ライフサイエンスコーパス: invasive cell

1 nclude cytotrophoblasts differentiating into invasive cells).

2 migration/invasion and metastasis of highly invasive cells.

3 that Shisa3 was highly expressed in the low invasive cells.

4 s as well as by promoting chemoresistance in invasive cells.

5 otentiating EGFR1 signalling at the front of invasive cells.

6 eceptor 1 (ESR1) were highly enriched in the invasive cells.

7 n dampens expression of the miRs in post-EMT invasive cells.

8 erentially expressed between preinvasive and invasive cells.

9 13, MMP15, and MMP17 was up-regulated in the invasive cells.

10 n and the gain of phenotypes associated with invasive cells.

11 in the conversion of normal keratinocytes to invasive cells.

12 n of the mesenchymal phenotype in migrating, invasive cells.

13 nding assay, was elevated in the PC-3 highly invasive cells.

14 , and motility activities of the PC-3 highly invasive cells.

15 m stationary, epithelial cells to migratory, invasive cells.

16 prevents migration and induces apoptosis of invasive cells.

17 f Matrigel for the study of morphogenesis of invasive cells, a simple and visual assay, adaptable to

18 Although invasive cells activate protective programs to survive u

19 RhoA expression was found in the PC-3 highly invasive cells as compared with the PC-3 low invasive ce

20 Here, we employed minimally invasive cell-attached patch-clamping, single-cell qPCR

21 roteolytically active form on the surface of invasive cells, based on its ability to bind directly in

22 molecular factors in the characterization of invasive cell behavior and, more generally, in epithelia

23 immobilized cryptic ECM epitopes to regulate invasive cell behavior may lead to the development of no

24 el role for steroid hormones, in stimulating invasive cell behavior, independent of effects on prolif

25 sion and formation of invadopodia, promoting invasive cell behavior.

26 of proteinases/inhibitors closely related to invasive cell behavior.

27 tastasis in two opposing ways, by supporting invasive cells but also by generating a barrier to invas

28 to laminin and a laminin-binding integrin by invasive cells but had no effect on their adhesion to th

29 cellular matrix, is highly expressed in non-invasive cells but undetectable levels in highly invasiv

30 o-oncogene, were found to be elevated in the invasive cells compared with the parental.

31 ized epithelial cells convert into migratory invasive cells during a number of developmental processe

32 Thus, in invasive cells, ECM-rigidity signals lead to increased m

33 ed actin assembly in cooperation with FAK at invasive cell edges, but WRC depletion can promote 3D ce

34 asive, E-cadherin-positive cells produces an invasive cell, even though these cells continue to expre

35 ing squamous and basal characteristics, with invasive cells exhibiting features of higher-grade tumor

36 Together, these results suggest that invasive cell fate requires G1 arrest and that strategie

37 ncer cells transition into highly motile and invasive cells for dissemination.

38 tasis, we systematically selected for highly invasive cells from breast cancer cell lines, MCF7 and M

39 ding stage of invasion, pattern of invasion, invasive cell grade, and composite histological tumor sc

40 Strikingly, RNAi of seprase in invasive cells greatly diminished their invasive potenti

41 gers a complex biological program leading to invasive cell growth by activating the c-Met receptor ty

42 G245D and other GOF p53 mutants enhances the invasive cell growth of p53-deficient head and neck squa

43 inhibiting aerobic glycolytic potential and invasive cell growth.

44 erimental data, and indicates that the U87WT invasive cells have a stronger directional motility bias

45 Microarray analysis of invasive cells identified potential downstream mediators

46 Exogenous expression of TNS4 marks invasive cells in an epithelial sheet.

47 tumor cells in culture that closely resemble invasive cells in primary breast carcinoma tissue.

48 l motility were most dramatically changed in invasive cells indicating a population that is neither d

49 diment has been the challenge of visualizing invasive cell interactions with basement membrane in viv

50 Only the invasive cell line, FaDu, released active stromelysin-1

51 as a variant form, are expressed in the most invasive cell lines but not in any of the noninvasive ce

52 The invasive cell lines displayed increased receptor tyrosin

53 three-dimensional trajectories of two highly invasive cell lines, the human HT-1080 fibrosarcoma and

54 had higher expression of E2F-1 than the less invasive cell lines.

55 vasive HNSCC cell lines compared with poorly invasive cell lines.

56 aining podosomes in invasive, but not in non-invasive cell lines.

57 ancer cell lines when compared with four non-invasive cell lines.

58 that netrin signaling orients a specialized invasive cell membrane domain toward the basement membra

59 UNC-40, however, MIG-10 localization to the invasive cell membrane is also dependent on the integrin

60 in receptor UNC-40 (DCC) localization to the invasive cell membrane of the AC.

