Ethanol extract of Ardisiae Japonicae Herba inhibits hepatoma carcinoma cell proliferation in vitro through regulating lipid metabolism / 中草药·英文版

Objective: The aim of this study is to discover the possible working mechanisms of Ardisiae Japonicae Herba (AJH) on hepatoma carcinoma (HCC). Methods: In this study, ethanol extract of AJH was prepared and used to treat HCC cell in vitro. Furthermore, a genomic wide RNA sequencing (RNA-seq) was performed to screen deregulated genes in HCC cells after the treatment of AJH extract. The gene and protein expression related to lipid metabolism in HCC cells were also investigated to validate the results obtained from RNA-seq. Results: AJH extract could inhibit HCC cell proliferation in vitro. RNA-seq analysis has identified 1,601 differentially expressed genes (DEGs, fold change ≥ 2.0 or fold change ≤ 0.5, P < 0.05) in HCC after AJH extract treatment, which included 225 up-regulated genes and 1,376 down-regulated genes. KEGG pathway analysis of DEGs demonstrated that lipid metabolism was a potential pathway related to AJH treatment. In agreement with the RNA-seq data, qPCR and Western-blot analysis indicated that expression of genes and proteins related to lipid metabolism (SREBP1, ACC, ACLY and FASN) were significantly down-regulated in AJH treatment group as compared with the control group. Furthermore, AJH extract could also decrease lipid contents and cellular free fatty acid levels in HCC cells. Conclusion: Ethanol extract of AJH could inhibit HCC cell proliferation in vitro, the possible mechanism may be related to the inhibition of lipid metabolism.

Activation of hepaticstellate cells cocultured with hepatoma carcinoma cells in vitro and in vivo / 西安交通大学学报(医学版)

Objective: To investigate the activation of hepatic stellate cells (HSCs) cocultured with hepatoma carcinoma cells. Methods: MHCC97H cells and HSCs were cocultured by cell-cell contact method, fibrinogen-thrombin paste technique, conditioned media from MHCC97H(MHCC97H-CM) and Transwell coculture technique, respectively. MHCC97H cells and HSCs were inoculated s. c. into nude mice. The expression of α-SMA in HSCs was assessed by immunocytochemical staining and Western blotting. Proliferation and migration of HSCs was determined using Cell-Counting Kit-8 (CCK-8) and wound healing and Transwell technique, respectively. Results: The activation of HSCs was significantly increased in the all cocultured system. The expression of α-SMA was up-regulated by cell-cell contact method, MHCC97H-CM, Transwell coculture technique in vitro and in cancer-bearing mice in vivo. The increased chemotaxis of MHCC97H cells and HSCs was observed by cell-cell contact method, fibrinogen-thrombin paste technique and in cancer-bearing mice. The proliferation and migration abilities of HSCs were significantly enhanced. Conclusion: Hepatoma carcinoma cells can promote the activation, proliferation and migration of HSCs under the cocultured system in vitro and in vivo.

The long non-coding RNA H19 induces hypoxia/reoxygenation injury by up-regulating autophagy in the hepatoma carcinoma cells

BACKGROUND: Long non-coding RNA H19 (H19) plays an important role by regulating protein expression in different tissues and organs of the body. However, whether H19 induces hypoxia/reoxygenation (h/R) injury via increase of autophagy in the hepatoma carcinoma cells is unknown. RESULTS: H19 was expressed in the hepatoma carcinoma cells (Hep G2 and HCCLM3 cells) and its expression was most in 8 h/24R. The knockdown of H19 and 3-MA (an autophagy inhibitor) protected against h/R-induced apoptosis, cell damage, the expression of cleaved caspase-3 and cleaved caspase-9, the release of cytochrome c (Cyt c). The knockdown of H19 and 3-MA also decreased the autophagic vesicles (AVs) and the expression of Beclin-1 and the ration of LC3-II/LC3-I, and increased cell viability, the expression of Bcl-2 and P62 and the phosphorylation of PI3K, Akt and mTOR. In addition, chloroquine (CQ, an inhibitor of autophagy flux) markedly decreased formation of autophagy flux (the ration of LC3-II/LC3-I). The results of the knockdown of H19 group were similar to those of the 3-MA (or CQ) group. Rapamycin (a mTOR inhibitor, an autophagy activator) further down-regulated h/R-induced decrease of the phosphorylated PI3K, Akt and mTOR. The knockdown of H19 cancelled the effect of rapamycin. The overexpression of H19 further expanded h/R-induced increase of the ration of LC3-II/LC3-I and decrease of the phosphorylated PI3K, Akt and mTOR. CONCLUSIONS: Our results suggest that the long non-coding RNA H19 induces h/R injury by up-regulation of autophagy via activation of PI3K-Akt-mTOR pathway in the hepatoma carcinoma cells.

