ライフサイエンスコーパス: tumor cell invasion

1 of ROK-regulated cytoskeleton function (e.g. tumor cell invasion).

2 HA modification, cathepsin B activation, and tumor cell invasion).

3 an modification, cathepsin B activation, and tumor cell invasion).

4 ase activating protein that was required for tumor cell invasion.

5 hown that increased ECM stiffness stimulates tumor cell invasion.

6 exchange factor, regulates cell adhesion and tumor cell invasion.

7 cal MKK4 substrates, and PPARgamma2 enhanced tumor cell invasion.

8 egradation, and matrix proteolysis-dependent tumor cell invasion.

9 ion, Rho-kinase (ROK) activation, and breast tumor cell invasion.

10 tein (HOXD10), RhoGTPase-ROK activation, and tumor cell invasion.

11 ion in anchorage-independent cell growth and tumor cell invasion.

12 e phosphoinositide 3-kinase (PI3K)-dependent tumor cell invasion.

13 factor (TNF)-induced apoptosis but inhibited tumor cell invasion.

14 and nontumor stromal cells during collective tumor cell invasion.

15 t into the mechanisms by which Pyk2 mediates tumor cell invasion.

16 rix degradation all accompany the process of tumor cell invasion.

17 podia, extracellular matrix degradation, and tumor cell invasion.

18 in promotes beta-catenin transactivation and tumor cell invasion.

19 SCC progression and play a critical role in tumor cell invasion.

20 ing in amoeboid and mesenchymal movement and tumor cell invasion.

21 n in the localization of proteins that drive tumor cell invasion.

22 collagenase activity, which is required for tumor cell invasion.

23 cells resulted in a significant reduction of tumor cell invasion.

24 t al. describe a unique mechanism regulating tumor cell invasion.

25 ion of the protease by the integrin promotes tumor cell invasion.

26 oproteinases has been reported to facilitate tumor cell invasion.

27 ession by cDNA transfection led to increased tumor cell invasion.

28 specific set of genes that together mediate tumor cell invasion.

29 asing antiapoptotic functions, and enhancing tumor cell invasion.

30 oteins, inhibits activated FAK, and prevents tumor cell invasion.

31 iRNA-mediated depletion of CD44 v5 decreases tumor cell invasion.

32 family protein inactivation and also induced tumor cell invasion.

33 cated in cell motility, differentiation, and tumor cell invasion.

34 lts define a novel role for EPO in mediating tumor cell invasion.

35 ional proteins from cell contacts, and focal tumor cell invasion.

36 r target that is involved in HGF/SF-mediated tumor cell invasion.

37 ced or bypassed tissue stiffness and limited tumor cell invasion.

38 brane metalloproteinase that is critical for tumor cell invasion.

39 (cathepsin B) activation resulting in breast tumor cell invasion.

40 bly and function of structures implicated in tumor cell invasion.

41 hancing MMP-2 gene transcription and in turn tumor cell invasion.

42 cadherin inhibits human mammary and prostate tumor cell invasion.

43 at degrade the extracellular matrix to drive tumor cell invasion.

44 nd CD44-mediated branching morphogenesis and tumor cell invasion.

45 n, has been identified as a key component in tumor cell invasion.

46 oteolytic and collagenolytic activity during tumor cell invasion.

47 fic blockade of CD44 significantly decreased tumor cell invasion.

48 regulates cellular adhesion, migration, and tumor cell invasion.

49 ulminates in the activation of pro-MMP-1 and tumor cell invasion.

50 of membrane-bound proteases occurring during tumor cell invasion.

51 Decreased adhesion is thought to promote tumor cell invasion.

52 o the specific functions of integrins during tumor cell invasion.

53 including the induction of angiogenesis and tumor cell invasion.

54 regulates cellular adhesion, migration, and tumor cell invasion.

55 ontacts and to be crucial for the process of tumor cell invasion.

56 lloproteinase stromelysin 3, is required for tumor cell invasion.

57 R3) promotes adhesion disassembly and breast tumor cell invasion.

58 ious effect on cell adhesion associated with tumor cell invasion.

59 to-mesenchymal transition (EMT) and inducing tumor cell invasion.

60 sitioning and reduces MT1-MMP exocytosis and tumor cell invasion.

61 al effects on cell proliferation but blocked tumor cell invasion.

