ライフサイエンスコーパス: anchorage-independent growth

1 The soft agar assay was used as a measure of anchorage independent growth.

2 t wild-type doubling times, cytokinesis, and anchorage-independent growth.

3 suppressed HCC cell migration, invasion, and anchorage-independent growth.

4 ploidy cells, and attenuation of cancer cell anchorage-independent growth.

5 T352A) attenuated the induction of PDAC cell anchorage-independent growth.

6 h Cat-1, the cells are again able to undergo anchorage-independent growth.

7 xpressed in TNBCs and 10 proved critical for anchorage-independent growth.

8 l lines reduced cell migration, invasion and anchorage-independent growth.

9 increased the proliferation rate and induced anchorage-independent growth.

10 ogate its actions as a negative regulator of anchorage-independent growth.

11 t expression reduced anchorage-dependent and anchorage-independent growth.

12 of epithelial characteristics and decreased anchorage-independent growth.

13 l lines and decreased cell proliferation and anchorage-independent growth.

14 l lines caused ATP reduction and compromised anchorage-independent growth.

15 cell proliferation, migration, invasion, and anchorage-independent growth.

16 ression of aromatase significantly increased anchorage-independent growth.

17 liation and increased both proliferation and anchorage-independent growth.

18 lected in their relative abilities to confer anchorage-independent growth.

19 also find that reduction of NOS1AP enhances anchorage-independent growth.

20 s of ROCK substrates, migration, invasion or anchorage-independent growth.

21 ration and invasion, anoikis resistance, and anchorage-independent growth.

22 ion forces, cell migration and invasion, and anchorage-independent growth.

23 ion of these activities inhibits PAK1-driven anchorage-independent growth.

24 on displayed higher activation of ERK1/2 and anchorage-independent growth.

25 l transition (EMT), increased migration, and anchorage-independent growth.

26 affected E1A-mediated cell proliferation and anchorage-independent growth.

27 s, activation of death programs, and loss of anchorage-independent growth.

28 r (CTGF) and Cyr61 target genes, and exhibit anchorage-independent growth.

29 increased proliferation, clonogenicity, and anchorage-independent growth.

30 ut not Exo84 was necessary for inhibition of anchorage-independent growth.

31 atment with an inhibitor of ERRalpha impeded anchorage-independent growth.

32 enic RAS but also conferred the capacity for anchorage-independent growth.

33 found no inhibition of KRAS mutant CRC cell anchorage-independent growth.

34 -RasV12 was sufficient to reduce Ras-induced anchorage-independent growth.

35 B56gamma3 to inhibit cell proliferation and anchorage-independent growth.

36 rRNA transcription and repressed EGF-induced anchorage-independent growth.

37 7b overexpression on migration, invasion and anchorage-independent growth.

38 ncy on ETV1 expression for proliferation and anchorage-independent growth.

39 ing, and are dependent on FGFR signaling for anchorage-independent growth.

40 cked the ability of EGFR mutations to induce anchorage-independent growth.

41 inotransferase is essential for Kras-induced anchorage-independent growth.

42 a tTG inhibitor blocks their EGF-stimulated anchorage-independent growth.

43 broblast cell morphologic transformation and anchorage-independent growth.

44 essive phenotype with increased motility and anchorage-independent growth.

45 ritical role in regulating proliferation and anchorage-independent growth.

46 tant, Y254F, was enhanced in Wrch-1-mediated anchorage-independent growth.

47 vPK also augments cellular proliferation and anchorage-independent growth.

48 ain prostate cancer migration, invasion, and anchorage-independent growth.

49 ed cell growth, clonogenicity, mobility, and anchorage-independent growth.

50 er proliferation, cell cycle progression and anchorage-independent growth.

51 cy, including cell migration, metastasis and anchorage-independent growth.

52 4C-E) resulted in a significant increase in anchorage-independent growth.

53 towards ULK1 and require ULK1 for sustained anchorage-independent growth.