Regulatory effects and mechanism of aconitine on proliferation,invasion and migration of hepatoma carcinoma cell MHCC97 / 中国免疫学杂志

Objective:To investigate the anticancer activity and mechanism of aconitine on cell proliferation,invasion and migration of hepatoma carcinoma cell(HCC).Methods:The effect of aconitine at different concentrations on proliferation was calculated by MTT assay.The effects of aconitine on invasion and migration of HCC were measured by Transwell and wound healing assay.Western blot was employed to detect the protein levels of P38MAPK signaling pathway-related proteins.Results:The concentrations of 5,10,20 μg/ml were selected according to the results of pre-experiment.Aconitine(10,20 μg/ml) inhibits proliferation and invasion of MHCC97 cells markedly after cells were treated with aconitine for 4 days.Treatment with aconitine down-regulated the ability of migration and decreased the ratio of p-P38/P38 and protein levels of p-MAPKAPK and p-HSP27.Conclusion:Aconitine inhibits prolif-eration,invasion and migration,and the mechanism may related with P38MAPK signaling pathway.

A new mitochondria-targeted platinum complex Mor-platin inhibits HepG2 cell prolif-eration and cell invasion / 中国肿瘤临床

Objective:To investigate the effects of Mor-platin, a novel mitochondrial platinum complex, on proliferation and migration of human hepatoma carcinoma HepG2 cells. Methods:Cell counting kit-8 (CCK-8) assay was used to analyze cell proliferation of Mor-platin and classic anticancer drugs, particularly cisplatin, in HepG2 cells. A laser confocal microscope was used to observe whether Mor-platin can target mitochondria. The morphological changes in cellular mitochondria after treatment with Mor-platin were ob-served on a transmission electron microscope. Cell apoptosis was measured by flow cytometry, and cell invasion was evaluated by three-dimensional tumor spheroid model. Results:Mor-platin can inhibit cell proliferation and is dose dependent. The half inhibitory concentration (IC50) of Mor-platin is lower than that of cisplatin. Laser confocal images showed that Mor-platin can target cell mito-chondria and enrich cell mitochondria. Transmission electron microscopy images showed that cell mitochondrial morphology changed after Mor-platin treatment. Furthermore, cell mitochondrial membrane is incomplete and mitochondrial cristae are reduced. Cell apoptosis caused by Mor-platin is dose dependent. The three-dimensional tumor spheroid model showed that the cell areas of the group subjected to Mor-platin treatment are smaller than those of the control group. Conclusion:Mor-platin can target cell mitochon-dria, change the cell mitochondrial morphology, inhibit cell proliferation, and thus promote cell apoptosis. It also showed better anti-cancer effects than cisplatin. Furthermore, Mor-platin can inhibit three-dimensional tumor spheroid invasion. These results suggest that Mor-platin is a potential antitumor drug.

Influence of Toxoplasma gondii on in vitro proliferation and apoptosis of hepatoma carcinoma H7402 cell

Objective: To discuss the influence of tachyzoite of Toxoplasma gondii (T. gondii) RH strain on proliferation and apoptosis of hepatoma carcinoma (HCC) H7402 cell. Methods: The HCC H7402 cell in logarithmic phase and tachyzoite of T. gondii RH strain in different concentrations (1 × 10

Influence of Toxoplasma gondii on in vitro proliferation and apoptosis of hepatoma carcinoma H7402 cell

