ライフサイエンスコーパス: invasive cell

1 nclude cytotrophoblasts differentiating into invasive cells).

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

3 ssion in MITF(high) proliferative and poorly invasive cells.

4 prevents migration and induces apoptosis of invasive cells.

5 ted reactive oxygen species (ROS) markers in invasive cells.

6 highest NIK expression observed in the most invasive cells.

7 otentiating EGFR1 signalling at the front of invasive cells.

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

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

10 migration/invasion and metastasis of highly invasive cells.

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

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

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

14 erentially expressed between preinvasive and invasive cells.

15 13, MMP15, and MMP17 was up-regulated in the invasive cells.

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

17 in the conversion of normal keratinocytes to invasive cells.

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

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

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

21 Although invasive cells activate protective programs to survive u

22 While these datasets cannot determine if the invasive cells are inherent to the population or if diff

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

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

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

26 gulated in human cancers, where it increases invasive cell behavior and correlates with poor patient

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

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

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

30 s unique insights into the roles of Piezo in invasive cell behavior.

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

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

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

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

35 was observed in the population of MITF(low) invasive cells but not in the population of MITF(high) d

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

37 Thus, without MMPs, an invasive cell can alter its BM-breaching tactics, sugges

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

39 These highly invasive cells continued to move throughout the 48 h exp

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

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

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

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

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

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

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

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

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

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

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

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

52 inhibiting aerobic glycolytic potential and invasive cell growth.

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

54 Microarray analysis of invasive cells identified potential downstream mediators

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

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

57 ve WERI Rb1 and Y79 cells as compared to non-invasive cells in vitro.

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

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

60 ing of human embryos using live imaging, non-invasive cell labeling, and computational predictions to

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

62 ly is HML-6 uniquely overexpressed in highly invasive cell lines and tissue samples, but also its gen

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

64 The invasive cell lines displayed increased receptor tyrosin

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

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

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

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

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

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

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

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

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

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

75 tive enrichment of the Arp2/3 complex at the invasive cell membrane, which drives formation of an F-a

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

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

78 Invasive cell migration in both normal development and m

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

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

81 s required for ECM-dependent cell growth and invasive cell migration under amino acid starvation, as

82 Invasive cell migration was temporally quantified by cal

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

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

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

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

87 formation of active invadopodia but impairs invasive cell migration.

88 n make-up is reset to regulate EGF-dependent invasive-cell migration.

89 ines increased proliferation, migration, and invasive cell motility in both infected and noninfected

90 zing discrete cellular mechanisms underlying invasive cell motility.

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

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

93 s, as well as metabolic reprogramming of the invasive cell phenotype, effectively reducing invasive c

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

95 crucial events during the progression toward invasive cell phenotype.

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

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

98 Within these GSCs, we identify an invasive cell population similar to outer radial glia (o

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

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

101 ression in tumors with highest expression in invasive cell populations.

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

103 Less clear, however, is how invasive cells provide energy, specifically ATP, to powe

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

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

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

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

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

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

110 ing up the possibility of building minimally invasive cell-specific structures and interfaces.

111 -TRIO-Rho-GTPase signaling network regulates invasive cell spread in both physiological and pathologi

112 markers, leading to a robust enhancement in invasive cell spread, which may lead to a worsened clini

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

114 pt to identify novel factors of the melanoma invasive cell state, we previously investigated the natu

115 mic rewiring associated with a quiescent but invasive cell state.

116 among GlialCAM, Mlc1, and aquaporin-4 in the invasive cell state.

117 n of TGM2 did not affect the SOX10-deficient invasive cell state; however, overexpression of TGM2 in

118 point toward targeted modulation of specific invasive cell states as a therapeutic strategy in GBM.

119 key factors that determine proliferative and invasive cell states in GBM.

120 lly at the invasive front of leader cells in invasive cell strands.

121 Highly and lowly invasive cell sublines were established using a repetiti

122 sion in 3D microenvironments and probing the invasive cell subpopulations.

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

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

125 contains subpopulations of proliferative and invasive cells that coordinately drive primary tumor gro

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

127 glioblastoma (GBM) contains groups of highly invasive cells that drive tumor progression as well as r

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

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

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

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

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

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

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

135 Non-invasive cell tracking can provide an important opportun

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

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

138 ted by cancer cells to enhance migratory and invasive cell traits.

139 In contrast, non-invasive cell type-specific ablation by induced apoptosi

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

141 and we demonstrate AAV-delivered, minimally invasive, cell-type-specific gene editing in wild-type m

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

143 (2% O(2)), but differentiate into tumorlike invasive cells under well-oxygenated conditions such as

144 Invasive cells use small invadopodia to breach basement

145 , proteases, and distinct modes of migration invasive cells use to overcome ECM barriers.

146 Invasive cells use transient, energy-consuming protrusio

147 es induced by cell crowding, focusing on pro-invasive cell volume reduction in ductal carcinoma in si

148 ade DCIS and indicates the presence of a pro-invasive cell volume reduction mechanotransduction pathw

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

150 The most invasive cells were stiffer, developed higher mechanical

151 KK-47 (non-invasive), T24 and 5637 (invasive) cells were used in experiments.

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

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

154 suppresses the default invasive state in non-invasive cells, which complements transcriptional regula

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

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

157 lastoma is the inability to eliminate highly invasive cells with chemotherapy, radiation, or surgical

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

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

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

161 rmatic analysis reveal that rounded-amoeboid invasive cells with high CD73-ROCK-Myosin II activity an

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

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