61 or cell-matrix adhesion molecules propelled invasive cell membrane protrusions, which in turn promot

62 es defects in polarization of F-actin to the invasive cell membrane, a process required for the AC to

63 s with azathioprine inhibited Vav1-dependent invasive cell migration and matrix degradation, through

64 pression of oncogenic mutants of p53 promote invasive cell migration by enhancing endosomal recycling

65 Invasive cell migration in both normal development and m

66 tween signal transduction, cell adhesion and invasive cell migration in Drosophila border cells.

67 s being important for cell proliferation and invasive cell migration of primary brain tumors cells.

68 Invasive cell migration was temporally quantified by cal

69 the vascular wall matrix thereby inhibiting invasive cell migration, and as such, provides an import

70 lonogenicity, formation of pancreatospheres, invasive cell migration, and CSC function in human pancr

71 provides an excellent model system to study invasive cell migration, however it is still unclear how

72 demonstrate a role for this mechanoenzyme in invasive cell migration.

73 formation of active invadopodia but impairs invasive cell migration.

74 zing discrete cellular mechanisms underlying invasive cell motility.

75 t, MAP-2-positive dermal nevus cells and the invasive cells of primary melanomas were TYRP1-negative.

76 LamR overexpression correlates with a highly invasive cell phenotype and increased metastatic ability

77 crucial events during the progression toward invasive cell phenotype.

78 n have a major role in the development of an invasive cell phenotype.

79 ivity were required for the generation of an invasive cell phenotype.

80 either pathologic complete response (pCR) or invasive cells (pINV).

81 characterized by a poorly defined and highly invasive cell population.

82 ogeneous cell environment have revealed that invasive cell populations can induce dissemination by ot

83 s markedly different between the in situ and invasive cell populations.

84 e whether a novel approach using a minimally invasive cell sampling device, the Cytosponge, coupled w

85 tors to a neuroendocrine phenotype, and that invasive cells shared molecular features with NECs arisi

86 One of the sequences overexpressed by the invasive cells showed 99% homology to the P311 gene, the

87 Invasive cells showed a reduced expression of CD44v7/8,

88 In response to HGF/SF, the highly invasive cells signal through the MAPK pathway, whereas

89 but also promoted a robust growth of highly invasive cells, similar to effects produced by CAFs.

90 xpression de-differentiates cells into a pro-invasive cell state concomitant with TGFbeta activation.

91 imilar results were obtained in other tissue-invasive cells such as vascular endothelial cells, sugge

92 n experimental settings to emerge within the invasive cell system and are believed to express the sys

93 roteins was not detected in lysates from non-invasive cells that do not form invadopodia.

94 Only invasive cells that exhibited a 4p15.3-16 deletion were

95 ategies that remained stable in culture: (i) invasive cells that produce an acidic environment via up

96 ermined that, in contrast to its presence in invasive cells, this complex of proteins was not detecte

97 invasive cells as compared with the PC-3 low invasive cells through cDNA array and Western blot analy

98 a potential mechanism whereby adhesion of an invasive cell to the extracellular matrix regulates subs

99 cells, allowing small populations of highly invasive cells to be detected and differentiated from ot

100 actin-rich cell membrane projections used by invasive cells to penetrate the basement membrane.

101 ing of selected cell populations in vivo.Non-invasive cell tracking is a powerful method to visualize

102 Non-invasive cell tracking techniques are, however, necessar

103 ignaling, leukocyte adhesion and diapedesis, invasive cell type-specific markers, and complement syst

104 rix degradation, and have been found in many invasive cell types.

105 (2% O(2)), but differentiate into tumorlike invasive cells under well-oxygenated conditions such as

106 Invasive cells use small invadopodia to breach basement

107 In contrast, the number of viable cells and invasive cells was decreased in sFRP3 mRNA knockdown met

108 esis exclusively partitioned with the highly invasive cells, whereas the highly proliferative subclon

109 in metastasis of the pathways identified in invasive cells, which are regulated by ZBP1.

110 ects by LKB1 inactivation creates a uniquely invasive cell with aberrant polarity and adhesion signal

111 EN (PTEN-positive) if any core or WS had any invasive cells with >/= 1+ staining.

112 more, stable transfection of the PC-3 highly invasive cells with constitutively active RhoA Q63L resu

113 The intensity and percentage of invasive cells with cytoplasmic PTEN staining were deter

114 Transfection of these highly invasive cells with dominant negative RhoA N19 or treatm

115 Treatment of metastatic but not normal/non-invasive cells with TGF-beta1 caused a rapid and profoun

116 so codistributed with intracellular EphA2 in invasive cells within human breast carcinomas.