OBJECTIVE@#To discuss the influence of tachyzoite of Toxoplasma gondii (T. gondii) RH strain on proliferation and apoptosis of hepatoma carcinoma (HCC) H7402 cell.@*METHODS@#The HCC H7402 cell in logarithmic phase and tachyzoite of T. gondii RH strain in different concentrations (1 × 10(7)/mL, 2 × 10(7)/mL, 4 × 10(7)/mL, 8 × 10(7)/mL and 16 × 10(7)/mL) were co-cultured. CCK-8 was utilized to determine the inhibition rate of T. gondii tachyzoite on H7402 cell growth. Flow cytometry was used to detect the change of cell cycle. RT-PCR method was used to detect the expression of cyclinB1 and cdc2-two genes related to cell cycle. Western blot method was used to detect the expression of apoptosis-related proteins Caspase-3 and Bcl-2.@*RESULTS@#The tachyzoite of T. gondii RH strain can inhibit the proliferation of HCC H7402 cells. The inhibition rate of tumor cell growth increased with the increase of concentration of T. gondii tachyzoite. With the increase of concentration of T. gondii tachyzoite, the proportion of G0/G1 phase of H7402 cell increased, the proportion of S phase decreased, and PI value decreased accordingly. The expression of cyclinB1 and cdc2 genes decreased with the increase of the concentration of T. gondii tachyzoite. With the increase of the concentration of tachyzoite of T. gondii RH strain, the expression quantity of Caspase-3 in H7402 cell increased, but the expression quantity of Bcl-2 protein decreased.@*CONCLUSIONS@#T. gondii can inhibit the in vitro proliferation of HCC H7402 cell, and induce its apoptosis. This effect shows a trend of concentration-dependent increase. Moreover, it is related to the down-regulation of cyclinB1 and cdc2 (cell cycle-related genes), the increase of apoptosis-related protein Caspase-3, and the decrease of Bcl-2 expression.

The effects of HSPC238 on the expression of RB in hepatoma carcinoma cells / 国际检验医学杂志

Objective To investigate the effect of up‐regulation and down‐regulation of HSPC238 on the RB gene mRNA and pRb protein .Methods PcDNA3 .1‐HSPC238 vector and PLL3 .7‐HSPC238 vector was transiently transfected into HepG2 cells re‐spectively .The level of RB mRNA was detected by real‐time PCR and pRb was detected by Western blotting .Results The level of RB mRNA and pRb in up‐regulation group both increased compared with control grops respectively .Conversely ,the level of RB mRNA and pRb in up‐regulation group both decreased compared with control grops respectively .Above results were all statistically significant(P<0 .05) .Conclusion HSPC238 could have a positive effect on the expression of the RB gene .

Effects of Propofol on Hepatoma Carcinoma HepG2 Cell Invasion / 中国药房

OBJECTIVE:To study the effects of propofol on invasion of hepatoma carcinoma HepG2 cell. METHODS:MTT method was used to detect the viability of HepG2 cells which were cultured with 0(negative control),1,3 and 10 μg/ml propofol for 48 h. The ability of cell invasion was detect by Tranaswell method. The phosphorylation level of nuclear factor-κB p65(NF-κB p65) and the expression of matrix metalloproteinase 2 (MMP-2),MMP-9,E-cadhherin and Snail were detected by Western blot method. RESULTS:Compared with negative control,1,3,10 μg/ml propofol inhibited the cell viability and invasion,down-regu-lated the expression of Snail and the phosphorylation level of NF-κB p65,and up-regulated the expression of E-cadherin (P<0.01). 3,10μg/ml propofol down-regulated the expression of MMP-2 and MMP-9(P<0.01). Above effects depended on drug con-centration(P<0.01). CONCLUSIONS:Propofol can suppress HepG2 invasion,which might be related to the inhibition of NF-κB/Snail signal pathway.

Research on inhibition mechanism of polypeptide extract from scorpion venom combined with Rapamycin on angiogenesis of H22 hepatoma / 中草药

Objective: To study the inhibition of polypeptide extract from scorpion venom (PESV) combined with Rapamycin (RAPA) on angiogenesis of H22 hepatoma and its mechanism. Methods: The H22 carcinoma cell suspension was subcutaneously inoculated into 40 Kunming mice. Then tumor-bearing mice were randomly divided into four groups, i.e., control group, PESV group (20 mg/kg), RAPA group (2.5 mg/kg), and PESV + RAPA group, 10 mice in each group. The intervention was lasted 14 d. The tumor volume was measured once every other day, the tumor volume growth curve was drawn, and the tumor inhibitory rate was calculated. The protein expression levels of mammal target of RAPA (mTOR), hypoxia-inducible factor-1α (HIF-1α), and vascular endothelial growth factor-A (VEGF-A) were detected by immunohistochemical assay. Microvessel was signed by factor VIII and then detected by immunohistochemical assay. Results: The growth speed of H22 hepatoma transplantation tumor was obviously inhibited in the PESV group, RAPA group, and PESV + RAPA group compared with control group after 14 d intervention (P 22 hepatoma, the mechanism maybe related to the inhibition on the protein expression of mTOR, HIF-1α, and VEGF-A.

