ライフサイエンスコーパス: liver cancer cell

1 er CD133, which is located on the surface of liver cancer cells.

2 he monodisperse CDs in MCF-7 cells and Huh-7 liver cancer cells.

3 ctrochemical biosensors for the detection of liver cancer cells.

4 f SCP1 increased the c-Myc protein levels in liver cancer cells.

5 n the enrichment of nuclear FBP1 and FBP2 in liver cancer cells.

6 bearing liver, limits intrahepatic spread of liver cancer cells.

7 rial homeostasis, and a signaling network in liver cancer cells.

8 in repressing c-MYC-induced CSC phenotype in liver cancer cells.

9 he most potent conjugate against HepG2 human liver cancer cells.

10 p in the regulation of invasive potential in liver cancer cells.

11 on of YAP/TEAD transcriptional activation in liver cancer cells.

12 hibited proliferation and migration of human liver cancer cells.

13 l is growth-suppressive and pro-apoptotic in liver cancer cells.

14 by the TCF and FoxA transcription factors in liver cancer cells.

15 H) concentration in vitro and in HepG2 human liver cancer cells.

16 the anti-apoptotic function of IL-6 in human liver cancer cells.

17 ents SAMe level to reach high enough to kill liver cancer cells.

18 ression and consequently its function in the liver cancer cells.

19 molecular probes for specific recognition of liver cancer cells.

20 hepatocytes and stimulating the apoptosis of liver cancer cells.

21 s directly affecting malignant properties of liver cancer cells.

22 and the growth response to TGF-beta in human liver cancer cells.

23 inhibitor celecoxib on the growth control of liver cancer cells.

24 yses cells, and spreads only poorly in Hep3B liver cancer cells.

25 ination with Bcl-XL inhibition on a panel of liver cancer cells.

26 from MAT1A to MAT2A gene expression in human liver cancer cells.

27 tiforme) cell lines and knocked out in HUH7 (liver cancer) cells.

28 ate induced apoptosis in the HepG2 and Hep3B liver cancer cells; 5-azaC treatment alone produced G2 a

29 ingly, CCDC3, as a secreted protein, targets liver cancer cells and increases long chain polyunsatura

30 can efficiently replicate in HepG2 and Hep3B liver cancer cells and produce high titers of virus.

31 The expression of FAM83H is elevated in liver cancer cells, and nuclear expression of FAM83H pre

32 CD133+ liver cancer cells are characterized by resistance to ch

33 SAMe and MTA are also proapoptotic in liver cancer cells by selectively inducing Bcl-x(S) expr

34 monstrate in vivo overexpression of MAT1A in liver cancer cells can suppress tumor growth.

35 up-regulated and exhibited high stability in liver cancer cells compared with other cells.

36 gged form of MAN2A1-FER in NIH3T3 and HEP3B (liver cancer) cells; Golgi were isolated for analysis.

37 nsports citrate across cell membranes, halts liver cancer cell growth by altering both energy product

38 at MAT2A and MAT2beta genes are required for liver cancer cell growth that is induced by the profibro

39 of CaMKK2 function is sufficient to inhibit liver cancer cell growth, and the growth defect resultin

40 pendent protein kinase 4 (CaMKIV) to control liver cancer cell growth.

41 nucifera was found to exert cytotoxicity on liver cancer cells HepG2 in a dose-dependent manner.

42 EMT in hepatic stellate cell (HSC) and human liver cancer cells (HepG2) and the potential role of EVE

43 thereby enabling the efficient detection of liver cancer cells (HepG2).

44 A similar differential activity was seen in liver cancer cells (HepG2, Huh7, and Hep3B).

45 e selective aptamers could specifically bind liver cancer cells in a mouse model.

46 ver stem cells (LSCs) into highly metastatic liver cancer cells in premalignant liver tissue.

47 Expression of this miRNA in liver cancer cells in vitro induces cell-cycle arrest as

48 aMKK2 with STO-609 impairs tumorigenicity of liver cancer cells in vivo.

49 limit proliferation and induce apoptosis of liver cancer cells in vivo.

