ライフサイエンスコーパス: soft agar

1 ouse embryo fibroblasts (colony formation in soft agar).

2 ttenuating their ability to form colonies in soft agar.

3 endent growth of gastric epithelial cells in soft agar.

4 activation, and inhibits the cell growth in soft agar.

5 resensitizes the DDR and restrains growth in soft agar.

6 -dependent tumor cell motility and growth in soft agar.

7 of colony formation, and impaired growth in soft agar.

8 ut had little effect on swimming motility in soft agar.

9 re necessary for TGF-beta-mediated growth in soft agar.

10 , resulting in increased colony formation in soft agar.

11 medium-stimulated epithelial cell growth in soft agar.

12 fewer colonies in both monolayer culture and soft agar.

13 zomib inhibited estrogen-dependent growth in soft agar.

14 etic basement membranes, and their growth in soft agar.

15 ted spontaneous mutants able to move through soft agar.

16 UMUC3) were dependent on FGFR1 for growth in soft agar.

17 mary epithelial cells caused their growth in soft agar.

18 ing in a viscous medium or on the surface of soft agar.

19 d growth of human glioblastoma T98G cells in soft agar.

20 ayer culture and growth of large colonies in soft agar.

21 one induced little or no colony formation in soft agar.

22 d by a screen for restoration of motility in soft agar.

23 as assessed by measuring colony formation in soft agar.

24 feration and anchorage-independent growth in soft agar.

25 s tumor cell anchorage-independent growth in soft agar.

26 cancer, BT-20 cells do not form colonies in soft agar.

27 n to inhibit anchorage-independent growth in soft agar.

28 BT-20 cells the ability to form colonies in soft agar.

29 sform primary mouse embryonic fibroblasts in soft agar.

30 roliferation, colony formation and growth in soft agar.

31 erin levels, and reduced colony formation in soft agar.

32 and reduced clonogenicity on plastic and in soft agar.

33 cultures and anchorage-independent growth in soft agar.

34 feration and anchorage-independent growth on soft agar.

35 orage-independent growth of cell colonies on soft agar.

36 red by the ability to form large colonies in soft agar.

37 ells reduces anchorage-independant growth in soft agar.

38 mation in mice, as well as foci formation in soft agar.

39 f v-Rel transformed CEFs to form colonies in soft agar.

40 s to form xenografts in mice and colonies in soft agar.

41 binant retrovirus suppressed their growth in soft agar.

42 eration, and anchorage-independent growth in soft agar.

43 ble to inhibit HC11-Int3 colony formation in soft agar.

44 TT assay and anchorage-independent growth in soft agar.

45 tion of the MNKs reduces colony formation in soft agar.

46 layer cell proliferation, but blocked AIG in soft agar.

47 ptor (EGFR), induced transformed colonies in soft agar.

48 tion with vSrc, resulted in robust growth in soft agar.

49 established from the mammary tumors grew in soft agar.

50 e of calcium and enhances clone formation in soft agar.

51 sed cyclin D1 and c-Myc levels and growth in soft agar.

52 leus, an overgrowth phenotype, and growth in soft agar.

53 was determined by cell cluster formation in soft agar.

54 a nude mice model (57% of inhibition) and in soft agar.

55 led to larger and more numerous colonies in soft agar.

56 med RelA-deficient cells to form colonies in soft agar.

57 horylation and inhibited colony formation in soft agar.

58 ent on IRS1 activity for colony formation in soft agar.

59 59 led to a reduction of colony formation in soft agar.

60 nes enhances the ability to form colonies in soft agar.

61 of prostate cancer cells to form colonies in soft agar.

62 melanoma proliferation in both monolayer and soft agar.

63 ration but essential for colony formation in soft agar.

64 cell transformation as assessed by growth in soft agar.

65 lution conditions and clonogenic activity in soft agar.

66 ters growth properties and induces growth in soft agar.

67 lls enhanced anchorage-independent growth in soft agar.

68 in the spontaneous formation of colonies in soft agar.

69 ed cells and anchorage-independent growth in soft agar.

70 nd migration, as well as reduced survival in soft agar (a measure of anoikis).