62 g, impairs membrane dynamics, and suppresses tumor cell invasion.

63 etastatic niches, promoting angiogenesis and tumor cell invasion.

64 of matrix-degrading invadopodia in CAFs and tumor cell invasion.

65 ppression caused mTORC1-dependent pancreatic tumor cell invasion.

66 ssociated with decreased macrophage-mediated tumor cell invasion.

67 nclear how Stx4 function is regulated during tumor cell invasion.

68 ke of tumor-derived exosomes, which leads to tumor cell invasion.

69 of chemokines and cytokines associated with tumor cell invasion.

70 es that have been previously associated with tumor cell invasion.

71 the plasma membrane, where they function in tumor cell invasion.

72 their inhibition by hypoxia and facilitates tumor cell invasion.

73 ations for tissue engineering and studies of tumor cell invasion.

74 ributed to the inhibitory effect of FOXL1 on tumor cell invasion.

75 , which is required for vitronectin-mediated tumor cell invasion.

76 eficiency and leads to similar inhibition of tumor cell invasion.

77 expression and LPA1-dependent chemotaxis and tumor cell invasion.

78 enhancing MMP-2 gene transcription and thus tumor-cell invasion.

79 related focal adhesion kinase (FAK) regulate tumor cell invasion, albeit via distinct mechanisms.

80 icated the small GTP-binding protein ARF6 in tumor cell invasion, although the molecular basis by whi

81 ilencing resulted in a dramatic reduction of tumor cell invasion and angiogenesis in vitro.

82 the precise mechanism by which PDGF-D causes tumor cell invasion and angiogenesis remain unclear.

83 F, and MMP-9, resulting in the inhibition of tumor cell invasion and angiogenesis.

84 s a multifunctional cytokine that stimulates tumor cell invasion and angiogenesis.

85 ors in axonal pathfinding and may facilitate tumor cell invasion and angiogenesis.

86 miR-10b appears to play an important role in tumor cell invasion and breast cancer progression.

87 Met plays an important role in tumor cell invasion and cell migration.

88 RhoGTPases and survival proteins leading to tumor cell invasion and cisplatin resistance.

89 ession of COX-2 showed that it has a role in tumor cell invasion and cross-talk to endothelial cells.

90 ) tumors, exhibit a reduced ability to drive tumor cell invasion and decreased secretion of prometast

91 erapeutic interventions targeted at limiting tumor cell invasion and dispersal.

92 These data suggest that Arg promotes tumor cell invasion and dissemination, while simultaneou

93 the extracellular matrix, thereby promoting tumor cell invasion and dissemination.

94 val protein up-regulation as well as reduces tumor cell invasion and enhances chemosensitivity.

95 nd M2a macrophages and were found to promote tumor cell invasion and express M2a markers, confirming

96 ented that tumor suppressive maspin inhibits tumor cell invasion and extracellular matrix remodeling.

97 ellular organization of F-actin and inhibits tumor cell invasion and filipodia formation.

98 omoted macrophage-tumor cell interaction and tumor cell invasion and indicate that VCAM-1 is a potent

99 n contribute to metastasis through enhancing tumor cell invasion and intravasation in vivo and that E

100 rusions that are thought to be important for tumor cell invasion and intravasation.

101 ne SH3BGRL (mSH3BGRL) strongly promoted both tumor cell invasion and lung metastasis.

102 tiple requisite proteolytic steps underlying tumor cell invasion and may provide insight into potenti

103 ng expression of RhoC, a potential marker of tumor cell invasion and metastases.

104 Disruption of adherens junctions promotes tumor cell invasion and metastasis and is often associat

105 (CaM) antagonists have been shown to inhibit tumor cell invasion and metastasis and to induce apoptos

106 Maspin has been shown to inhibit tumor cell invasion and metastasis in breast tumor cells

107 EDD9/HEF1/Cas-L scaffolding protein promotes tumor cell invasion and metastasis in multiple cancer ce

108 Acid pH has been shown to stimulate tumor cell invasion and metastasis in vitro and in cells

109 r factor (HGF/SF) plays an important role in tumor cell invasion and metastasis that is mediated thro

110 ortance of the extracellular matrix (ECM) in tumor cell invasion and metastasis, and culminated in th

111 pite the well-established role of hypoxia in tumor cell invasion and metastasis, and resistance to th

112 Ectopic expression of miR-34a decreased tumor cell invasion and metastasis, inhibited the format

113 mor-associated fibroblasts as a modulator of tumor cell invasion and metastasis, using retroviral del

114 are critically involved in the processes of tumor cell invasion and metastasis, we investigated the

115 are critically involved in the processes of tumor cell invasion and metastasis, we investigated whet

116 rane-associated extracellular cathepsin B in tumor cell invasion and metastasis, we used the yeast tw

117 tic cytokines (chemokines) can help regulate tumor cell invasion and metastasis.

