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1 s they selectively bind and internalize into liver cancer cells.
2 s directly affecting malignant properties of liver cancer cells.
3 and the growth response to TGF-beta in human liver cancer cells.
4 inhibitor celecoxib on the growth control of liver cancer cells.
5 yses cells, and spreads only poorly in Hep3B liver cancer cells.
6 from MAT1A to MAT2A gene expression in human liver cancer cells.
7 ion, protein synthesis remains unhindered in liver cancer cells.
8 phagic ferroptosis in beta-catenin-activated liver cancer cells.
9 idate due to its action on resistant Mahlavu liver cancer cells.
10 n-cofilin to favor migration and invasion of liver cancer cells.
11  when compared to 2D and 3D mono-cultures of liver cancer cells.
12 ssessed on colorectal, breast, cervical, and liver cancer cells.
13  outcomes induced by HNF4alpha deficiency in liver cancer cells.
14  higher migratory and invasive properties of liver cancer cells.
15  L18 was enhanced by LARP1 overexpression in liver cancer cells.
16 er CD133, which is located on the surface of liver cancer cells.
17 p in the regulation of invasive potential in liver cancer cells.
18 ination with Bcl-XL inhibition on a panel of liver cancer cells.
19 he monodisperse CDs in MCF-7 cells and Huh-7 liver cancer cells.
20 ctrochemical biosensors for the detection of liver cancer cells.
21 e many photoreceptor-specific exons in HepG2 liver cancer cells.
22 f SCP1 increased the c-Myc protein levels in liver cancer cells.
23 n the enrichment of nuclear FBP1 and FBP2 in liver cancer cells.
24 bearing liver, limits intrahepatic spread of liver cancer cells.
25 rial homeostasis, and a signaling network in liver cancer cells.
26 in repressing c-MYC-induced CSC phenotype in liver cancer cells.
27 he most potent conjugate against HepG2 human liver cancer cells.
28 on of YAP/TEAD transcriptional activation in liver cancer cells.
29 hibited proliferation and migration of human liver cancer cells.
30 l is growth-suppressive and pro-apoptotic in liver cancer cells.
31 by the TCF and FoxA transcription factors in liver cancer cells.
32 H) concentration in vitro and in HepG2 human liver cancer cells.
33 the anti-apoptotic function of IL-6 in human liver cancer cells.
34 ents SAMe level to reach high enough to kill liver cancer cells.
35 ression and consequently its function in the liver cancer cells.
36 is genes and blocked metabolic adaptation in liver cancer cells.
37 molecular probes for specific recognition of liver cancer cells.
38 hepatocytes and stimulating the apoptosis of liver cancer cells.
39 tiforme) cell lines and knocked out in HUH7 (liver cancer) cells.
40 ate induced apoptosis in the HepG2 and Hep3B liver cancer cells; 5-azaC treatment alone produced G2 a
41 h the antiproliferative effect against HepG2 liver cancer cells, a representative of metabolizing cel
42  to determine the metabolic changes of HepG2 liver cancer cells after EV treatment.
43 e, CRISPR-mediated knockout of FN3K in human liver cancer cells altered the abundance of redox metabo
44  and scaffold-based 3D-culture techniques of liver cancer cells and fibroblasts, we aimed to establis
45 ingly, CCDC3, as a secreted protein, targets liver cancer cells and increases long chain polyunsatura
46 can efficiently replicate in HepG2 and Hep3B liver cancer cells and produce high titers of virus.
47 nduced cell death in pancreatic, breast, and liver cancer cells and reduced the growth of breast tumo
48 s on CL1-0 and A549 lung cancer cells, Huh-7 liver cancer cells, and MCF-7 breast cancer cells using
49 f both the PI3K/Akt and MAPK/ERK pathways in liver cancer cells, and Nqo1 ablation blocked metabolic
50      The expression of FAM83H is elevated in liver cancer cells, and nuclear expression of FAM83H pre
51 a six-letter DNA library to selectively bind liver cancer cells; and 2) in a six-letter self-assembli
52                                       CD133+ liver cancer cells are characterized by resistance to ch
53 our growth and lung metastasis of breast and liver cancer cells are inhibited by anti-Cnx antibodies.
54 richia coli (E. coli) interacting with human liver cancer cells, at [Formula: see text] multicolor 3D
55                                     In vivo, liver cancer cells but not hepatocytes display cell surf
56        SAMe and MTA are also proapoptotic in liver cancer cells by selectively inducing Bcl-x(S) expr
57 monstrate in vivo overexpression of MAT1A in liver cancer cells can suppress tumor growth.