54 well as for Ewing sarcoma proliferation and anchorage-independent growth.

55 ndrial function, cellular proliferation, and anchorage-independent growth.

56 with CK2alpha had enhanced proliferation and anchorage-independent growth.

57 lticellular spheroids that were generated by anchorage-independent growth.

58 ncer-like gene expression but do not exhibit anchorage-independent growth.

59 ll death and reducing metabolic activity and anchorage-independent growth.

60 esults in preventing migration, invasion and anchorage-independent growth.

61 uired to support replicative immortality and anchorage independent growth, a predictor of tumorigenes

62 pha silencing in ras-transformed IEC reduced anchorage-independent growth, a criterion for malignant

63 ere we report that p100 inhibits cancer cell anchorage-independent growth, a hallmark of cellular mal

64 ction of glucose metabolism for Kras-induced anchorage-independent growth, a hallmark of transformed

65 cer cells inhibits cell proliferation and an anchorage-independent growth, a hallmark of tumorigenic

66 These cell lines exhibit anchorage-independent growth, a lack of contact inhibiti

67 ction to ECM-induced signals is required for anchorage-independent growth, a property of most maligna

68 These cells (hNCPCs(V600E)) acquired anchorage-independent growth ability and were weakly tum

69 of apico-basal polarity in 3D cultures, and anchorage-independent growth, accompanied by expression

70 osis, epithelial-mesenchymal transition, and anchorage-independent growth activities in vitro and on

71 UBE3, ZSCAN18, CCDC8 and FBN2 resulted in an anchorage-independent growth advantage.

72 ns for CAP1 in cancer cell proliferation and anchorage-independent growth, again in a cell context-de

73 d strikingly, cooperated with OSM to promote anchorage-independent growth (AIG), a property associate

74 ired and sufficient to control PKD1-mediated anchorage-independent growth and anchorage-dependent pro

75 n a subset of these cell lines inhibits both anchorage-independent growth and cell invasion in a GAP-

76 investigation revealed that miR-185 impedes anchorage-independent growth and cell migration, in addi

77 CHPT1 silencing inhibited anchorage-independent growth and cell proliferation, als

78 lpha expression was required for Myc-induced anchorage-independent growth and cell proliferation.

79 I in H460 cells also impaired cell adhesion, anchorage-independent growth and cell seeding to the lun

80 ons, ectopic expression of Myc-nick promotes anchorage-independent growth and cell survival at least

81 tment; second, in a separate assay measuring anchorage-independent growth and colony formation by imm

82 mary epithelial cells evidenced by decreased anchorage-independent growth and decreased cell migratio

83 ive melanoma and lung cancer cells increased anchorage-independent growth and elevated the expression

84 embrane localization and activation, impeded anchorage-independent growth and enhanced stress-induced

85 ormed characteristics of cancer cells (e.g., anchorage-independent growth and enhanced survival capab

86 al features of human cancer cells, including anchorage-independent growth and escape from contact inh

87 n immortalized cells, although essential for anchorage-independent growth and evasion of apoptosis, d

88 pression was sufficient to suppress in vitro anchorage-independent growth and in vivo tumor formation

89 -kappaB termination, could suppress in vitro anchorage-independent growth and in vivo tumor formation

90 hat LARP1 promotes cell migration, invasion, anchorage-independent growth and in vivo tumorigenesis.

91 ermore, depletion of K-Ras and RalB inhibits anchorage-independent growth and invasion and interferes

92 ing ATAD3A also results in loss of both cell anchorage-independent growth and invasion and suppressio

93 nes were heterogeneous in their capacity for anchorage-independent growth and invasion.

94 amate receptor-1 (GRM1) blockade on melanoma anchorage-independent growth and invasion.