118 ases and integrins play an essential role in tumor cell invasion and metastasis.

119 h suppression of early lesions and enhancing tumor cell invasion and metastasis.

120 eptors and integrins play essential roles in tumor cell invasion and metastasis.

121 ); its collagenase activity facilitates both tumor cell invasion and metastasis.

122 Cell migration plays an important role in tumor cell invasion and metastasis.

123 d enhancement of cell motility essential for tumor cell invasion and metastasis.

124 ation- and IRES-dependent translation during tumor cell invasion and metastasis.

125 lar matrix degradation, which may facilitate tumor cell invasion and metastasis.

126 broblast migration during wound healing, and tumor cell invasion and metastasis.

127 are important determinants in the control of tumor cell invasion and metastasis.

128 -MMP; also known as MMP-14), a key enzyme in tumor cell invasion and metastasis.

129 acellular signaling pathways responsible for tumor cell invasion and metastasis.

130 tion of branching tubules, angiogenesis, and tumor cell invasion and metastasis.

131 egulation of cortactin levels contributes to tumor cell invasion and metastasis.

132 cer, expression of uPA/uPAR is essential for tumor cell invasion and metastasis.

133 hways that may be involved into Met mediated tumor cell invasion and metastasis.

134 in disease processes including arthritis and tumor cell invasion and metastasis.

135 ding extracellular matrix, thus facilitating tumor cell invasion and metastasis.

136 ta receptor (TGFbetaR) is required for local tumor cell invasion and metastasis.

137 brane destruction associated with late-stage tumor cell invasion and metastasis.

138 tumor cells, and are believed to facilitate tumor cell invasion and metastasis.

139 toma cells allowed us to kinetically monitor tumor cell invasion and metastasis.

140 ate, increased tumor stiffness, and enhanced tumor cell invasion and metastasis.

141 man cancer and are associated with increased tumor cell invasion and metastasis.

142 molecular mechanism by which talin enhances tumor cell invasion and metastasis.

143 the mechanism of action of SPDEF in prostate tumor cell invasion and metastasis.

144 (MET), are fundamental processes involved in tumor cell invasion and metastasis.

145 in activation has important implications for tumor cell invasion and metastasis.

146 owth and motility, fundamental components of tumor cell invasion and metastatic spread of melanoma ce

147 c-Src signaling complex, leading to enhanced tumor cell invasion and metastatic spread.

148 type typically is characterized by augmented tumor cell invasion and migration in addition to tumor c

149 ven our previous finding of VEGFR-1-mediated tumor cell invasion and migration in pancreatic carcinom

150 events under hypoxia, causing alterations in tumor cell invasion and migration in vitro, as well as m

151 erin and inhibited Snail expression and both tumor cell invasion and migration.

152 jection; (2) Rac1 activation; and (3) breast tumor cell invasion and migration.

153 RNA-mediated suppression of Fkbp1a increases tumor cell invasion and MMP9 levels, while down-regulati

154 cell movement is a crucial mechanism in both tumor cell invasion and morphogenetic cell movements dur

155 roenvironment (TME) are crucial in promoting tumor cell invasion and progression.

156 alinosporamide A also suppressed TNF-induced tumor cell invasion and receptor activator of nuclear fa

157 inducer (CD147) is a crucial process during tumor cell invasion and regulation of blood supply.

158 un thus contributes to ErbB2-induced mammary tumor cell invasion and self-renewal.

159 We confirmed that these miRNA can stimulate tumor cell invasion and show that SS can attenuate their

160 Tumor cell invasion and the expression of matrix metallo

161 More notably, ARC deficiency also limited tumor cell invasion and the number of circulating cancer

162 te may provide new targets for modulation of tumor cell invasion and tissue remodeling.