58 up-regulated and exhibited high stability in liver cancer cells compared with other cells.
59 el of H3K27me3 and suppressed cell growth in liver cancer cells, compared with EZH1 or EZH2 single kn
60 ion in AATD liver-impacting genes related to liver cancer, cell cycle, and fibrosis, as well as key r
61 arrying miR122 and PTX were delivered to the liver cancer cells efficiently due to their rubber-like
62 ing sensitivity to bromodomain inhibitors in liver cancer cells exhibiting NSUN7 epigenetic silencing
63 ting effects of 14-3-3z were eliminated when liver cancer cells expressed mutant MATa1 unable to inte
64 gged form of MAN2A1-FER in NIH3T3 and HEP3B (liver cancer) cells; Golgi were isolated for analysis.
65 nsports citrate across cell membranes, halts liver cancer cell growth by altering both energy product
66 at MAT2A and MAT2beta genes are required for liver cancer cell growth that is induced by the profibro
67  of CaMKK2 function is sufficient to inhibit liver cancer cell growth, and the growth defect resultin
68 pendent protein kinase 4 (CaMKIV) to control liver cancer cell growth.
69  nucifera was found to exert cytotoxicity on liver cancer cells HepG2 in a dose-dependent manner.
70 EMT in hepatic stellate cell (HSC) and human liver cancer cells (HepG2) and the potential role of EVE
71  thereby enabling the efficient detection of liver cancer cells (HepG2).
72  A similar differential activity was seen in liver cancer cells (HepG2, Huh7, and Hep3B).
73 e selective aptamers could specifically bind liver cancer cells in a mouse model.
74  charged with doxorubicin, selectively kills liver cancer cells in culture, as the selectivity of the
75 ver stem cells (LSCs) into highly metastatic liver cancer cells in premalignant liver tissue.
76                  Expression of this miRNA in liver cancer cells in vitro induces cell-cycle arrest as
77  limit proliferation and induce apoptosis of liver cancer cells in vivo.
78 aMKK2 with STO-609 impairs tumorigenicity of liver cancer cells in vivo.
79             Blocking lipogenesis in cultured liver cancer cells is sufficient to decrease cell viabil
80 porters which cause high drug effluxion from liver cancer cells, leading to chemoresistance and a dim
81 omoter was hypermethylated in both colon and liver cancer cells, leading to the production of high le
82 profile the uptake and excretion fluxes of a liver cancer cell line (HepG2) and use genome-scale meta
83 cognition, two liver cell lines were used: a liver cancer cell line BNL 1ME A.7R.1 (MEAR) and a nonca
84 nd GPC3 antigens on the surface of the human liver cancer cell line Hep3B using anti-EpCAM-CdTe- and
85                  In the present study, human liver cancer cell line HepG2, having high intracellular
86 ter overexpressed in hepatocarcinoma and the liver cancer cell line HepG2.
87 ression data from the well-established human liver cancer cell line, HepG2.
88 nerated during ethanol metabolism in a human liver cancer cell line, highlighting the potential of th
89                 We screened a large panel of liver cancer cell lines (LCCLs) to identify agents that
90 croarray analysis of gene re-expression in 4 liver cancer cell lines after their exposure to reagents
91 plied this new approach in hematological and liver cancer cell lines and confirm the feasibility of t
92 o main actors in exosome biogenesis, in both liver cancer cell lines and HCC patient samples.
93 eceptor inhibitor (AEE788) were evaluated in liver cancer cell lines and in a xenograft model.
94 alian target of rapamycin signaling in human liver cancer cell lines and in both an in vitro and in v
95 in normal liver tissue but at high levels in liver cancer cell lines and in hepatocellular carcinoma
96 ession of GNMT inhibits the proliferation of liver cancer cell lines and prevents carcinogen-induced
97 lation and expression status was assessed in liver cancer cell lines and primary tumors.
98 ZNF198 and SUZ12 were also observed in human liver cancer cell lines derived from HBV-related tumors
99          BACKGROUND & AIMS: Human tumors and liver cancer cell lines express the product of a fusion
100 ficantly higher anti-proliferation effect on liver cancer cell lines Hep3B and SNU-449 than on liver
101                                        Human liver cancer cell lines HepG2 and Hep3B were treated wit
102 ression of GADD45beta was decreased in human liver cancer cell lines HepG2 and Hep3B, but not in norm
103                      Similarly, treatment of liver cancer cell lines HepG2 and Huh7, colon cancer cel
104 y, leptin was shown to be mitogenic in human liver cancer cell lines HepG2 and Huh7.