95 ransfectants of truncated FasL showed strong anchorage-independent growth and lung metastasis potenti

96 -dependent growth was ROCK-independent, both anchorage-independent growth and Matrigel invasion were

97 example is the importance of active RalA in anchorage-independent growth and membrane raft trafficki

98 lower cell cycle progression and compromised anchorage-independent growth and migration ability in vi

99 has an obligate role in TGF-beta-stimulated anchorage-independent growth and migration.

100 phosphorylation of MEK, leading to increased anchorage-independent growth and migration.

101 ivation of MEK and NF-kappaB, migration, and anchorage-independent growth and reduce its mitochondria

102 nt-derived colon cancer cell line suppressed anchorage-independent growth and reduced tumor growth in

103 operties of MCF10-2A cells with induction of anchorage-independent growth and self-renewal in 3D-sphe

104 bset of lung cancer cell lines reduces their anchorage-independent growth and significantly decreases

105 abrogated the ability of hypoxia to increase anchorage-independent growth and significantly reduced t

106 pensates for AMPK activation and facilitates anchorage-independent growth and solid tumour formation

107 ess conditions, such as glucose limitations, anchorage-independent growth and solid tumour formation

108 ts expression in NIH-3T3 fibroblasts induces anchorage-independent growth and stimulates cell invasio

109 KSR2 expression alone induced anchorage-independent growth and synergized with the tra

110 egulated kinase pathway activation, promoted anchorage-independent growth and tumor formation in mice

111 gulation of the miR-200 family, and enhanced anchorage-independent growth and tumor formation in nude

112 cells harboring wild-type PPP2R1A increased anchorage-independent growth and tumor formation, and tr

113 in signaling, cell migration, proliferation, anchorage-independent growth and tumor growth in a mouse

114 Phosphorylation of WASp at Y102 enhances anchorage-independent growth and tumor growth in an in v

115 significant increases in cell proliferation, anchorage-independent growth and tumor growth in vivo.

116 ation of PEAK1 levels in cancer cells alters anchorage-independent growth and tumor progression in mi

117 ies associated with tumorigenesis, including anchorage-independent growth and tumor progression.

118 nally important in alveolar rhabdomyosarcoma anchorage-independent growth and tumor-cell proliferatio

119 s or their inhibition with imatinib enhanced anchorage-independent growth and tumorigenesis induced b

120 tion of EGFR expression reduced HER2-induced anchorage-independent growth and tumorigenesis.

121 nhibits proliferation, NF-kappaB activation, anchorage-independent growth and tumorigenesis.

122 c and/or Akt and examined the cell lines for anchorage-independent growth and tumorigenesis.

123 We showed that depletion of FoxM1 inhibits anchorage-independent growth and tumorigenicity in mouse

124 ants strongly promoted cell focus formation, anchorage-independent growth, and cell invasion.

125 rmation of the HA cable structure, increased anchorage-independent growth, and cell-cell adhesion.

126 ing FGFR3 and kdFGFR3 reduced clonogenicity, anchorage-independent growth, and disintegration of the

127 gnificantly decreased cell proliferation and anchorage-independent growth, and impaired migration and

128 ediated signaling, inhibiting cell invasion, anchorage-independent growth, and in vivo dissemination

129 imensional culture, increased proliferation, anchorage-independent growth, and increased migration an

130 creased proliferation and survival, promoted anchorage-independent growth, and induced migration and

131 phosphorylation increased autophagy, reduced anchorage-independent growth, and inhibited Akt-driven t

132 cluded rates of proliferation and apoptosis, anchorage-independent growth, and invasiveness, were ass

133 orrelated with increased cell proliferation, anchorage-independent growth, and migration and invasion

134 as, suppresses SW-480 cell proliferation and anchorage-independent growth, and promotes caspase- and

135 KSRP decreased cell proliferation, reversed anchorage-independent growth, and reduced migration/inva

136 duced apoptosis, inhibited proliferation and anchorage-independent growth, and rendered glioma cells

137 asTF promotes oncogenic gene expression, anchorage-independent growth, and strongly up-regulates

138 ogic transformation by H-RasV12 or K-RasV12, anchorage-independent growth, and survival of anoikis of

139 , KAP1, CHD1, and EIF3L collectively support anchorage-independent growth, and the SUMOylation of KAP

140 JNK2alpha had decreased cellular growth and anchorage-independent growth, and the tumors were four-f

141 n, elevated clonogenic activity, accelerated anchorage-independent growth, and transformation and wer

142 changes, an increase in cell proliferation, anchorage-independent growth, and tumor growth in vivo.