71 cells and monitored its effects on growth in soft agar, a hallmark of cellular transformation, and al

72 vasiveness and decreased colony formation in soft agar across multiple melanoma cell lines.

73 e ability of these cells to form colonies in soft agar, an in vitro measure of tumorgenicity.

74 ERK and Akt activity and inhibited growth in soft agar and ability of these cells to migrate.

75 morigenic phenotype with increased growth in soft agar and an invasive phenotype in three-dimensional

76 44, and displayed increased clonogenicity in soft agar and broad drug-resistance in vitro and in vivo

77 and FLLL32 also inhibit colony formation in soft agar and cell invasion and exhibit synergy with the

78 nhibition of anchorage-independent growth in soft agar and cell migration in each of four NSCLC lines

79 d cell proliferation and colony formation in soft agar and cell-cycle arrest.

80 c Mullerian epithelial marker genes, grow in soft agar and develop ectopic invasive tumors in recipie

81 s, increased anchorage-independent growth in soft agar and enhanced tumor growth in severe combined i

82 Similar results were seen in soft agar and focus-formation assays, where p110beta was

83 so inhibited anchorage-independent growth in soft agar and growth in an orthotopic xenograft model.

84 on is associated with higher tumor growth in soft agar and in a xenograft model.

85 horage-independent survival of HeLa cells in soft agar and in athymic mice.

86 density, and acquired the ability to grow in soft agar and in Matrigel compared with the parental rel

87 reby, to be essential for melanoma growth in soft agar and in nude mice.

88 roliferation, migration, invasion, growth in soft agar and in vivo tumorigenicity, whereas downregula

89 he ability of neuroblastoma cells to grow in soft agar and induce tumors in immunodeficient mice.

90 ability of neurospheres to form colonies in soft agar and inhibited their capacity to propagate subc

91 H1299 lung cancer cells inhibited growth in soft agar and invasive colony formation in Matrigel and

92 h the MAPK inhibitor U0216 reduced growth in soft agar and invasive phenotype, whereas the combinatio

93 adhesion, cell invasion, colony formation in soft agar and metastasis in a rat model system.

94 olayers, but developed into colonospheres in soft agar and nodules/tumors in nude mice.

95 ormed monolayers as well as colonospheres in soft agar and nodules/tumors in nude mice.

96 mediated CTSD induction, inhibited growth in soft agar and partially restored tamoxifen sensitivity o

97 Long-term-infected TIVE cells (LTC) grew in soft agar and proliferated under reduced-serum condition

98 ir growth rate, enhanced colony formation in soft agar and promoted tumor formation in nude mice.

99 d cells contained HPV-16, formed colonies in soft agar and rapidly produced tumors in immunodeficient

100 ased cell proliferation, colony formation in soft agar and strikingly diminished cell migration and i

101 mutant mtDNA were tested by growth assay in soft agar and subcutaneous implantation of the cells in

102 breast cancer cells in liquid culture and in soft agar and suppresses the tumorigenicity of MCF-7 cel

103 of tumor cell growth and colony formation in soft agar and the extent of such inhibition appeared to

104 cell lines (R(-)3) formed large colonies in soft agar and the transformation of these T antigen-expr

105 utant failed to exhibit swarming motility on soft agar and this phenotype was rescued by a plasmid-bo

106 ability of tumorigenic rat cells to grow in soft agar and to form tumors.

107 ed anchorage-independent colony formation in soft agar and tumor burden in an allograft model.

108 TGM2 suppressed colony formation in soft agar and tumor formation in a xenograft mouse model

109 to impair RasV12-driven colony formation in soft agar and tumor growth in mice.

110 haracteristics and inhibited their growth in soft agar and tumor growth in vivo.

111 epidermoid cancer cells inhibited growth in soft agar and tumorigenesis in nude mice, and suppressed

112 TPA-mediated anchorage-independent growth in soft agar and tumorigenicity in nude mice.

113 5 in HaCaT cells induced colony formation in soft agar and tumorigenicity in nude mice.

114 ed ability of HeLa cells to form colonies in soft agar and tumors in nude mice.

