE cells. No significant difference in the expression level of TKT and TKTL2 gene between the CNE cells transfected with siRNA TKTL1 construct and the cells transfected with control vector or untransfected CNE cells was observed (P>0.05). However, the expression level of TKTL1 gene was significantly downregulated in the CNE cells transfected with siRNA TKTL1 construct compared with the cells transfected with control vector.Cancer cells were arrested in G0/G1 phase, and cancer cell proliferation was significantly inhibited in the CNE cells transfected with siRNA TKTL1 construct. CONCLUSION: TKTL1 plays an important role in the total transketolase activity and cell proliferation of human nasopharyngeal carcinoma. TKTL1 may be considered as a potential target for novel anti-cancer therapy.     

Expression of miR-625-3p in colorectal carcinoma tissues and cells

AIM: To investigate the expression of microRNA-625-3p (miR-625-3p) in colorectal carcinoma (CRC) and its underlying mechanism. METHODS: Quantitative real-time PCR was employed to detect the levels of miR-625-3p expression in different CRC cell lines, CRC tissues and pair-matched adjacent normal tissues. The relationships between the expression levels of miR-625-3p and the patients' clinicopathological parameters were estimated. The effects of miR-625-3p on the apoptosis and the cell mitotic cycle of CRC cells were analyzed with propidium iodide staining and flow cytometry. The effect of miR-625-3p on the apoptosis-related proteins was analyzed by Western blot. RESULTS: The expression level of miR-625-3p in the CRC tissues was higher than that in the pair-matched adjacent normal tissues (P<0.05). The expression of miR-625-3p in the CRC tumor tissues was significantly correlated with the tumor infiltrative depth, TNM stage and distant metastasis (P<0.05). The expression levels of miR-625-3p in CRC SW620 cells were higher than that in SW480 cells. The CRC cell mitotic cycle was significantly inhibited and cell apoptosis was significantly promoted when the expression of miR-625-3p was inhibited (P<0.05). The expression of Bax protein didn't change and the expression of Bcl-2 protein increased after miR-625-3p mimics were transfected into CRC SW620 cells(P<0.05). CONCLUSION: miR-625-3p may be a promising approach for the treatment of CRC by promoting cell proliferation and inhibiting apoptosis.     

miRNA-7 inhibits proliferation of human nasopharyngeal 5-8F carcinoma cells via EGFR/PI3K/Akt pathway

AIM:To investigate the relationship of microRNA-7 (miRNA-7) over-expression and epidermal growth factor receptor (EGFR)/phosphatidylinositol kinase-3 (PI3K)/protein kinase B (PKB, also called Akt) pathway in human nasopharyngeal carcinoma 5-8F cells. METHODS:The 5-8F cells were transfected with miRNA-7 mimics (carrying by Lipofectamine 2000). The expression of miRNA-7 was detected by real-time PCR. The cell proliferation was analyzed by CCK-8 assay. The cell colony-forming capability was determined by cell colony formation test. The expression of EGFR/PI3K/Akt at mRNA and protein levels was examined by real-time PCR and Western blotting. RESULTS:The expression level of miRNA-7 was significantly increased in 5-8F cells compared with negative control (NC) group and control group (P<0.01). The proliferation of NPC 5-8F cells was decreased extremely after tansfected with the miRNA-7 mimics (P<0.01), so did the result of the cell colony-formation test. The expression of EGFR/PI3K/Akt at mRNA and protein levels was significantly down-regulated compared with NC group and control group (P<0.01). CONCLUSION: Over-expression of miRNA-7 significantly inhibits the proliferation and colony-forming ability of nasopharyngeal carcinoma 5-8F cells by down-regulation of EGFR/PI3K/Akt pathway.     

miR-509 regulates growth,invasion and migration of human hepatocellular carcinoma LM3 cells and survival of nude mice

AIM: To investigate the effect of microRNA-509 (miR-509) on the growth, invasion and migration of human hepatocellular carcinoma (HCC) LM3 cells and survival of tumor-bearing nude mice. METHODS: LM3 cells were transferred with miR-509 mimic and pcDNA Ras-related C3 botulinum toxin substrate 1 (pcRac1), and the expression of Rac1 was measured by Western blot. The relationship between miR-509 and Rac1 was determined by luciferase reporter assay. The invasion ability was determined by Transwell assay, and the migration ability was measured by wound healing assay. Xenograft model of HCC was established by subcutaneous injection with LM3 cells into nude mice. The survival rate of the mice were recorded and the protein level of Rac1 was determined by Western blot. RESULTS: miR-509 mimic inhibited the expression of Rac1 in the LM3 cells (P<0.05). pcRac1 attenuated the effect of miR-509 on Rac1. miR-509 also alleviated luciferase activity of wild Rac1 (P<0.05). Meanwhile, miR-509 mimic decreased the number of invasive LM3 cells and inhibited the migration of LM3 cells (P<0.05). In addition, over-expression of miR-509 up-regulated survival rate of model mice and decreased the protein level of Rac1 in the tumor tissue (P<0.01). CONCLUSION: miR-509 inhibits the invasion and migration of HCC cells and promotes the survival of tumor-bearing nude mice through inhibiting the expression of Rac1.     