Effect of magnetic nanocomposites on proliferation ability of human hepatoma carcinoma cells / 器官移植

Objective To investigate the effect of magnetic nanocomposites on proliferation ability of human hepatoma carcinoma (HCC)cells (HepG2 cell line).Methods Leucine-rich repeat-containing G protein-coupled receptor (LGR) 5-small interfering ribonucleic acid (siRNA ) was composited with polyethylenimine wrapped superparamagnetic iron oxide nanoparticle (PEI-SPIO)as the gene vector.PEI group was established by transfecting HepG2 cells when cell fusion reached 60% and SI group was established by transfecting HepG2 cells with equivalent simple LGR5-siRNA.Control (Ctrl)group was also established without transfecting.The efficiency of nanocomposites entering cells was scanned with MRI T2.The inhibition rate of cell proliferation was detected by (cell count kit,CCK)-8 assay.The expression level of messenger ribonucleic acid (mRNA)in LGR5 of cells was detected by reverse transcriptase polymerase chain reaction (RT-PCR)and the protein expressions of LGR5 and cyclin D1 were detected by western blotting.Results MRI T2 signal of HepG2 cells in PEI group decreased significantly.Compared with Ctrl group,the inhibition rate of cell proliferation of HepG2 cells in PEI group was significantly increased.The relative expression of LGR5 mRNA and the relative expression of LGR5 and cyclin D1 protein were both significantly decreased (all in P <0.05),while the corresponding indexes of the cells in SI group had no statistical significance (all in P>0.05 ).Conclusions Magnetic nanocomposites PEI-SPIO composited with LGR5-siRNA may effectively transfect HepG2 cells.Its mechanism may take effect through down-regulating the expression of cyclin D1 to inhibit the proliferation ability of hepatocellular carcinoma HepG2 cells.

The effect of simvastatin on the gap junction function of hepatocellular carcinoma cells / 中国癌症杂志

Background and purpose:It has been reported that gap junctional (GJ) function was signiifcantly decreased in hepatocellular carcinoma (HCC) tissues and cell lines. However, the increased GJ suppress tumorigenesis and the development of liver cancer. This study therefore aimed to examine the effect of simvastatin on GJ function between Hep3b cells. Thus, the exploition of drugs to increase GJ function between liver cancer cells will provide an efifcient approach to ifght against liver tumor as well as increase cytotoxicity of antitumor agents.Methods:SRB was used to assay the toxicity of simvastatin. The effect of simvastatin on GJ function was determined by “Parachute” dye-coupling assay and scrape loading/dye transfer assay.Results:Pretreated Hep3b cells with simvastatin at the concentration of 1, 5 or 10 μmol/L for 24 h did not induce the cytotoxicity. So simvastatin at the concentration of 5 and 10 μmol/L would not reduce the amount of GJ on cell membranes. “Parachute” dye-coupling assay showed that the treatment with 5 and 10 μmol/L simvastatin for 4 h enhanced the dye spread through GJ in Hep3b cells. Similarly, scrape loading/dye transfer assay showed that simvastatin could induce the increasing spread of lucifer yellow (Ly, Sigma) around the scoifng cells with increasing concentrations.Conclusion:Simvastatin could increase the GJ function of Hep3b cells.

Antitumor effect of volatile oil from Sinapis Albae Semen on H22-bearing mice and its mechanism / 中草药

Objective: To investigate the antitumor effect of volatile oil from Sinapis Albae Semen (VOSAS) on H22-bearing mice and to determine the mechanism. Methods: To establish the H22 implanted hepatocellular carcinoma animal model which was used to analyze the effect of VOSAS on the growth of transplanted tumor. Mice were divided into five groups 24 h after modeling: model, cytoxan (CTX, 25 mg/kg) positive control, low-, mid-, and high-dose (20, 40, and 80 mg/kg) VOSAS groups. The mice were ip administered once daily for 10 d. Morphological changes in H22 solid tumor cells were observed by both Hematoxylin-eosin (HE) and acridine orange (AO) staining. The expression of Bax and Bcl-2 in the tumor tissue was determined using immunohistochemistry. Results: VOSAS could inhibit the tumor growth and extend the life span of H22-bearing mice (P < 0.01); and it could also raise the expression of Bax while suppress the expression of Bcl-2; the antitumor effect of VOSAS on H22-bearing mice demonstrated a good dose-effect relationship, but the high-dose group of the volatile oil has obvious toxicity and side effects on the mice. Conclusion: VOSAS could inhibit the growth of H22 tumor cells and the mechanism may be related to up-regulating the expression of Bax and down-regulating the expression of Bcl-2, and the induction of apoptosis.