115 insult formed significantly more colonies in soft agar and were significantly more invasive when grow

116 clones showed dramatically reduced growth in soft agar and when implanted s.c.

117 ed in the transformation of keratinocytes in soft agar and xenograft establishment, thus also implica

118 eration and reduced both colony formation in soft agar and xenograft tumor growth in immunodeficient

119 rmation activity (focus formation, growth in soft agar) and activation of PI3K and MAPK signaling.

120 rongly stimulated cell growth in culture, in soft agar, and accelerated tumor formation in a ligand i

121 oliferation, anchorage-independent growth in soft agar, and enhanced metastatic potential.

122 of transformed cells to form clones, grow in soft agar, and form tumors in severe combined immunodefi

123 igher growth rate, produced more colonies in soft agar, and formed larger tumor upon xenograft inject

124 in monolayer culture, suspension culture, or soft agar, and in vivo in tumor xenografts.

125 ncer drug, invasion, and colony formation in soft agar, and in vivo tumor growth in nude mice.

126 A, increased anchorage-independent growth in soft agar, and increased migration.

127 um, enhanced anchorage-independent growth in soft agar, and increased tumorigenicity in nonobese diab

128 feration, enhanced tumor colony formation in soft agar, and increased xenograft tumor growth in nude

129 h cell proliferation and colony formation in soft agar, and induces apoptosis in cancer cells.

130 l proliferation, reduced colony formation in soft agar, and induction of apoptosis.

131 osis in culture, reduced colony formation in soft agar, and inhibited invasion of melanoma cells.

132 ced apoptosis, abolished colony formation in soft agar, and inhibited localized and metastatic tumor

133 pe, acquired anchorage-independent growth in soft agar, and led to enlarged, disorganized, three-dime

134 dine decreased cell proliferation, growth in soft agar, and methylcytosine content of malignant chola

135 cycle progression, small colony formation in soft agar, and no tumor formation in nude rats.

136 er, HBx stimulated cell migration, growth in soft agar, and spheroid formation.

137 growth rate in culture, colony formation in soft agar, and tumor progression in nude mice.

138 oliferation, anchorage-independent growth in soft agar, and tumorigenesis in severe combined immunode

139 m foci in tissue culture plates, colonies in soft agar, and tumors in nude mice.

140 itro cell proliferation, colony formation in soft agar, and xenograft growth in athymic mice.

141 of cell proliferation, migration, growth in soft agar, apoptosis, senescence, and gene expression re

142 r growth of human pancreatic cancer cells in soft agar as well as in athymic nude mice.

143 helial cell line induced colony formation in soft agar as well as s.c. tumor growth in severe combine

144 Results obtained using a soft agar assay and shRNA Nrf2-transfected cells show th

145 w the anticancer activity of SC66 by using a soft agar assay as well as a mouse xenograft tumor model

146 Transformation in a single layer soft agar assay could be documented as early as 2 to 3 d

147 ndependent cell growth ability was tested by soft agar assay following FA exposure.

148 The results of the soft agar assay indicated that chlorogenic acid suppress

149 The soft agar assay was used as a measure of anchorage indep

150 In a soft agar assay, treatment of HC11-Int3 cells with P50-s

151 anchorage-independent growth as revealed by soft agar assay.

152 Cell transformation was assessed by soft agar assay.

153 nditions and is strongly correlated with the soft-agar assay.

154 ntified and tumorigenesis was assessed using soft agar assays and xenograft analysis of severe combin

155 Soft agar assays revealed that anchorage-independent gro

156 A has transforming activities when tested in soft agar assays, and CoAA is homologous to oncoproteins

157 as evidenced by enhanced colony formation in soft agar assays.

158 s, and blocked contact-independent growth in soft agar assays.

159 is BRCA1 dependent shown by 3D-matrigel and soft agar assays.

160 K knockdown in a xenotransplant model and in soft agar assays.

161 Lin28 was determined by colony formation and soft agar assays.

162 sed the colony formation of human T cells in soft-agar assays.

163 invasive properties, and formed colonies in soft-agar assays.

164 d cell proliferation and colony formation in soft-agar assays.