143 ll lines compromised cell cycle progression, anchorage-independent growth, and tumorigenesis in nude

144 s exhibit epithelial-to-mesenchymal changes, anchorage-independent growth, and upregulated RAS/MAPK s

145 by shRNA suppressed PCa cell proliferation, anchorage-independent growth, and xenograft tumor format

146 lignant melanoma cells resulted in increased anchorage-independent growth, as evidenced by enhanced c

147 increased invadopodia-dependent invasion and anchorage-independent growth, as well as by inhibition o

148 Results of MTT- and anchorage-independent growth assays and cell cycle analy

149 ting contact inhibition and oncogene-induced anchorage-independent growth, because of a failure to pr

150 n of KLF5 expression significantly decreased anchorage-independent growth, but did not affect prolife

151 on of RalA expression reduced CRC tumor cell anchorage-independent growth, but surprisingly, stable s

152 tive CCND1/CDK2 activity effectively confers anchorage independent growth by inhibiting p53 or replac

153 cell (HCEC) model to identify suppressors of anchorage-independent growth by conducting a soft agar-b

154 mors inhibited their anchorage-dependent and anchorage-independent growth by inducing senescence and/

155 melanocytes and in melanoma cells increased anchorage-independent growth by providing GAB2-expressin

156 antly, Orai3 knockdown selectively decreased anchorage-independent growth (by approximately 58%) and

157 1)/S transition of the cell cycle as well as anchorage-independent growth capability of breast cancer

158 y active forms of Akt1 and Akt2 restores the anchorage-independent growth capability of HeLa cells de

159 tive-tissue growth factor (CTGF), as well as anchorage-independent growth, capacity to invade Matrige

160 cessary for actin cytoskeletal organization, anchorage-independent growth, cell migration, and experi

161 unctionally, the Tsc2(-/-) cells demonstrate anchorage-independent growth, cell scattering, and anoik

162 each variant on NB cell adhesion, migration, anchorage-independent growth, co-precipitation with alph

163 Here, we used 2D and 3D Matrigel, anchorage-independent growth conditions and a breast can

164 nder magnesium-deprived situations and under anchorage-independent growth conditions, demonstrating a

165 PC re-expression exerted profound effects in anchorage-independent growth conditions, however, includ

166 icted by Helios found ten conferred enhanced anchorage-independent growth, demonstrating Helios's exq

167 y and cellular transformation as assessed by anchorage-independent growth, focus formation, invasion,

168 ificantly reduced cellular proliferation and anchorage-independent growth from control melanomas, whe

169 ased proliferation, migration, invasion, and anchorage-independent growth; impaired growth of an orth

170 bypass the requirement for oncogenic Ras in anchorage independent growth in vitro and tumor formatio

171 transcripts identified in this tumor induced anchorage-independent growth in 3T3 cells and tumor form

172 of human kinases for their ability to induce anchorage-independent growth in a derivative of immortal

173 tivity in maintaining metabolic activity and anchorage-independent growth in breast cancer cells.

174 ficantly reduces both cell proliferation and anchorage-independent growth in EAC cells.

175 together with FGFR2 isoform IIIb, increases anchorage-independent growth in immortalized Barrett's e

176 d that its depletion inhibits clonogenic and anchorage-independent growth in multiple patient-derived

177 duces the ability of Ran(K152A) to stimulate anchorage-independent growth in NIH-3T3 cells and in SKB

178 ated Akt phosphorylation, proliferation, and anchorage-independent growth in parental cells, but had

179 ated Akt phosphorylation, proliferation, and anchorage-independent growth in parental cells.

