ライフサイエンスコーパス: hepatoma

1 oncolytic Ad safely and efficiently to treat hepatoma.

2 ch has high affinity and selectivity towards hepatoma.

3 miR-21 and TIAM1 expression in patients with hepatoma.

4 d, malignant hepatocellular carcinoma Morris hepatoma 7777 was systematically optimized to yield the

5 The erythropoietin-producing hepatoma A2 receptor (EphA2) is a tyrosine kinase overex

6 was also shown that sesamol has potent anti-hepatoma activity in a xenograft nude mice model.

7 PHY906 may potentiate the anti-hepatoma activity of Sorafenib by multiple mechanisms ta

8 d migration, we used primary hepatocytes and hepatoma and macrophage cell lines.

9 al RNA transfer mechanism by human and mouse hepatoma and nonhepatoma cells that replicate the negati

10 Mice that lack GNMT develop fibrosis and hepatomas and have alterations in signaling pathways inv

11 ally altered in cachectic muscles of Yoshida hepatoma-bearing rodents but not in those with diabetes,

12 ABP-PEG-HCBP1 delivered oAd efficiently into hepatoma cancer cells.

13 ressing ad, (Ad/GFP)-ABP-PEG-HCBP1, showed a hepatoma cancer specific uptake and transduction compare

14 icantly decreased Met and VEGF expression in hepatoma cancer, but not in non-hepatoma cancer.

15 xpression in hepatoma cancer, but not in non-hepatoma cancer.

16 tis C virus (HCV) clones propagated in human hepatoma cell cultures yield relatively low infectivity

17 hyroid hormone receptor (TRalpha1) regulates hepatoma cell growth and pathophysiology, but the underl

18 assay showed that pEpo-AFPL-Luc transfected hepatoma cell increased gene expression under hypoxic co

19 in primary rat hepatocytes (PRHs) and human hepatoma cell line (HepG2) were quantified by dichlorofl

20 We found that JB12 was required in human hepatoma cell line 7 (Huh-7) liver cancer cells to maint

21 Hepatoma cell line and immortalized human hepatocytes tr

22 ment of a polarizable, HBV-susceptible human hepatoma cell line and studies of primary hepatocytes fr

23 on of CYP1A1 mRNA and EROD activity in human hepatoma cell line Hep3B.

24 iver mitochondria and in the cultured murine hepatoma cell line Hepa1c1c7.

25 Removing serum from the medium of the human hepatoma cell line HepG2 increased Rdh10 and Rdh16 (huma

26 In the human hepatoma cell line HepG2, retinoic acid, clofibric acid,

27 e to efficiently block HCV attachment to the hepatoma cell line Huh-7.5 as well as primary human hepa

28 ls comparable to the highly permissive human hepatoma cell line Huh-7.5.

29 sly shown that confluent growth of the human hepatoma cell line Huh7 substantially induces the CYP3A4

30 In the human hepatoma cell line Huh7, the coexpression of the coactiv

31 In this study, we differentiated the human hepatoma cell line Huh7.5 by supplementing tissue cultur

32 We confirmed these findings in the human hepatoma cell line Huh7.5.1.

33 Transfection of 20 such mutants in a human hepatoma cell line identified many with severe impairmen

34 Transient overexpression of IFNL4 in a hepatoma cell line induced STAT1 and STAT2 phosphorylati

35 onversely, expression of LSP1 in the JM2 rat hepatoma cell line led to decreased proliferation.

36 tissue, and knockout of the CIDEB gene in a hepatoma cell line results in multiple aspects of lipid

37 HCV life cycle, we established a stable Huh7 hepatoma cell line that contained an HCV subgenomic RNA

38 s of the G6pc promoter by glucotoxicity in a hepatoma cell line then in primary hepatocytes and in th

39 e of QSG-7701 (human hepatocyte) with HepG2 (hepatoma cell line) increases QSG-7701's proliferation,

40 imary human hepatocytes (PHHs) and the human hepatoma cell line, HepaRG, is restricted to differentia

41 d in VA-13 cells, an EtOH-metabolizing human hepatoma cell line, which displayed marked defects in bo

42 hput screening performed in the Hepa-1 mouse hepatoma cell line, which revealed that SIN3A is necessa

43 ly knock down LSP1 expression in the JM1 rat hepatoma cell line.