163 matrix degrading protrusions, important for tumor cell invasion and transendothelial migration and t

164 ignaling in MDA-MB-231 cells is required for tumor cell invasion and tumor angiogenesis.

165 ctional studies suggest it causes aggressive tumor cell invasion and tumor cell vessel-like structure

166 ppression in cancer, in angiogenesis, and in tumor cells' invasion and metastases.

167 r of normal TM morphology and of TM-mediated tumor-cell invasion and proliferation.

168 sociated with altered embryonic development, tumor cell invasion, and abnormal wound repair.

169 a (PEA-15) are linked to insulin resistance, tumor cell invasion, and cellular senescence; these chan

170 tem cell properties, including self-renewal, tumor cell invasion, and chemotherapy resistance in HA/C

171 rget genes such as MIA, which is involved in tumor cell invasion, and H19, a long noncoding RNA precu

172 ovel epigenetic mechanism regulating EMT and tumor cell invasion, and has important implication in ta

173 rmation of colonies in soft agar, stimulated tumor cell invasion, and induced liver metastasis in an

174 ion adaptively induced by PI3K therapy fuels tumor cell invasion, and may provide an important antime

175 l migration, chemotaxis, cell-cell adhesion, tumor cell invasion, and metastasis.

176 MRTFs are important regulators of fibrosis, tumor cell invasion, and metastasis.

177 may play a key role in MMP-2 production and tumor cell invasion, and that perturbation of this molec

178 red for maximal responses to fibronectin and tumor cell invasion, and this operates through an enhanc

179 E-cadherin serves as a suppressor of tumor cell invasion, and when tumor cells turn on the ex

180 an promote angiogenesis, cell proliferation, tumor-cell invasion, and immune evasion.

181 ns, which can lead to development of tumors, tumor-cell invasion, and metastasis.

182 A, which resulted in a marked suppression of tumor cell invasion, angiogenesis and metastasis in a mo

183 C3 cells resulted in a dramatic reduction of tumor cell invasion as indicated by a Matrigel invasion

184 tions and "scatter" during processes such as tumor cell invasion as well as some stages of embryonic

185 l compounds from series 1 (10 muM) inhibited tumor cell invasion but none from the non-nitrate panel

186 es RhoGTPase/survival protein expression and tumor cell invasion, but also increases chemosensitivity

187 AP20 may be an important regulator of breast tumor cell invasion by a CaM-mediated mechanism that lea

188 family proteins, plays an essential role in tumor cell invasion by altering gene expression.

189 Inhibition of tumor cell invasion by antibodies against alpha1 and alp

190 Although Pyk2 regulates tumor cell invasion by controlling invadopodium-mediated

191 ppressor in lung adenocarcinoma and inhibits tumor cell invasion by decreasing PPARgamma2 levels.

192 Mechanistically, miR-520f inhibited tumor cell invasion by directly targeting ADAM9, the TGF

193 estingly, in humans, LIMK1 activity promotes tumor cell invasion by modulating actin and microtubule

194 The inhibition of tumor cell invasion by N6L demonstrated in this study, i

195 opulations express Mena(INV), which promotes tumor cell invasion by potentiating EGF responses.

196 sociated macrophages (TAMs), in turn, aid in tumor cell invasion by secreting epidermal growth factor

197 These results show that SS can inhibit tumor cell invasion by suppressing NF-kappaB-mediated tr

198 Here we show that hypoxia increases tumor cell invasion by the modulation of Rab11, an impor

199 These novel findings suggest that tumor cell invasion can be therapeutically targeted by i

200 genes resulted in significant reductions in tumor cell invasion compared to a nontargeting siRNA con

201 have developed a new 3-dimensional model of tumor cell invasion, demonstrated protein and collagen d

202 ne loop mechanism, and in particular whether tumor cell invasion depends on spatial ligand gradients

203 enchyma near the growing tumor mass, or from tumor cell invasion directly into the parenchyma.

204 ch maspin regulates cell-matrix adhesion and tumor cell invasion does not involve the serpin mechanis

205 ntegrin in human GBM cells leads to impaired tumor cell invasion due to hyperactivation of the Rho GT

206 This mechanism likely enhances tumor cell invasion during metastasis.

207 Matrix metalloproteases promote tumor cell invasion, epithelial-to-mesenchymal transitio

208 r the expression of proteins associated with tumor cell invasion (estrogen receptor alpha and cycloox

209 induction of apoptosis, but their effect on tumor cell invasion has not been well studied.