180 , morphological transformation and increased anchorage-independent growth in response to FGF2 ligand

181 Here, we found substantial inhibition of anchorage-independent growth in soft agar and cell migra

182 ll lung cancer (NSCLC) cell lines, increased anchorage-independent growth in soft agar and enhanced t

183 Interestingly, miR-193a controls anchorage-independent growth in soft agar through K-Ras,

184 by growth factor-independent proliferation, anchorage-independent growth in soft agar, and enhanced

185 ormation between GRIN1 and GRIN2A, increased anchorage-independent growth in soft agar, and increased

186 o-mesenchymal transition phenotype, acquired anchorage-independent growth in soft agar, and led to en

187 reased cell proliferation, colony formation, anchorage-independent growth in soft agar, cell migratio

188 own of CAPC by siRNA in LNCaP cells enhanced anchorage-independent growth in soft agar.

189 ze of transformed foci in cultured cells and anchorage-independent growth in soft agar.

190 functionally relevant; through induction of anchorage-independent growth in TGF-beta1-dependent norm

191 ERRalpha expression, metabolic capacity, and anchorage-independent growth in the absence of KSR1.

192 icient to enhance metabolic capacity but not anchorage-independent growth in the absence of KSR1.

193 signaling pathway-mediated cell invasion and anchorage-independent growth in U1242 MG cells.

194 s of contact growth inhibition and increased anchorage-independent growth in vitro and in vivo.

195 colon cancer cells reduces cell survival and anchorage-independent growth in vitro and inhibits tumor

196 esses prostate cancer cell proliferation and anchorage-independent growth in vitro and inhibits tumor

197 negatively regulates anchorage-dependent and anchorage-independent growth in vitro and restrains tumo

198 ific expression of CD24 (NLS-CD24) increased anchorage-independent growth in vitro and tumor formatio

199 encing inhibits NSCLC cell proliferation and anchorage-independent growth in vitro and tumor formatio

200 ispensable for breast cell proliferation and anchorage-independent growth in vitro and tumor growth i

201 tion of ETS1 in breast cancer cells promotes anchorage-independent growth in vitro and tumor growth i

202 sufficient to promote cell proliferation and anchorage-independent growth in vitro and tumorigenesis

203 ts elevated activity in tumor cells promotes anchorage-independent growth in vitro as well as pancrea

204 Notch4 function in vasculogenic mimicry and anchorage-independent growth in vitro is due in part to

205 MEM16A overexpression significantly promoted anchorage-independent growth in vitro, and loss of TMEM1

206 cancer cell stemness in a mammosphere assay, anchorage-independent growth in vitro, and lung cancer c

207 ificantly inhibited invasion, migration, and anchorage-independent growth in vitro, and orthotopic tu

208 P2 overexpression suppressed foci formation, anchorage-independent growth in vitro, and tumorigenicit

209 s to tumor cell proliferation, invasion, and anchorage-independent growth in vitro.

210 inhibited oral cancer cell invasiveness and anchorage-independent growth in vitro.

211 ls significantly increased proliferation and anchorage-independent growth in vitro.

212 ressive versus MMTV-PyVT;Nedd9(+/+) cells in anchorage-independent growth, in growth on three-dimensi

213 ited an increased capacity for AKT-dependent anchorage-independent growth, in support of a tumor supp

214 n several malignant phenotypes, particularly anchorage-independent growth, indicating that this often

215 A synthesis, and the anchorage-dependent and anchorage-independent growth induced by insulin and GPCR

216 roliferation in vitro and in vivo, decreases anchorage-independent growth, induces apoptosis, and dra

217 ULK2 overexpression inhibited anchorage independent growth, inhibited astrocyte transf

218 ilization, G2/M growth arrest induction, and anchorage-independent growth inhibition of cancer cells.