44 BV and HDV receptor activity in a permissive hepatoma cell line.

45 egrades clathrin heavy chain expression in a hepatoma cell line.

46 d the aminoglycosides G418 and gentamicin in hepatoma cell lines (HepG2, Hep3B and Hepa1-6) and in ex

47 Three hepatoma cell lines (HepG2, Hepa-1, and Huh-7) were trea

48 Cell viability of two human hepatoma cell lines (Huh7 and Hep-G2) was quantitatively

49 In rat hepatoma cell lines and mouse liver in vivo, LSP1 functi

50 f SMAD6 blocked the binding and infection of hepatoma cell lines and primary human hepatocytes by HCV

51 In studies of hepatoma cell lines and primary human hepatocytes, we fo

52 expression of bile acid homeostasis genes in hepatoma cell lines and primary human hepatocytes.

53 tein expression were studied in HCV-infected hepatoma cell lines and primary human hepatocytes.

54 FQ potently inhibited HCV infection of hepatoma cell lines by affecting an early step of the vi

55 Human hepatoma cell lines exhibited high levels of MKlp2; howe

56 The pEpo-AFPL-TK was transfected into hepatoma cell lines in the presence of ganciclovir (GCV)

57 Finally, depletion of iron in the medium of hepatoma cell lines incubated with the iron chelator des

58 ilencing or inhibition of endogenous TAK1 in hepatoma cell lines leads to an upregulation of HBV repl

59 ing, but also that sterol depletion of human hepatoma cell lines reduced HNRNPA1 mRNA levels, an effe

60 (HBV) receptor enabled researchers to create hepatoma cell lines susceptible to HBV infection.

61 , decreased SIRT6 expression was observed in hepatoma cell lines that are known to be apoptosis-insen

62 ver models of infection typically use either hepatoma cell lines that exhibit aberrant physiology or

63 These viruses were used to infect hepatoma cell lines that express different levels of HCV

64 ere further assessed in IFN-gamma-stimulated hepatoma cell lines with (HepG2.2.15 cells) and without

65 ndent tetracycline-inducible systems in four hepatoma cell lines with different p53 mutational status

66 silencing of SLC13A5 expression in two human hepatoma cell lines, HepG2 and Huh7, profoundly suppress

67 In human hepatoma cell lines, SUGP1 knockdown stimulated 3-hydrox

68 lication of diverse HCV genotypes in several hepatoma cell lines.

69 the miR-200 family were conducted using the hepatoma cell lines.

70 ding and infection were tested in transduced hepatoma cell lines.

71 titis B surface antigen (HBsAg) particles of hepatoma cell lines.

72 imary human hepatocytes, liver biopsies, and hepatoma cell lines.

73 ver following partial hepatectomy (PHx), and hepatoma cell lines.

74 Overexpression of miR-21 promoted hepatoma cell migration and invasion, similar to that ob

75 3) and subsequent TIAM1 suppression promotes hepatoma cell migration and invasion.

76 ted that miR-224 played an oncogenic role in hepatoma cell migration and tumor formation through sile

77 ng hepatic energy homeostasis to influencing hepatoma cell proliferation and suggest a potential role

78 with 2-DG produces synergistic inhibition on hepatoma cell proliferation by dual targeting of apoptos

79 ed human HCC samples, a mouse HCC model, and hepatoma cell/myofibroblast cocultures to examine the hy

80 ts were given intrahepatic injections of rat hepatoma cells (H4IIE); 24 tumor-bearing rats (mean tumo

81 bling isolates of all HCV genotypes in human hepatoma cells (HCVcc), production efficacy varies.

82 ls (capital A, Cyrillic549) as compared with hepatoma cells (Hep3b).