210 in-like sequences within NC1 (FNC1) promoted tumor cell invasion in a laminin 5-dependent manner and

211 Because Thy-1 (CD90) marks CAFs that promote tumor cell invasion in a murine model of Kras(G12D)-driv

212 se the SPARC gene product is associated with tumor cell invasion in a variety of different cancers, w

213 also showed that knockdown of Eps8 inhibited tumor cell invasion in an organotypic model of OSCC.

214 olipase Cgamma-1 (PLCgamma-1) contributes to tumor cell invasion in experimental systems when activat

215 differential control of angiogenesis versus tumor cell invasion in GBM.

216 little is known about the factors governing tumor cell invasion in HNSCC.

217 In turn, this results in enhanced tumor cell invasion in low nutrients and metastatic diss

218 mbospondin-1, and Wnt-5A expression, reduced tumor cell invasion in organotypic culture, and restrict

219 fostered by a stiff matrix, and critical for tumor cell invasion in our assays.

220 observations suggest that MMAC/PTEN inhibits tumor cell invasion in part by regulating MMP-2 gene tra

221 g its stability in the membrane, and blocked tumor cell invasion in tissues.

222 cPA has previously been shown to inhibit tumor cell invasion in vitro and cancer cell metastasis

223 This, in turn, enhances tumor cell invasion in vitro and in vivo.

224 receptor for secreted Hsp90alpha reduces the tumor cell invasion in vitro and lung colonization and t

225 hly metastatic breast cancer cells inhibited tumor cell invasion in vitro and lung metastatic coloniz

226 NA significantly inhibits uPA expression and tumor cell invasion in vitro and tumor growth and incide

227 The ability of dysadherin to promote tumor cell invasion in vitro was dependent on the establ

228 epression and overexpression of NNMT blocked tumor cell invasion in vitro.

229 ucer of apoptosis and was able to knock down tumor cell invasion in vitro.

230 K tyrosine phosphorylation and inhibition of tumor cell invasion in vitro.

231 ng promotes cell motility and enhancement of tumor cell invasion in vitro.

232 EphB2 was found to increase tumor cell invasion in vivo using an internally controll

233 oproteinase-2 (MMP-2), an enzyme involved in tumor-cell invasion, in SNB19 cells expressing p16 was s

234 es its transcriptional activity and promotes tumor cell invasion, indicating that AKT-dependent regul

235 ct of alpha(5)beta(1)-integrin inhibition on tumor cell invasion, indicating that alpha(5)beta(1)-int

236 Neutralizing antibodies against uPAR block tumor cell invasion induced by hypoxia or HIF-1 alpha ov

237 supports pericellular matrix degradation and tumor cell invasion into different pathologically releva

238 mammary tumor-associated lymphangiogenesis, tumor cell invasion into lymphatics, and metastasis.

239 he diaphragm, frequently with indications of tumor cell invasion into the diaphragm.

240 Furthermore, Rab25-driven tumor-cell invasion into a 3D extracellular matrix envir

241 aring mice exhibit significant reductions in tumor cell invasion, intravasation into blood vessels an

242 Tumor cell invasion involves targeted localization of pr

243 Tumor cell invasion is a highly integrated and complex p

244 Tumor cell invasion is a major contributor to cancer mor

245 Tumor cell invasion is a primary event in the metastatic

246 Tumor cell invasion is a process regulated by integrins,

247 This review will summarize the evidence that tumor cell invasion is the result of oncogene-mediated s

248 Tumor cell invasion is vital for cancer progression and

249 which regulates pericellular proteolysis and tumor cell invasion, is a new binding partner of DLC1 in

250 of matrix metalloproteinases, necessary for tumor cell invasion, is also regulated by these HA/CD44-

251 lloproteinase (MT1-MMP), a key proteinase in tumor cell invasion, is essential for the design of pote

252 ast cancer, TAMs enhance tumor angiogenesis, tumor cell invasion, matrix remodeling, and immune suppr

253 Therefore, inhibition of tumor cell invasion may provide an effective therapy for

254 g the expression of MMP9, which could affect tumor cell invasion mediated by TGF-beta.