219 RNA Rad9 cells restores migration, invasion, anchorage-independent growth, integrin beta1 expression,

220 However, selective PDK1 inhibition impairs anchorage-independent growth, invasion, and cancer cell

221 In contrast, PKCdelta attenuation enhanced anchorage-independent growth, invasion, and migration in

222 e-mediated attenuation of PKCdelta inhibited anchorage-independent growth, invasion, migration, and t

223 cells, miR-22 decreased cell proliferation, anchorage-independent growth, invasiveness, and promoted

224 Anchorage independent growth is one of the hallmarks of

225 major source of ROS generation required for anchorage-independent growth is the Q(o) site of mitocho

226 the loss of KSR2 in metabolic signaling and anchorage-independent growth, KSR2 RNAi, MEK inhibition,

227 s treated with bisphosphonates inhibited the anchorage-independent growth, migration and invasion of

228 oviocytes, and cell proliferation, survival, anchorage-independent growth, migration, and invasion we

229 gnant properties such as cell proliferation, anchorage-independent growth, migration, invasion, and a

230 tionally cooperate with NF-kappaB to promote anchorage-independent growth, motility and invasion of m

231 nhibition of sAPPalpha significantly reduced anchorage independent growth of the cancer cells.

232 Silencing ITSN1 significantly inhibits the anchorage independent growth of tumor cells in vitro and

233 PAK4 substrate GEF-H1 (IC(50) = 1.3 nM) and anchorage-independent growth of a panel of tumor cell li

234 l migration, invasion, colony formation, and anchorage-independent growth of aggressive lung cancer c

235 gulation of survivin, which in turn supports anchorage-independent growth of alphavbeta6-expressing c

236 has also acquired the property to facilitate anchorage-independent growth of breast cancer cells.

237 we found that Nrf2 activation inhibited the anchorage-independent growth of breast cancer cells.

238 entiation and impaired the proliferation and anchorage-independent growth of cells with protective al

239 firmed by finding that DeltaNp73 facilitates anchorage-independent growth of gastric epithelial cells

240 UC338 decreased both anchorage-dependent and anchorage-independent growth of HCC cells.

241 f focal complexes, is also essential for the anchorage-independent growth of HeLa cervical carcinoma

242 The motility, survival, and anchorage-independent growth of HMGB1-secreting malignan

243 not RKI-11 inhibits migration, invasion and anchorage-independent growth of human breast cancer cell

244 preading of murine embryonic fibroblasts and anchorage-independent growth of human cancer cell lines.

245 tion, CDK2 inhibition drastically diminishes anchorage-independent growth of human cancer cells and c

246 ounds disrupt NR0B1 complexes and impair the anchorage-independent growth of KEAP1-mutant cancer cell

247 CPIC treatment also reduced the anchorage-independent growth of LAPC-4 prostate cancer c

248 Depletion of AR suppressed Sema4D-induced anchorage-independent growth of LNCaP and LNCaP-LN3 cell

249 cycle arrest and inhibited proliferation and anchorage-independent growth of lung cancer cells.

250 The anchorage-independent growth of MCF-10A(arom) cells can

251 gammaS inhibited, whereas adenosine promoted anchorage-independent growth of MDA-MB-231 cells.

252 for SLFN5 in the regulation of invasion and anchorage-independent growth of melanoma cells.

253 x), resulting in increased proliferation and anchorage-independent growth of melanoma cells.

254 Aspirin decreased viability and anchorage-independent growth of mutant PIK3CA breast can

255 mediated knockdown of C3G or SOS1 suppressed anchorage-independent growth of NIH-3T3 cells overexpres

256 Igammai2 and Src synergistically induced the anchorage-independent growth of nonmalignant cells.

257 INPP4B increases proliferation and triggers anchorage-independent growth of normal colon epithelial

258 nd in cells and suppressed proliferation and anchorage-independent growth of pancreatic cancer by inh

259 enzymatic product of LTA(4)H, and suppressed anchorage-independent growth of pancreatic cancer cells.