Effects of substrate stiffness on confluent growth of hepatic and hepatoma carcinoma cells / 医用生物力学

Objective To investigate the cause of differences in confluent growth between hepatic(L02) and hepatoma carcinoma(HCCLM3) cells by comparing responses of the two cells to different substrate stiffness (0.5, 4 kPa and glass). MethodsThe real-time photomicrography, immunofluorescence staining, flow cytometry, and Western Blotting techniques were respectively employed to observe the morphological characteristics, the cytoskeleton conformation and the distribution of E-cad of confluent L02 and HCCLM3 cells on different substrates, and test the changes in expression of E-cad, Integrinβ1 and p-Src. Results (1) Confluent L02 cells displayed a round or cubic shape, while HCCLM3 cells showed a polygon shape. The morphology of HCCLM3 cells were spread and polarized more obviously than that of L02 cells. With the increase of substrate stiffness, the variation of L02 cells with time was smaller than that of HCCLM3 cells. (2) The cytoskeleton of confluent L02 cells showed a ring-like conformation under the cortex, and E-cad was located at the cell-cell contact sites. However, the ring-like cytoskeleton of HCCLM3 cells was incomplete and distributed radially along the basement, while E-cad was dispersed in cytoplasm. (3) As the substrate stiffness increased, expression of E-cadherin in both L02 and HCCLM3 cells was significantly decreased (P<0.01), while the level of p-Src and integrinβ1 was increased significantly, with greater changes in HCCLM3 cells than in L02 cells. Conclusions The assembling of cortical ring-like cytoskeleton was positively correlated with the location of E-cad at the cell-cell contact sites. The substrate stiffness showed a more obvious impact on the balanced regulation between cadherin and integrin mediated adhesion system of hepatocarcinoma cells than that of hepatic cells.

Effects of substrate stiffness on the migration of hepatic and hepatoma carcinoma cells / 医用生物力学

Objective To investigate the cause of tumor cell migration by comparing the effect of substrate stiffness on hepatic and hepatoma carcinoma cell migration so as to understand the invasive characteristics of tumor cells. Methods Immunofluorescence staining, morphological analysis and transwell were employed to observe the morphological characteristics of HCCLM3 and L02 cells on different substrates and test their migration characteristics with the quantitative analysis. Results (1) The migration rate and net translocation of HCCLM3 and L02 cells on 4 kPa substrate was higher than those both on 0.5 kPa(most soft one) and on glass (the hardest one) substrates, and L02 cells also displayed higher migration efficiency than HCCLM3 cells on such substrates. (2) The mean squared displacement of HCCLM3 and L02 cells on different substrates showed consistent tendency, and the directional persistence of L02 cells on the softer substrate was significantly higher than that of HCCLM3 cells. (3) In 0.5 and 1 mg/mL three dimensional collagen environment, the number of invasive cells of HCCLM3 was remarkably more than that of L02 cells. After adding MMPs inhibitor GM6001 (40 μg/mL), the number of invasive cells was notably increased in HCCLM3 cells, but notably decreased in L02 cells. Conclusions (1) In two dimensional comparatively soft environment, L02 cells displayed an efficient migration due to its higher directional persistence. (2) In three-dimensional collagen environment, the invasion efficiency of HCCLM3 cells was significantly higher due to the various modes of migration adaptation to the microenvironment.

Effect of N-Ras by RNA interference on radiosensitivity of hepatoma carcinoma cell MHCC97-H line / 中华放射医学与防护杂志

Objective To investigate the radiosensitivity of silencing N-Ras by RNA interference in hepatoma carcinoma cell MHCC-97.Methods N-Ras RNA interference (RNAi) vector was constructed by using pcDNA 6.2-GW/EmGFP-mir plamid.The RNAi effect was detected by RT-PCR,Western bolt,immunohistochemisty and MTT method.Survival curve for each cell line were obtained by measuring the clone forming abilities of irradiated cell populations.Results After silencing the N-Ras by RNAi,The expression level of N-Ras mRNA,N-Ras protein,immunohistochemisty were decreased 96.9% ±0.159%(t=40.377,P＜0.05),89.8%±0.012% (t=31.595,P＜0.05),90%,respectively,and The survival of hepatoma carcinoma cell MHCC-97 line were inhibited 21.9% (F = 4.63,P < 0.05).Which have significant difference in statistics.The SER of hepatoma carcinoma cell MHCC-97 line after interference was 1.15.Conclusions RNAi targeting silence N-Ras may increase the radiosensitivity of hepatoma carcinoma cell MHCC-97 line.

