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 with alpha-actinin 4 is required to promote tumor cell invasion.

5 fibroblasts (CAF) that facilitate epithelial tumor cell invasion.

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

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

8 their inhibition by hypoxia and facilitates tumor cell invasion.

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

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

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

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

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

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

15 hown that increased ECM stiffness stimulates tumor cell invasion.

16 r cells to promote collagen crosslinking and tumor cell invasion.

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

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

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

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

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

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

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

24 and nontumor stromal cells during collective tumor cell invasion.

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

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

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

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

29 vo as a potential mechanism for early breast tumor cell invasion.

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

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

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

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

34 oproteinases has been reported to facilitate tumor cell invasion.

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

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

37 l-mesenchymal transition (EMT) and increased tumor cell invasion.

38 asing antiapoptotic functions, and enhancing tumor cell invasion.

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

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

41 family protein inactivation and also induced tumor cell invasion.

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

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

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

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

46 brane metalloproteinase that is critical for tumor cell invasion.

47 e localized matrix degradation necessary for tumor cell invasion.

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

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

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

51 cadherin inhibits human mammary and prostate tumor cell invasion.

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

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

54 oteolytic and collagenolytic activity during tumor cell invasion.

55 fic blockade of CD44 significantly decreased tumor cell invasion.

56 actin-binding protein alpha-actinin 4 during tumor cell invasion.

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

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

59 n glioblastoma cancer stem cells that drives tumor cell invasion.

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

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

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

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

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

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

66 including the induction of angiogenesis and tumor cell invasion.

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

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

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

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

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

72 tory mechanisms are well orchestrated during tumor cell invasion.

73 etastatic niches, promoting angiogenesis and tumor cell invasion.

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

75 ppression caused mTORC1-dependent pancreatic tumor cell invasion.

76 ssociated with decreased macrophage-mediated tumor cell invasion.

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

78 of chemokines and cytokines associated with tumor cell invasion.

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

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

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

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

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

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

85 s a multifunctional cytokine that stimulates 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 b, a VEGFA-blocking antibody, may accelerate tumor cell invasion and induce alternative angiogenic pa

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

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

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

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

104 ically permissive tumor microenvironment for tumor cell invasion and metastases.

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

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

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

108 talk between PDGFR/SDF-1 signaling regulates tumor cell invasion and metastasis in human and mouse ad

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 oles in the development of various malignant tumor cell invasion and metastasis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 ed type I collagen linearization facilitates tumor cell invasion and promotes spontaneous breast canc

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

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

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

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

159 Tumor cell invasion and the expression of matrix metallo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

185 r microenvironment, which directly regulates tumor cell invasion by affecting immune cell function, c

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

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

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

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

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

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

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

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

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

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

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

197 oproteinases (MMPs) and thus associated with tumor cell invasion, clinical studies demonstrated incre

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

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

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

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

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

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

204 This mechanism likely enhances tumor cell invasion during metastasis.

205 rapy-mediated senescence, and suppression of tumor cell invasion endpoints.

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

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

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

209 (MRI), which is unable to precisely identify tumor cell invasion, impairing effective surgery and rad

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 entially adjust energy production or promote tumor cell invasion in response to microenvironment cond

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

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

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

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

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

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

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

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

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

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

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

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

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 cal inhibition of PDGFRbeta and JNK impaired tumor cell invasion induced by integrin alpha11-positive

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

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

240 mor matrix regulates metastasis by fostering tumor cell invasion into the stroma and migration toward

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

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

243 Tumor cell invasion involves targeted localization of pr

244 Tumor cell invasion is a highly integrated and complex p

245 Tumor cell invasion is a major contributor to cancer mor

246 Tumor cell invasion is a primary event in the metastatic

247 Tumor cell invasion is a process regulated by integrins,

248 Tumor cell invasion is one result of the bidirectional i

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

250 Tumor cell invasion is vital for cancer progression and

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

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

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

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

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

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

257 atologic malignancies and is associated with tumor cell invasion, metastasis, and a poor patient prog

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

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

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

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

262 Dissemination encompasses tumor cells invasion of stroma, followed by intravasatio

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

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

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

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

267 ction in extracellular matrix regulation and tumor cell invasion, processes replicated by invasive tr

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

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

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

271 tion of tumor microenvironment acidosis with tumor cell invasion, relatively little is known regardin

272 Tumor cell invasion requires the molecular and physical

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

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

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

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

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

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

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

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

281 J8H inhibited tumor cell invasion through Matrigel.

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

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

284 Tumor cell invasion through the extracellular matrix is

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

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

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

288 lpha11 promotes CAF invasion and CAF-induced tumor cell invasion upon PDGF-BB stimulation.

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

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

291 Tumor cell invasion was studied using organotypic raft c

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

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

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

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

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

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