165 anchorage-independent growth by conducting a soft agar-based short hairpin RNA (shRNA) screen within

166 hibits Src-Y527F-induced colony formation in soft agar, but not Ras-G12V-induced colony formation.

167 nine reduced colony formation of WT cells in soft agar by more than 80% and induced apoptosis under c

168 significant reduction in both monolayer and soft-agar cell growth.

169 y formation, anchorage-independent growth in soft agar, cell migration, and epithelial-mesenchymal tr

170 ates of cell proliferation, clonogenicity in soft agar, changes in the actin cytoskeleton, and induct

171 additional novel DNA methylation targets in soft-agar clones derived from CSC-exposed HBEC; a CSC ge

172 The soft agar clonogenic assay showed that T80/KLF8 cells fo

173 1 in cultured SCLC resulted in inhibition of soft agar clonogenic capacity and induction of apoptosis

174 by CSC coincided with a dramatic increase in soft-agar clonogenicity.

175 Soft agar colonies of CLP-expressing cells had rough bou

176 n, glycolytic flux to lactate, and growth as soft agar colonies or tumors in athymic mice.

177 hat have undergone an EMT form mammospheres, soft agar colonies, and tumors more efficiently.

178 horylated at Ser79/81 (S79/81A) formed fewer soft agar colonies.

179 nhibited but were unable to efficiently form soft-agar colonies or tumor xenografts, suggesting that

180 s apoptosis and suppresses proliferation and soft agar colonization.

181 cts of Bcr-Abl in a solid tumor model and in soft agar colony assays.

182 rming Matrigel invasion, cell proliferation, soft agar colony formation and scratch closure assays.

183 Soft agar colony formation assays and xenograft studies

184 ion in EBER-expressing cells was examined in soft agar colony formation assays.

185 cells and mouse epidermal JB6 cells promoted soft agar colony formation by downregulating Pdcd4 prote

186 or chemical inhibition of Gln uptake blocks soft agar colony formation by Hace1(-/-) MEFs.

187 d with reduced in vitro proliferation rates, soft agar colony formation efficiency, and migration rat

188 lls by TSC2 siRNA, and decreased Myc-induced soft agar colony formation following retroviral transduc

189 growth factor-independent proliferation and soft agar colony formation in MCF10A cells, and hLsm1 in

190 protein function decreased proliferation and soft agar colony formation of ESFT cells.

191 ransition) signaling, transwell invasion and soft agar colony formation, and in vivo promoted lung me

192 ets of miR-7, reduced cell proliferation and soft agar colony formation, and increased apoptosis.

193 rigenic variables including cellular growth, soft agar colony formation, and tumor formation in athym

194 associated with altered cellular phenotypes, soft agar colony formation, and tumorigenesis in nude mi

195 2-yl)-2,5-diphenyltetrazolium bromide assay, soft agar colony formation, as well as tumor growth in a

196 ificantly suppresses cell growth in culture, soft agar colony formation, cell invasion and growth of

197 ion of wild-type full-length TMEFF2 inhibits soft agar colony formation, cellular invasion, and migra

198 sive SK-N-SH neuroblastoma cells resulted in soft agar colony formation, which was inhibited by a GRP

199 ells led to decreased transwell invasion and soft agar colony formation, without affecting proliferat

200 ibited their growth, motility, invasion, and soft agar colony formation.

201 ation, or cell transformation as measured by soft agar colony formation.

202 shRNAs leads to increased proliferation and soft agar colony formation.

203 co-expression of PEA-15 resulted in enhanced soft agar colony growth and increased tumor growth in vi

204 stable suppression of RalB greatly enhanced soft agar colony size and formation frequency.

205 enhancement of cell proliferation, increased soft agar colony size, and elevated ERK1/2 phosphorylati

206 lls and completely blocks their invasive and soft agar colony-forming abilities, but it spares nontra

207 A soft-agar colony assay showed that PLK1 silencing impair

208 SHP2 activity attenuates cell proliferation, soft-agar colony formation and orthotopic GBM growth in

209 but not CRAF WT, transformed NIH3T3 cells in soft-agar colony formation assays, increased kinase acti

210 investigated using mammosphere formation and soft-agar colony formation assays.