X-ray ionizing radiation induces epithelial-mesenchymal transition in human nasopharyngeal carcinoma CNE-2 cells

AIM:To investigate the effect of X-ray ionizing radiation on epithelial-mesenchymal transition (EMT) in human nasopharyngeal carcinoma CNE-2 cells and its involved potential signaling pathway. METHODS:The nasopharyngeal carcinoma CNE-2 cells were irradiated with different doses (0 Gy, 2 Gy, 4 Gy and 8 Gy) of X-ray. The morphological changes of the cells were observed under inverted microscope after 24 h. The migration and invasion abilities were detected by wound healing and Transwell assays. The mRNA and protein levels of E-cadherin, N-cadherin and vimentin in nasopharyngeal carcinoma CNE-2 cells were determined by real-time PCR and Western blot, respectively. The protein levels of Akt and p-Akt were detected by Western blot. RESULTS:After X-ray irradiation, the CNE-2 cells exhibited typical ‘cobblestone’ or spindle-like shape, with extended pseudopodia and dilated intercellular space. The invasiveness and metastatic abilities of the CNE-2 cells were enhanced (P<0.01). The mRNA and protein expression levels of E-cadherin were significantly decreased (P<0.01), while the mRNA and protein expression levels of N-cadherin and vimentin were markedly increased after irradiation as compared with the control group (no irradiation) (P<0.05). The protein level of p-Akt was significantly enhanced (P<0.01), while the protein level of Akt showed little change after irradiation. CONCLUSION:X-ray ionizing radiation induces EMT in nasopharyngeal carcinoma CNE-2 cells, which may be related to the activation of PI3K/Akt signaling pathway.     

Role of ClC-3 chloride channel in inhibition of nasopharyngeal carcinoma cell cycle by metformin

AIM: To study the roles of ClC-3 chloride channel in the inhibition of nasopharyngeal carcinoma cell cycle by metformin. METHODS: The CNE-2Z cells were treated with metformin at different concentrations. The viability of CNE-2Z cells was measured by CCK-8 assay. The cell cycle distribution was detected by flow cytometry. The protein expression of ClC-3 was determined by Western blot. The Cl^- currents was record by the patch-clamp technique. In addition, the cell cycle distribution was analyzed in the nasopharyngeal carcinoma CNE-2Z cells which over-expressed ClC-3 by pEZ-M03-ClC-3 plasmid transfection. RESULTS: Metformin inhibited the viability of CNE-2Z cells at 5, 10 and 20 mmol/L. Metformin at 10 mmol/L prevented the activation of chloride currents induced by hypotonicity, inhibited the protein expression of ClC-3 chloride channel and arrested the nasopharyngeal carcinoma CNE-2Z cells at G₀/G₁ phases. ClC-3 chloride channel protein over-expression reversed the effect of metformin on the cell cycle distribution of CNE-2Z cells. CONCLUSION: Metformin inhibits the CNE-2Z cell cycle, which may be related to the inhibition of ClC-3 chloride channel function and protein expression.     

miR-556-3p regulates viability,migration and invasion of endometrial cancer cells by targeting SASH1