83 lycoprotein (P-gp) encoded by ABCB1 in human hepatoma cells (HepG2) without modifying the expression

84 To this end, we exposed human hepatoma cells (Huh7) to 0.5 muM (nontoxic concentration

85 Conditioned medium from HCV-infected hepatoma cells (Huh7.5 cells) or immortalized human hepa

86 Coculture of NK cells (NK3.3) with human hepatoma cells (Huh7.5) expressing HCV core or NS5A prot

87 atoma cells (JFH-1), and not with uninfected hepatoma cells (Huh7.5), induced IFN-alpha production.

88 icity of HCV-infected HLA-A2-positive Huh7.5 hepatoma cells (Huh7.5A2 cells) in activating HCV-specif

89 tter complexes were highly toxic against rat hepatoma cells (IC(50) = 0.40-2.0 muM) and less toxic ag

90 nant hepatitis type 1 (JFH-1) virus-infected hepatoma cells (JFH-1), and not with uninfected hepatoma

91 Human NK cells recognize HCV-infected hepatoma cells after IFN-alpha stimulation in a DNAM-1-d

92 comprehensive peptidome from GPC3-expressing hepatoma cells after immune-affinity purification of hum

93 e effect of PD-L1 expression on HCV-infected hepatoma cells against HCV-specific CD8 T cells.

94 refore, indicate that the cross-talk between hepatoma cells and activated HSCs is an important featur

95 expression profiling was carried out on rat hepatoma cells and compared to profiles of hepatoma "var

96 culture-derived HCV-producing Huh7.5-derived hepatoma cells and confirmed its depletion by immunoblot

97 SMAD (SMAD7) promote HCV infection in human hepatoma cells and hepatocytes.

98 RMP inhibited ATX expression in human HepG2 hepatoma cells and hepatoma cells overexpressing the pre

99 ed completion of the HCV infectious cycle in hepatoma cells and HFLCs in a dose-dependent and time-de

100 n, entry, spread, production, and release in hepatoma cells and HFLCs.

101 Reduced expression of GNMT in mouse hepatoma cells and human HCC cells appears to increase a

102 search for FXR-interacting proteins in human hepatoma cells and identified AMPK as a coregulator of F

103 In human Hep3B hepatoma cells and in EPO-generating organs of hypoxic o

104 transporter mRNA levels were assessed in rat hepatoma cells and in mice by peptide injection or adeno

105 w that down-regulation of C/EBPbeta in mouse hepatoma cells and in mouse livers reduces C/EBPbeta-HDA

106 o increase entry of HCV pseudoparticles into hepatoma cells and inhibit signaling by interferon alpha

107 at Nox4 mediates LPS-TLR4 signaling in human hepatoma cells and murine hepatocytes and may contribute

108 can efficiently prevent infection of Huh-7.5 hepatoma cells and primary hepatocytes by cell-culture-d

109 Here we show that hepatoma cells and primary hepatocytes strongly up-regul

110 F on HCV infection of and spread among Huh-7 hepatoma cells and primary HFLCs.

111 the proteasome inhibitor bortezomib (BZB) in hepatoma cells and primary human hepatocytes as well as

112 Inhibition of HCV was measured in hepatoma cells and primary human hepatocytes using lucif

113 responses induced by these cytokines in Huh7 hepatoma cells and primary human hepatocytes.

114 H4IIE hepatoma cells and rat primary hepatocytes were incubate

115 LDL-DHA nanoparticle selectively kills hepatoma cells and reduces growth of orthotopic liver tu

116 2a) recombinant replicates spontaneously in hepatoma cells and releases infectious virus.

117 KB1 promoted proliferation of GNMT-deficient hepatoma cells and required mitogen-activated protein ki

118 cytotoxicity and potency toward Nrf2 in rat hepatoma cells and stably modifies specific cysteine res

119 Overexpression of KIF18B and CDCA3 in hepatoma cells and subsequent microarray analysis reveal

120 ted NK cells were cultured with HCV-infected hepatoma cells and subsequently analyzed (for degranulat

121 Nox4) in LPS-induced TLR4 responses in human hepatoma cells and wildtype and Nox4-deficient mice.

122 iosynthesis, as PGRMC1 depletion in cultured hepatoma cells and zebrafish blocked the ability of HISs

123 oth HCVcc and patient serum-derived virus to hepatoma cells as well as primary human hepatocytes.