50 Blocking lipogenesis in cultured liver cancer cells is sufficient to decrease cell viabil

51 omoter was hypermethylated in both colon and liver cancer cells, leading to the production of high le

52 cognition, two liver cell lines were used: a liver cancer cell line BNL 1ME A.7R.1 (MEAR) and a nonca

53 nd GPC3 antigens on the surface of the human liver cancer cell line Hep3B using anti-EpCAM-CdTe- and

54 In the present study, human liver cancer cell line HepG2, having high intracellular

55 ter overexpressed in hepatocarcinoma and the liver cancer cell line HepG2.

56 croarray analysis of gene re-expression in 4 liver cancer cell lines after their exposure to reagents

57 eceptor inhibitor (AEE788) were evaluated in liver cancer cell lines and in a xenograft model.

58 alian target of rapamycin signaling in human liver cancer cell lines and in both an in vitro and in v

59 in normal liver tissue but at high levels in liver cancer cell lines and in hepatocellular carcinoma

60 ZNF198 and SUZ12 were also observed in human liver cancer cell lines derived from HBV-related tumors

61 BACKGROUND & AIMS: Human tumors and liver cancer cell lines express the product of a fusion

62 Human liver cancer cell lines HepG2 and Hep3B were treated wit

63 ression of GADD45beta was decreased in human liver cancer cell lines HepG2 and Hep3B, but not in norm

64 Similarly, treatment of liver cancer cell lines HepG2 and Huh7, colon cancer cel

65 y, leptin was shown to be mitogenic in human liver cancer cell lines HepG2 and Huh7.

66 Depletion of IGF2BP1 from multiple liver cancer cell lines inhibits proliferation and induc

67 inducing ligand (TRAIL)-induced apoptosis of liver cancer cell lines requires death receptor-5 (DR5)-

68 s hypothesis, primary human cancer cells and liver cancer cell lines were treated with zebularine (ZE

69 Treatment of human liver cancer cell lines with FFAs exacerbated the EMT ph

70 -mediated hepatocyte transformation in human liver cancer cell lines, as well as during HBV replicati

71 with an upregulation of Hh markers in human liver cancer cell lines, in liver samples from HBV infec

72 lentiviral shRNA knockdown in several human liver cancer cell lines, we demonstrated that TTK boosts

73 hat all four compounds are effective in five liver cancer cell lines.

74 ivator GRIP1 in MCF-7 human breast and HepG2 liver cancer cell lines.

75 rm from a 1.2 kb mRNA was found in colon and liver cancer cell lines.

76 in both liver cancer tissues and established liver cancer cell lines.

77 14 of 15 colorectal, 1 of 8 lung, and 1 of 4 liver cancer cell lines.

78 s indicate a prominent novel role for Id1 in liver cancer cell metabolic adaptation.

79 ed in liver parenchymal cells, in preventing liver cancer cell metastasis.

80 P30, ACSL4, endophilin B1, or Rab5a in human liver cancer cells or genetic knock-out of Tip30 in mous

81 critical determinants of the growth of human liver cancer cells, providing a strong rationale to eluc

82 ibit Wnt/beta-catenin signaling in colon and liver cancer cells regardless of whether this pathway is

83 In contrast, degradation of the AhR in HepG2 liver cancer cells resulted in decreased G0/G1 --> S pha

84 In contrast to liver cancer cells, SAMe and MTA had no effect on Bcl-x(

85 ver, small molecule activation of miR-122 in liver cancer cells selectively induced apoptosis through

86 bjective of our current study is to identify liver cancer cell-specific molecular probes that could b

87 eam target and is functionally important for liver cancer cell survival and transformation.

88 from MAT1A to MAT2A gene expression in human liver cancer cells that may offer a growth advantage.

89 eported that IL-6 promoted survival of human liver cancer cells through activating STAT3 in response

90 quired in human hepatoma cell line 7 (Huh-7) liver cancer cells to maintain BOK at low levels, and BO

91 ally, c-MYC-induced self-renewal capacity of liver cancer cells was exerted in a p53-dependent manner

92 ter growth inhibition (IC50=50 nM for Hep G2 liver cancer cells) while exhibiting reduced toxicity to

93 Blocking Notch signaling in liver cancer cells with the Notch activation signature u