Roscovitine on cell cycle in mitotic hepatoma carcinoma cell / 国际外科学杂志

Objective To study the influences by a Cyelin-dependent kinase inhibitor Roscovitine on cell cycle in mitotic hepatoma carcinoma cell SMMC-7721. Methods Microscope,MTT, flow cytometry and R-T PCR were used to observe the effects of Roscovitine on morphology, proliferation, cell cycle, apoptosis and the mRNA expression of CDK2, Caspase-3, bcl-2 in SMMC-7721 cells. Results Roscovitine inhibited the proliferation of SMMC-7721 cells in dosage and time dependent manner and induced apoptosis. Flow cytometry showed the ratio of G0, G1 increased. R-T PCR showed that the expression of bcl-2 reduced, Caspase-3 increased. Conclusion Reseovitine can inhibit the growth, proliferation, block the cell cycle at G0/G1 and promotes apoptosis of mitotic SMMC-7721 cells, and the mechanism of apoptosis is dependent on the activity of bcl-2 and Caspase-3.

Influence of glypican-3 gene on proliferation,adhesion and invasion of hepatoma carcinoma cancer cell line SK-Hep-1 / 中国肿瘤生物治疗杂志

Objective:To study the influence of GPC3 gene on the proliferation,adhesion and invasion of hepatoma cell line SK-Hep-1.Methods:SK-Hep-1 cells were transfected with pEGFP-N2-GPC3 using Lipofectamine2000.RT-PCR was used to examine the GPC3mRNA expression in GPC3-SK-Hep-1 cells.MTT assay was used to examine the proliferation and calculate the adhesion rate of SK-Hep-1 cells.Transwell system was used to assess the migration and invasion of the cells.Results:SK-Hep-1 cells were successfully transfected with pEGFP-N2-GPC palsmid.GPC3 mRNA was detected in SK-Hep-1 cells.Transfection with CPC3 significantly suppressed the growth of SK-Hep-1 cells(P

Role of RhoC-siRNA expression vector on growth velocity and invasiveness of hepatoma carcinoma cells / 第三军医大学学报

Objective To construct a RhoC-siRNA expression vector, and study its role on the biological behaviors of hepatoma carcinoma cells. Methods RhoC-siRNA gene was synthesized and cloned into the expression vector pSilencer2.1. The constructed RhoC-siRNA expression vector was stably transfected into hepatoma carcinoma cell line SK-Hep1. The inhibitory effect of RhoC-siRNA on the expression of RhoC in transfected cells was detected by Western blotting. The morphous, growth velocity and the ability of cell adhesion, cell migration, cell invasion before and after transfection was observed. Results Enzyme digestion and DNA sequencing confirmed that the RhoC specific siRNA expression vector was constructed successfully. After transfection, RhoC expression was inhibited by 60%, and no marked difference was observed in cellular morphous and growth curve, while the ability of cell adhesion, cell migration, and cell invasion were markedly decreased. Conclusion The RhoC-siRNA expression vector can effectively suppress RhoC expression in transfected hepatoma carcinoma cells. Although having no effect on the morphous and growth velocity of hepatoma carcinoma cells, it decreases the potentiality of cell invasion and cell metastasis, which may provide a novel applicable strategy for gene therapy on hepatocellular carcinoma.

Effect of rutin on proliferation of HepG2 cells / 第三军医大学学报

Objective To observe the effect of rutin on growth and proliferation of human hepatic cancer line(HepG2).Methods HepG2 cells were cultured in vitro,then cocultured with 50 to 250 ?mol/L rutin for 24 h.The inhibition rate of rutin on growth and proliferation of HepG2 was determined by MTT,~(3)H-TdR,and apoptotic cells were observed in fluorescent staining by Olympus fluorescent microscopy,and cell cycle was analysed by flow cytometry.Results Rutin inhibited HepG2 cells from growth and proliferation,and evoked apoptosis.Flow cytometry showed that 50 to 250 ?mol/L rutin caused an increase at G_(0)/G_(1) phase and a decrease at G_(2)/M phase and arrest at G_(0)/G_(1) phase in the cell cycle.Conclusion Rutin markedly inhibits the proliferation of HepG2 cells and induces apoptosis in a concentration-dependent manner.