124 aVpu virus release from BST-2-positive HepG2 hepatoma cells but not HeLa cells, whereas Vpu failed to

125 were determined in plasma phospholipids and hepatoma cells by gas chromatography.Cellulose did not a

126 l data show that recognition of HCV-infected hepatoma cells by pDCs involves CD81- and CD9-associated

127 on primary human hepatocytes and Hep3B human hepatoma cells can mediate binding and uptake of very lo

128 nificant increasing of death rate in hypoxic hepatoma cells compared to controls.

129 at a high level of reprogramming occurs when hepatoma cells convert to a non-differentiated phenotype

130 t hairpin RNA-mediated attenuation of ISX in hepatoma cells decreased cell proliferation and malignan

131 nfluences the proliferation and migration of hepatoma cells during the metastasis process and support

132 -alpha-stimulated NK cells with HCV-infected hepatoma cells efficiently reduced HCV replication.

133 ificantly up-regulated in obese patients and hepatoma cells exposed to FFA.

134 se and cell death is less significant in the hepatoma cells following coincubation with NS5A TCR-tran

135 We studied hepatoma cells from GNMT knockout mice and analyzed the

136 Hepatoma cells from GNMT mice had defects in LKB1 signal

137 pression of SHP and its co-repressor EID1 in hepatoma cells Huh7, Hepa1, and stellate cells LX2.

138 passage of hepatitis C virus (HCV) in human hepatoma cells in an experimental design in which host c

139 (HCV) in the course of 200 passages in human hepatoma cells in an experimental design that precluded

140 These T cells killed GPC3-expressing hepatoma cells in culture and slowed growth of HCC xenog

141 ases the expression of ATF5 protein in HepG2 hepatoma cells in part by stabilizing the ATF5 protein.

142 HBV-specific T cells lysed HBV-producing hepatoma cells in vitro.

143 nduced metastatic colonization of epithelial hepatoma cells in vivo.

144 nhanced 2-fold in HAP1 and 1.6-fold in human hepatoma cells in which plasminogen receptor (KT) was ov

145 ng the pregnane X receptor (PXR), but not in hepatoma cells in which PXR was knocked down.

146 ced 0.35-fold in HAP1 and 0.33-fold in human hepatoma cells in which the plasminogen receptor (KT) wa

147 RNAi-mediated MKlp2 knockdown in hepatoma cells induced polyploidization consistent with

148 this study, we found that HEV replication in hepatoma cells inhibited poly(I.C)-induced beta interfer

149 The TSLP secreted by HCV-infected hepatoma cells is capable of activating human monocyte-d

150 ent evidence that miR-29 expression in human hepatoma cells is controlled in part by FOXA2, which is

151 , coculture of tonsillar cells with infected hepatoma cells lead to an expansion of germinal center T

152 green fluorescent protein (GFP) (E2-GFP) in hepatoma cells led to impaired phosphorylation of IRF-3

153 ll subpopulation, but not in less metastatic hepatoma cells or normal hepatocytes.

154 tenuated IFN-alpha induction by HCV-infected hepatoma cells or TLR ligands, and this inhibitory effec

155 expression in human HepG2 hepatoma cells and hepatoma cells overexpressing the pregnane X receptor (P

156 ols, we show the level at which HCV-infected hepatoma cells present endogenously processed HCV epitop

157 As hepatoma cells producing cell culture-derived HCV (HCVcc

158 IFN-alpha induction by HCV-containing hepatoma cells required viral replication, direct cell-c

159 Transient expression of hCH25H in human hepatoma cells restricted HCV infection in a genotype-in

160 We found that RB depletion in hepatoma cells resulted in a compromised immunological r

161 Passage of hepatitis C virus (HCV) in human hepatoma cells resulted in populations that displayed pa

162 BMCs from healthy subjects with HCV-infected hepatoma cells resulted in preferential expansion of cir

163 Mechanistic studies in hepatoma cells revealed that LysoPC enhances secretion o

164 , forced expression and knockdown of SPZ1 in hepatoma cells showed that SPZ1 was able to regulate the

165 with replicons, infectious virus, and human hepatoma cells that express a HCV polyprotein.