211 c cooperate in suppressing proliferation and soft-agar colony formation of neoplastic epithelial ovar

212 in vitro proliferation, migration, invasion, soft-agar colony formation, and survival in the presence

213 ckdown of CDH10 promoted cell proliferation, soft-agar colony formation, cell migration and cell inva

214 imatinib-induced apoptosis and inhibition of soft-agar colony formation.

215 resulted in impaired in vitro migration and soft-agar colony formation.

216 NT-3 promoted motility, migration, invasion, soft-agar colony growth and cytoskeleton restructuring i

217 icantly improved ability to form colonies in soft agar compared with control.

218 P cells had little colony-forming ability in soft agar compared with TonB210/GFP cells.

219 invasion, motility, and colony formation in soft agar compared with vector control-transfected cells

220 Assays on soft-agar confirmed that NsrR is a negative regulator of

221 ced SmgGDS expression form fewer colonies in soft agar, do not proliferate in culture due to an arres

222 These cells when trypsinized and regrown in soft agar, formed colonospheres/organoids that developed

223 melanocytes grew anchorage-independently in soft agar, formed pigmented lesions reminiscent of in si

224 neuploidy, and amplified colony formation in soft agar, further supporting the role of CHFR as a tumo

225 nement of a worm between a glass plate and a soft agar gel is controlled while recording the worm's m

226 x2 was necessary for its ability to increase soft agar growth and in vivo metastasis in an immunocomp

227 n of ZNF322A promoted cell proliferation and soft agar growth by prolonging cell cycle in S phase in

228 from CAN-genes, and experimentally verifying soft agar growth enhancement in response to depletion of

229 r in combination and observed the effects on soft agar growth of HC11 cells overexpressing Int3.

230 f the ITSN1 target, PI3K-C2beta, rescues the soft agar growth of ITSN1-silenced cells demonstrating t

231 owth inhibitory effects of TGF-beta, and the soft agar growth of these cells was increased upon TGF-b

232 Synergistic inhibition of soft agar growth was also observed.

233 d signaling pathways regulate proliferation, soft agar growth, and invasion of human lung adenocarcin

234 essed HBECs toward malignancy as measured by soft agar growth, including EGF-independent growth, but

235 ted resistance to redox stress and increased soft agar growth, while downregulation of SQSTM1 decreas

236 only 5 of 362 random shRNAs (1.4%) enhanced soft agar growth.

237 hibition in SUM44 cells dramatically reduced soft agar growth.

238 d bone matrix-related filaments and enhanced soft agar growth.

239 catalytic domain mutant was unable to induce soft-agar growth indicating that testisin protease activ

240 uding anchorage-independent proliferation in soft agar, growth factor-independent proliferation, and

241 ble knockdown of SLFN2 form more colonies in soft agar, implicating this protein in the regulation of

242 Also IGF1 enhanced colony formation in soft agar in an alpha6beta4-dependent manner.

243 ls but is required for transformed growth in soft agar in vitro and for tumorigenicity in vivo.

244 in human melanoma cells inhibited growth on soft agar in vitro and tumor formation in vivo, suggesti

245 ) cells enhanced proliferation and growth in soft agar in vitro but was insufficient to drive tumorig

246 reased the ability of these cells to grow in soft agar in vitro.

247 e Escherichia coli populations in semisolid (soft) agar in the concentration range C = 0.15-0.5% (w/v

248 ed increased anchorage-independent growth in soft agar, increased S-phase cell cycle distribution, in

249 creased Wnt activity and colony formation in soft agar induced by Apc siRNA treatment, whereas they d

250 f tumor cell anchorage-independent growth in soft agar, induction of the p130Cas cleavage, and anoiki

251 al for malignant transformation according to soft agar, invasion, and tumorigenicity assays, after th

252 he ability of breast cancer cells to grow in soft agar is enhanced following GREB1 transfection.

253 Colony formation in soft agar is the gold-standard assay for cellular transf

254 migration of this organism in tryptone-based soft agar media supplemented with different salts.

255 mutants for those that could migrate through soft agar medium lacking added magnesium.