AIM To investigate whether microRNA-556-3p （miR-556-3p） regulates the viability, migration and invasion of endometrial cancer cells by targeting SASH1 gene. METHODS The expression of miR-556-3p, and the mRNA and protein levels of SASH1 in endometrial cancer tissues were detected by RT-qPCR and Western blot. Anti-miR-556-3p or pcDNA-SASH1 was transfected into endometrial cancer Ishikawa cells. The cell viability was detected by MTT assay, the migration and invasion abilities of the cells were detected by Transwell chamber method, and the protein expression levels of cyclin D1, p21, matrix metalloproteinase-2 （MMP-2） and MMP-9 were detected by Western blot. StarBase prediction and dual-luciferase reporter experiments were used to analyze the targeting relationship between miR-556-3p and SASH1. Anti-miR-556-3p and si-SASH1 were co-transfected into the Ishikawa cells, and their effects on cell viability, migration and invasion were examined by the methods described above. RESULTS Compared with adjacent tissues, the expression of miR-556-3p in endometrial cancer tissues was increased significantly, and the expression of SASH1 at mRNA and protein levels was decreased significantly （P<0.05）. Inhibition of miR-556-3p expression or induction of SASH1 over-expression obviously reduced the viability of Ishikawa cells, the number of migratory cells, the number of invasive cells and the protein levels of cyclin D1, MMP-2 and MMP-9, and dramatically increased the protein level of p21 （P<0.05）. miR-556-3p targeted SASH1 and negatively regulated its expression. Knock-down of SASH1 expression reversed the inhibitory effect of miR-556-3p expression inhibition on the viability, migration and invasion of Ishikawa cells. CONCLUSION Inhibition of miR-556-3p expression suppresses the viability, migration and invasion of endometrial cancer cells. The mechanism is related to the regulation of its target gene SASH1.     

miR-140-3p inhibits viability,invasion and migration of non-small-cell lung cancer A549 cells by targeting PD-L1

AIM: To explore the target relationship between microRNA-140-3p (miR-140-3p) and programmed cell death ligand 1 (PD-L1) and their effect on the viability, migration and invasion of non-small-cell lung cancer A549 cells.METHODS: RT-qPCR was used to detect the miR-140-3p expression in HLF-1, A549 and H1299 cells, and then the A549 cells with the most significant difference were selected as the subsequent research object. TargetScan software and dual-luciferase reporter assay were performed to predict and confirm the target relationship between miR-140-3p and PD-L1. RT-qPCR and Western blot were used to determine the effects of miR-140-3p mimic and inhibitor on PD-L1 expression level. MTT assay was used to detect the viability of A549 cells. Transwell assay was performed to detect the migration and invasion abilities of the A549 cells.RESULTS: miR-140-3p was significantly down-regulated in the A549 cells and H1299 cells (P<0.05). Transfection with miR-140-3p mimic decreased the expression of PD-L1 and inhibited the viability, migration and invasion of the A549 cells. Transfection with pcDNA3.0-PD-L1 reversed the inhibitory effect of miR-140-3p on the viability, migration and invasion of the A549 cells.CONCLUSION: miR-140-3p inhibits the viability, migration and invasion of A549 cells by targeting PD-L1.     

Paeonol affects viability and migration ability of hepatocellular carcinoma cells by up-regulating miR-424-3p and inhibiting PI3K/AKT signaling pathway

AIM To investigate the effect of paeonol on the viability and migration ability of hepatocellular carcinoma cells and its molecular mechanism. METHODS Human hepatocellular carcinoma Hep3B cells was treated with paeonol at different concentrations (50, 100, 200 and 400 mg/L). The cell viability was measured by CCK-8 assay to determine the optimal drug concentration. The Hep3B cells were divided into normal control (NC) group, paeonol group, miR-NC group, miR-424-3p group, paeonol+anti-miR-NC and paeonol+anti-miR-424-3p group. The expression level of miR-424-3p was detected by RT-qPCR. The migration ability was detected by Transwell assay. The protein levels of cyclin D1, matrix metalloproteinase 2 (MMP2), MMP9 and PI3K/AKT signaling pathway-related molecules were determined by Western blot. RESULTS Paeonol intervention inhibited the viability of Hep3B cells in a concentration-dependent manner (P<0.05). The concentration of paeonol at 200 mg/L was selected for the following study. Paeonol intervention inhibited the protein expression of MMP2 and MMP9 in the Hep3B cells, and inhibited the migration ability of the Hep3B cells. Paeonol intervention promoted the expression of miR-424-3p in the Hep3B cells (P<0.05). Over-expression of miR-424-3p inhibited the expression of cyclin D1, MMP2 and MMP9 in the Hep3B cells and inhibited cell viability and migration ability (P<0.05). Inhibition of miR-424-3p reversed the effect of paeonol on the viability and migration ability of the Hep3B cells (P<0.05). Paeonol inhibited phosphorylation levels of PI3K and AKT in the Hep3B cells and inhibited the activation of PI3K/AKT signaling pathway (P<0.05). Inhibition of miR-424-3p reversed the effect of paeonol on PI3K/AKT signaling pathway in the Hep3B cells (P<0.05). CONCLUSION Paeonol inhibits the viability and migration ability of hepatocellular carcinoma cells by up-regulating miR-424-3p and inhibiting PI3K/AKT signaling pathway.