166 We cultured hepatoma cells that express luciferase-tagged subgenomic

167 al PC-to-PE ratio and cellular ATP levels in hepatoma cells that expressed various amounts of PEMT.

168 ll proliferation and tumorigenic activity in hepatoma cells through CCND1 induction.

169 tes that constitutive exposure to IFN causes hepatoma cells to become tolerant of ISG function.

170 HCV isolated from culture media of infected hepatoma cells to define viral and host-encoded proteins

171 s (HCV) positive-strand RNA from human Huh-7 hepatoma cells to human plasmacytoid dendritic cells (pD

172 HCV; TNF-alpha increased the permissivity of hepatoma cells to infection by Lassa, measles and vesicu

173 We developed a cell culture system using hepatoma cells to study persistent HCV infection during

174 eripheral blood mononuclear cells with Huh-7 hepatoma cells transfected with HCV RNA.

175 expression on LDLR transcript levels between hepatoma cells transfected with the rs6924995 A versus G

176 irus in permissive, transfected human Huh7.5 hepatoma cells upon serial passage.

177 gene was subsequently knocked down in human hepatoma cells using lentiviral vectors expressing small

178 s in mitochondrial metabolism by HepG2 human hepatoma cells using siRNA.

179 cked cell-cycle progression at G2-M phase in hepatoma cells via downregulation of CDK1, induction of

180 IFN-alpha production by HCV-infected hepatoma cells was decreased in pDCs from HCV-infected p

181 In addition, human hepatoma cells were incubated with different propionate

182 When Huh7 K2040 and Huh7 L2198S hepatoma cells were incubated with IFN-alpha-2a, express

183 Huh7.5.1 hepatoma cells were transfected with small interfering R

184 To determine mechanisms of action, rat hepatoma cells were treated with CE and eluates of CDSF

185 METHODS AND Human hepatoma cells were treated with Lp(a) purified from hum

186 Human hepatoma cells were treated with Lp(a) purified from hum

187 equence did not affect transfection of human hepatoma cells when inserted into the hypervariable regi

188 missing factors, we transduced Huh-7.5 human hepatoma cells with a pooled lentivirus-based human comp

189 ctive inhibition of HCV replication in human hepatoma cells with persistent HCV RNA replication.

190 Human primary hepatocytes, Huh7 hepatoma cells with silenced PTP1B, mouse hepatocytes fr

191 apacity to replicate efficiently in cultured hepatoma cells without cell culture-adaptive mutations.

192 ) consensus sequences, were viable in Huh7.5 hepatoma cells without requirement for adaptive mutation

193 te the cross-talk between hepatocytes (human hepatoma cells) and activated human HSCs.

194 ion 3-96 h following Tcf7l2 silencing in rat hepatoma cells, and combined this with ChIP-Seq to inves

195 ing of ApoE-deficient TRLs to HSPGs on human hepatoma cells, and decreased clearance of ApoE-deficien

196 ll lines: A549 lung adenocarcinoma and HuH-7 hepatoma cells, and for productive DENV infection of Aed

197 -2-induced HBV restriction was weak in Huh-7 hepatoma cells, and the interferon-induced anti-HBV effe

198 ntly to regulate S6 in an additive manner in hepatoma cells, but it uses mTORC1 as the primary pathwa

199 higher caspase activation and cell death in hepatoma cells, but not in primary hepatocytes.

200 F19 activated mTORC1 in HepG2 and HuH7 human hepatoma cells, differentiated 3T3-L1 adipocytes and mou

201 apoAIV overexpression increased MTP mRNA in hepatoma cells, indicating transcriptional regulation.