105           Depletion of IGF2BP1 from multiple liver cancer cell lines inhibits proliferation and induc
106                           Silencing PTPRK in liver cancer cell lines reduces colony-forming capacity
107 inducing ligand (TRAIL)-induced apoptosis of liver cancer cell lines requires death receptor-5 (DR5)-
108 s hypothesis, primary human cancer cells and liver cancer cell lines were treated with zebularine (ZE
109                           Treatment of human liver cancer cell lines with FFAs exacerbated the EMT ph
110 s activation against malignant B cell lines, liver cancer cell lines, and primary chronic lymphocytic
111 -mediated hepatocyte transformation in human liver cancer cell lines, as well as during HBV replicati
112  with an upregulation of Hh markers in human liver cancer cell lines, in liver samples from HBV infec
113                                However, most liver cancer cell lines, including HepG2 and Huh7, do no
114  lentiviral shRNA knockdown in several human liver cancer cell lines, we demonstrated that TTK boosts
115 14 of 15 colorectal, 1 of 8 lung, and 1 of 4 liver cancer cell lines.
116 hat all four compounds are effective in five liver cancer cell lines.
117 ivator GRIP1 in MCF-7 human breast and HepG2 liver cancer cell lines.
118 rm from a 1.2 kb mRNA was found in colon and liver cancer cell lines.
119 in both liver cancer tissues and established liver cancer cell lines.
120 s indicate a prominent novel role for Id1 in liver cancer cell metabolic adaptation.
121 ed in liver parenchymal cells, in preventing liver cancer cell metastasis.
122 , we developed a protocol to establish human liver cancer cell models at a success rate of around 50%
123 P30, ACSL4, endophilin B1, or Rab5a in human liver cancer cells or genetic knock-out of Tip30 in mous
124                                 Besides, the liver cancer cells overexpress the drug exporters which
125 n blocked metabolic adaptation and inhibited liver cancer cell proliferation and HCC growth in mice.
126  function as a therapeutic target to inhibit liver cancer cell proliferation and inhibit HCC.
127 nhibition of adiponectin secretion increases liver cancer cell proliferation, since adiponectin prote
128 critical determinants of the growth of human liver cancer cells, providing a strong rationale to eluc
129 ay a critical role in hNTCP dysregulation in liver cancer cells, providing insights into hepatocarcin
130            Importantly, SRSF1-depleted human liver cancer cells recapitulate this pathogenesis, illus
131        shRNA HK2 suppression in HK1(-)HK2(+) liver cancer cells reduced xenograft tumor progression,
132 ibit Wnt/beta-catenin signaling in colon and liver cancer cells regardless of whether this pathway is
133 In contrast, degradation of the AhR in HepG2 liver cancer cells resulted in decreased G0/G1 --> S pha
134                        KHK overexpression in liver cancer cells results in decreased fructose flux th
135                               In contrast to liver cancer cells, SAMe and MTA had no effect on Bcl-x(
136 ver, small molecule activation of miR-122 in liver cancer cells selectively induced apoptosis through
137 bjective of our current study is to identify liver cancer cell-specific molecular probes that could b
138 mentation effectively restores the growth of liver cancer cells starved of Trp.
139 finding suggested plausible effects of RS on liver cancer cell survival and invasion activities.
140 eam target and is functionally important for liver cancer cell survival and transformation.
141 from MAT1A to MAT2A gene expression in human liver cancer cells that may offer a growth advantage.
142 eported that IL-6 promoted survival of human liver cancer cells through activating STAT3 in response
143 quired in human hepatoma cell line 7 (Huh-7) liver cancer cells to maintain BOK at low levels, and BO
144 Mutations in the gene for beta-catenin cause liver cancer cells to release fewer exosomes, which redu
145 bilized DR5 and increased the sensitivity of liver cancer cells to the treatment of tumor necrosis fa
146 significantly improved the classification of liver cancer cells versus benign hepatocytes.
147 ally, c-MYC-induced self-renewal capacity of liver cancer cells was exerted in a p53-dependent manner
148 ter growth inhibition (IC50=50 nM for Hep G2 liver cancer cells) while exhibiting reduced toxicity to
149                  Blocking Notch signaling in liver cancer cells with the Notch activation signature u

 
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