255 ng localized actin polymerization, including tumor cell invasion, microbial pathogenesis, and T cell

256 hages can stimulate angiogenesis and enhance tumor cell invasion, motility, and intravasation.

257 The effects of ROCK on tumor cell invasion/motility and growth may derive from

258 ollagen IV degradation in vitro and mediates tumor cell invasion of G8 myoblast monolayers.

259 that drive mesenchymal programs may suppress tumor cell invasion of peritoneal tissues.

260 These enzymes are associated with tumor cell invasion of the basement membrane and stroma,

261 sion and suggest that semaphorin 7a promotes tumor cell invasion on collagen and lymphangiogenesis vi

262 al at metastatic sites, but had no effect on tumor cell invasion or extravasation.

263 The role of proteases in the tumor cell invasion process is multifaceted.

264 ccurring in the basement membrane during the tumor cell invasion process, and thus provide mechanisti

265 d protein, has previously been implicated in tumor cell invasion, proliferation and metastasis.

266 ownstream of uPA-uPAR that actively advances tumor cell invasion, proliferation, and survival of pros

267 Current models of tumor cell invasion propose that oncogenic signaling con

268 Tumor cell invasion relies on cell migration and extrace

269 Tumor cell invasion requires the molecular and physical

270 ral nervous system neoplasm characterized by tumor cell invasion, robust angiogenesis, and a mean sur

271 )-mediated signaling have been implicated in tumor cell invasion, survival, and metastasis in a varie

272 We used a tumor cell invasion system to identify the chemokine CCL

273 ay in which MMP-9 regulates uPA activity and tumor cell invasion through cleavage of PN-1.

274 from tumor cells has the capacity to promote tumor cell invasion through endothelial barriers by both

275 tor (VEGF) directly and negatively regulates tumor cell invasion through enhanced recruitment of the

276 matrix metalloproteinase (MT1-MMP) supports tumor cell invasion through extracellular matrix barrier

277 ession/processing contribute to Rac-promoted tumor cell invasion through interstitial collagen barrie

278 J8H inhibited tumor cell invasion through Matrigel.

279 axis of tumor cells, ET-1 and ET-2 increased tumor cell invasion through Matrigel.

280 operatively influence matrix degradation and tumor cell invasion through proteolytic cascades, with i

281 Tumor cell invasion through the extracellular matrix is

282 fficking of alpha5beta1 that is required for tumor cell invasion through three-dimensional matrices.

283 inases MMP-2 and MMP-9, which play a role in tumor cell invasion, through JNK1-independent and -depen

284 ain may play an important role in inhibiting tumor cell invasion, thus explaining the observed loss o

285 ll SNB19 glioma cells significantly inhibits tumor-cell invasion, thus suggesting a novel function of

286 correlated with enhanced tumorigenicity and tumor cell invasion using in vitro model systems.

287 d Src kinase in patient samples and promoted tumor cell invasion using intracranial mouse models.

288 essed tumor cell proliferation but increased tumor cell invasion via greater mitochondrial traffickin

289 ) expressed active RhoA enhanced LPA-induced tumor cell invasion via the activation of endogenous Rho

290 Tumor cell invasion was studied using organotypic raft c

291 Da gelatinase (MMP-9) is a known mediator of tumor cell invasion, we sought to determine whether and

292 and because stromal cells may contribute to tumor cell invasion, we used quantitative real-time reve

293 icellular matrix degradation and mesenchymal tumor cell invasion, whereas in MT1-MMP-negative cells,

294 D by small interfering RNA (siRNA) decreased tumor cell invasion, whereas PDGF-D overexpression by cD

295 ed MMP1 secretion by smooth muscle cells and tumor cell invasion, whereas selective blocking of exoso

296 ructural modulation" mechanism may exist for tumor cell invasion, whereby triple-helical collagen pro

297 lved typical features of neoangiogenesis and tumor cell invasion with a spatial resolution of ~5 micr

298 to HCC cell lines lacking Ink4a/Arf inhibits tumor cell invasion, without affecting cell proliferatio

299 ence (siRNA) reduces expression of MMP-9 and tumor cell invasion, without growth inhibition in cell c

300 ficantly impairs FA-mediated degradation and tumor cell invasion yet does not appear to affect invado