202 zole (BPTT) was most effective against human hepatoma cells, inhibits cell invasion, and decreases ne

203 an be effectively taken up by cultured human hepatoma cells, is nontoxic to the cultured cells and a

204 or-3 (TLR3) senses HCV infection in cultured hepatoma cells, leading to nuclear factor kappa B (NF-ka

205 tor aminopeptidase N and replicated in human hepatoma cells, suggesting a principal ability to cause

206 In human hepatoma cells, the apo(a) component from the internaliz

207 In human HepG2 hepatoma cells, the rare chr11:47227430 A allele disrupt

208 In contrast, in Huh7 hepatoma cells, the virus must acquire loss-of-function

209 V disables a key receptor ligand in infected hepatoma cells, thereby inhibiting the ability of infect

210 Before infection of naive hepatoma cells, we exposed cell culture-derived HCV stra

211 of cis-proline-containing proteins in human hepatoma cells, we found that combined knockdown of cycl

212 Using primary rat hepatocytes and human hepatoma cells, we found that treatment with the beta-AR

213 ed in DNA damage response in hepatocytes and hepatoma cells.

214 ouse brain and approximately 40,000 in human hepatoma cells.

215 eptor tyrosine kinase Axl in EMT-transformed hepatoma cells.

216 host interactions of all ten HCV proteins in hepatoma cells.

217 nced, HBV gene expression and replication in hepatoma cells.

218 duced secretion from primary hepatocytes and hepatoma cells.

219 P-1 and replication assessed after fusion to hepatoma cells.

220 d microdomains purified from hepatocytes and hepatoma cells.

221 domains (NLMs) purified from hepatocytes and hepatoma cells.

222 ows them to recognize and kill GPC3-positive hepatoma cells.

223 of a functional genomics screening in human hepatoma cells.

224 hepatitis C virus (HCV) entry into polarized hepatoma cells.

225 ransferrin (Tf)-receptor-mediated pathway in hepatoma cells.

226 hepatitis C virus (HCV) infection in Huh7.5 hepatoma cells.

227 be linked to cellular cholesterol states in hepatoma cells.

228 ar to that observed with T(3) stimulation in hepatoma cells.

229 tor-beta 1 (TGF-beta1) in HCV-infected human hepatoma cells.

230 lar vesicles and HBsAg particles secreted by hepatoma cells.

231 IFN-alpha induction in pDCs by HCV-infected hepatoma cells.

232 vimentin, and matrix metalloproteinase-2 in hepatoma cells.

233 olar antiviral activity against HBV in human hepatoma cells.

234 and cell-surface levels of ZIP8 in H4IIE rat hepatoma cells.

235 atic energy homeostasis and proliferation of hepatoma cells.

236 ies (11 and 12) were further analyzed on the hepatoma cells.

237 A responsive Cyp26a1 gene in hepatocytes and hepatoma cells.

238 IFN-gamma enhanced PD-L1 expression in hepatoma cells.

239 ar vesicles and HBsAg particles derived from hepatoma cells.

240 erin, restrict HBV spread in NTCP-expressing hepatoma cells.

241 with Pin1-null fibroblasts or PIN1-depleted hepatoma cells.

242 ess if these miRNAs are actively secreted by hepatoma cells.

243 RNA expression and activity in cultured Huh7 hepatoma cells.

244 on normal mouse NCTC hepatocytes, but not on hepatoma cells.

245 e inflammasome complex in HCV-infected human hepatoma cells.

246 transfecting HBV replication constructs into hepatoma cells.

247 ent was adapted for growth in HepG2C3A human hepatoma cells.

248 1b strain Con1 subgenomic replicon in human hepatoma cells.

249 directing T cells to target virally infected hepatoma cells.IMPORTANCE Due to the protective ability

250 examined in a tissue culture model of HCV in hepatoma cells: HCV infection induced extracellular rele

251 o induces Smad1/5/8 phosphorylation in human hepatoma-derived cells and, synergistically with IL-6 an

252 e sought to assess the relationship of serum hepatoma-derived growth factor (HDGF) with PAH disease s

253 athway as a functional target of miR-130a in hepatoma-derived Hep3B cells.

254 We recently showed that hepatoma-derived HepG2 cells support the entire HCV life

255 y short-term direct exposure to HCV-infected hepatoma-derived Huh-7.5 cells.

256 Therefore, the hypoxia/hepatoma dual specific gene expression vector with the E

257 this study, we developed a novel hypoxia and hepatoma dual specific gene expression vector.