260 depletion of srGAP3 promotes Rac dependent, anchorage-independent growth of partially transformed hu

261 a2 or SPRK3 inhibited both proliferation and anchorage-independent growth of RMS cells.

262 activation, and decreased the viability and anchorage-independent growth of the cells.

263 Anchorage-independent growth of the PC-3 cells and tumor

264 ncing LITAF by shRNA enhances proliferation, anchorage-independent growth of these cancer cells and t

265 hosphatases significantly reduced growth and anchorage-independent growth of TNBC cells to a greater

266 In addition, Akt3 was required for anchorage-independent growth of transformed astrocytes a

267 actin-binding domain drastically reduced the anchorage-independent growth of transformed cells.

268 The requirement for Cat-1 when assaying the anchorage-independent growth of transformed fibroblasts

269 t cannot be phosphorylated by AMPK increased anchorage-independent growth of tumor cells and helped t

270 hate 5-kinase (PIPK) Igammai2 in controlling anchorage-independent growth of tumor cells in coordinat

271 NAi-mediated knockdown of RASSF10-stimulated anchorage-independent growth of U87 glioma cells, increa

272 ) production, which led to cell invasion and anchorage-independent growth on soft agar plates.

273 owth, but inhibited PDAC cell proliferation, anchorage-independent growth, orthotopic tumor growth, a

274 biased determination of colony formation and anchorage independent growth over time.

275 s Wnt/beta-catenin activation, as well as an anchorage-independent growth phenotype.

276 esvirus 68 (gammaHV68) infection and achieve anchorage-independent growth, providing a cellular reser

277 ogenic H-Ras(V12) to regulate metabolism and anchorage-independent growth, providing novel targets fo

278 eads to markedly increased cell motility and anchorage-independent growth, reduced endocrine sensitiv

279 This diminished both cell proliferation and anchorage-independent growth required for cancer progres

280 The ability of PGC1alpha to promote anchorage-independent growth required interaction with E

281 activities, both RalA and RalB regulation of anchorage-independent growth required interaction with R

282 Hemizygous deletion promoted anchorage-independent growth, revealing that PKCbeta is

283 Overexpression of HOXD9 increases anchorage-independent growth, shortens population-doubli

284 ced migration and colony formation, impaired anchorage-independent growth, slower xenograft tumor gro

285 is, they exhibit much greater invasiveness, anchorage-independent growth, spheroid formation, and dr

286 malignant melanoma cell proliferation and/or anchorage-independent growth, suggesting key and non-ove

287 K2 expression alone was sufficient to impair anchorage-independent growth, supporting their nonoverla

288 es (ROS) which are required for Kras-induced anchorage-independent growth through regulation of the E

289 inhibited HBx stimulation of cell migration, anchorage-independent growth, tumor development in HBxTg

290 tively inhibits melanoma cell proliferation, anchorage-independent growth, tumorigenesis, and tumor m

291 ic cell line U251 reduces their capacity for anchorage-independent growth, two-dimensional migration,

292 ion gene to be dependent on VTI1A-TCF7L2 for anchorage-independent growth using RNA interference-medi

293 s leads to loss of contact inhibition and to anchorage-independent growth, vital traits acquired duri

294 Mechanistically, the block in anchorage-independent growth was associated with accumul

295 Anchorage-independent growth was tightly linked to dose-

296 Proliferation, migration, and anchorage independent growth were evaluated.

297 ocyst component was necessary for supporting anchorage-independent growth, whereas RalB interaction w

298 nduced apoptosis, faster cell migration, and anchorage-independent growth, whereas Yap knockdown resu

299 I-induced Akt activation, proliferation, and anchorage-independent growth while retaining responsiven

300 AXL inhibition suppressed mesothelioma anchorage-independent growth, with reduction in colony n