256 catechin-3-gallate (EGCG) inhibits growth in soft agar of breast cancer cells with Her-2/neu overexpr

257 phosphorylated ERK, and slows the growth in soft agar of HCT116 cells.

258 and obese human donors stimulated growth in soft agar of non-tumorigenic epithelial cells.

259 es individually promoted colony formation in soft agar or collaborated with each other functionally.

260 d RBM3 is downregulated in cells cultured in soft agar or exposed to stress.

261 the ability of C6 cells to form colonies in soft agar or spheres when grown in suspension.

262 pressing populations do not form colonies in soft agar or tumors in mice.

263 strain G27 resulted in decreased motility on soft agar plates, a defect that was complemented by a wi

264 invasion and anchorage-independent growth on soft agar plates.

265 rly flagellated counterparts in spreading on soft-agar plates and through medium-filled channels desp

266 gand-independent proliferation and growth in soft agar relative to cells expressing wt PR-B or phosph

267 Similarly, cell growth in soft agar required the PR DBD but was sensitive to disru

268 ack EP2 expression prevented their growth in soft agar, restored their cytostatic response to TGF-bet

269 ever, including impaired colony formation in soft agar, spheroid formation, and xenograft growth.

270 genesis as measured by growth of colonies in soft agar, spheroids in extracellular matrix and xenogra

271 orage-independent cell transformation assay (soft agar), stable expression of RSK2 in JB6 cells signi

272 iferation, promoted formation of colonies in soft agar, stimulated tumor cell invasion, and induced l

273 opment of compact multicellular spheroids in soft agar suggesting the ability to induce anchorage-ind

274 d prostate cells enabled colony formation in soft agar, suggesting that, in the proper cellular conte

275 -ras allele consistently increased growth in soft agar, suggesting tumor-suppressive properties of th

276 When grown on a soft agar surface in a rich medium, cells of Salmonella

277 , AgmU-mCherry clusters were not observed on soft agar surfaces or when cells were in large groups, c

278 y and formed significantly fewer colonies in soft agar than did cells treated with LipofectAMINE alon

279 g GRP78 and Cripto grow much more rapidly in soft agar than do cells expressing either protein indivi

280 e to growth inhibition by PDK1 inhibitors in soft agar than on tissue culture plastic, consistent wit

281 significantly fewer and smaller colonies in soft agar than their 2D-irradiated counterparts (gamma P

282 93a controls anchorage-independent growth in soft agar through K-Ras, whereas it affects invasive gro

283 In the soft agar transformation and Transwell metastasis assays

284 e, as shown by increased colony formation in soft agar, tumor formation in SCID (severe combined immu

285 invasion and anchorage-independent growth in soft agar, two fundamental biological events associated

286 ersely, silencing RBM3 or culturing cells in soft agar (under conditions that enrich for stem cell-li

287 PTEN into PEL inhibited colony formation in soft agar, verifying the functional dependence of PEL on

288 cant 3-fold increase in clonogenic growth in soft agar was also noted.

289 Growth of transformed cells in soft agar was enhanced by alpha-4 and suppressed by alph

290 Colony formation by RCC 786-O in soft agar was markedly inhibited by DPI.

291 colonies of the NSCLC cell line, H1,299, in soft agar was strongly inhibited by the Abl kinase inhib

292 li in liquid and embedded in glucose-limited soft agar, we evaluate the fit of this model to experime

293 prevents HeLa cells from forming colonies in soft agar, when paxillin is knocked down together with C

294 e cells), and these cells formed colonies in soft agar, whereas BCR-ABL+ NIH 3T3 cells lacking IL-3 r

295 s promotes their ability to form colonies in soft agar, whereas ectopically expressing paxillin in th

296 ll lines to proliferate and form colonies in soft agar, whereas EWSAT1 inhibition had no effect on ot

297 ion through collagen and decreased growth in soft agar, whereas the second was enriched in cells with

298 nduced colony formation of JB6 Cl41 cells in soft agar, which was associated with inhibition of histo

299 o stimulated cancer cell colony formation in soft agar, which was reduced by a chemical inhibitor of

300 igration, invasion, and colony formation, in soft agar with CD66(high) cells.