258 Hepatoma exhibits a series of heterogeneous subpopulatio

259 Treating of rat hepatoma FAO cells with Wy14,643, an agonist of peroxiso

260 dielectric characterization of cancer cells (Hepatoma G2, HepG2).

261 ed the phosphorylation state of JNK1 in both hepatoma H4IIE cells and mouse primary hepatocytes in bo

262 8, and the other expresses low levels (human hepatoma: Hep3B and HepG2; human prostate cancer: PC3 an

263 Exposure of mouse hepatoma (Hepa-1) and human hepatoblastoma (HepG2) cells

264 investigated using the differentiated human hepatoma HepaRG cells.

265 In hepatoma/hepatocarcinoma cell lines, FGFR3 isoforms were

266 In hepatoma/hepatocarcinoma cells, up-regulated FGFR3-IIIb

267 ctivated receptor alpha (PPARalpha) in human hepatoma HepG2 cells and mouse liver.

268 his is based on stable transfection of human hepatoma HepG2 cells with a plasmid that encodes the red

269 nitrogen-containing membrane lipids in human hepatoma HepG2 cells.

270 uptake and accessible to chromatin in human hepatoma HepG2 cells.

271 We analyzed human hepatoma (HepG2) cells and mouse primary hepatocytes to

272 ompatibility was assessed by culturing human hepatoma (HepG2) cells on treated surfaces.

273 e/xanthine and adenine/hypoxanthine in human hepatoma (HepG2) cells were detected simultaneously.

274 ells, but not in mouse liver, cultured human hepatoma (HepG2) cells, or AC16 cultured human cardiomyo

275 n monocyte-macrophage cells but not in human hepatoma (HepG2) cells.

276 Knockdown of Prox1 by siRNAs in human hepatoma Huh-7 cells increased the expression of RORgamm

277 not replicate efficiently in wild-type human hepatoma Huh-7 cells, but it replicates robustly in cert

278 Human hepatoma (Huh-7 and Huh-7.5) and primary HFLCs were incu

279 ipid droplet content were performed in human hepatoma Huh7 and HepG2 cells using confocal microscopy

280 and FXR isoform expression was confirmed in hepatoma Huh7 and HepG2 cells.

281 Knockdown of CREB3L1 mRNA in human hepatoma Huh7 cells and immortalized human fibroblast SV

282 ble of transmitting infection to naive human hepatoma Huh7.5.1 cells and establishing a productive in

283 ed exosomes isolated from HCV-infected human hepatoma Huh7.5.1 cells were shown to contain full-lengt

284 We used human hepatoma (Huh7.5) cells and those that had undergone pro

285 emically or due to mutations repressed it in hepatomas in a dose-dependent manner, whereas beta-caten

286 ty of LDL-DHA to reduce growth of orthotopic hepatomas in rats.

287 replication and infectivity in Leghorn male hepatoma (LMH) chicken liver cells and in chickens.

288 ression in humans as well as mouse and human hepatoma models of the disease.

289 s highlight ISX as an important regulator in hepatoma progression with significant potential as a pro

290 Incubating McArdle rat hepatoma RH7777 cells with 2-monoacylglycerol caused DGA

291 enhancer and AFP promoter may be useful for hepatoma specific gene therapy.

292 usly demonstrated that the CD133(-)/EpCAM(-) hepatoma subpopulation was more metastatic than its coun

293 ly expressed gene clusters upon encountering hepatoma target cells presenting endogenously expressed

294 f hepatocellular carcinoma (HCC, also called hepatoma) therapy.

295 fectoprotein (AFP) promoter and enhancer for hepatoma tissue specific gene expression.

296 A high positive correlation existed in human hepatoma tumors between ISX and CCND1 expression.

297 Human hepatoma up-regulated protein (HURP) is a substrate of A

298 t hepatoma cells and compared to profiles of hepatoma "variant" cell lines derived via a stringent se

299 lic steatosis and in ethanol-incubated human hepatoma VL17A cells.

300 n = 15) and tumor growth in a remote BNL 1ME hepatoma xenograft tumor (n = 28).

301 transduction efficiency of dcAd5-CMV/NIS in hepatoma xenografts.