ライフサイエンスコーパス: glioma cell

1 ivity and feedforward expression of NLGN3 in glioma cells.

2 p-regulates SK1 expression during hypoxia in glioma cells.

3 ss of EGFRvIII-driven Met phosphorylation in glioma cells.

4 c interaction between EGFRwt and EGFRvIII in glioma cells.

5 l cells treated with conditioned medium from glioma cells.

6 tion of the Fas receptor pathway in p53(+/+) glioma cells.

7 ng NK immune surveillance that can eradicate glioma cells.

8 w role for Myc in the proficient division of glioma cells.

9 TR) is a novel mediator of invasion of human glioma cells.

10 H1 into Ras-transformed cells or established glioma cells.

11 maitotoxin-elicited Ca(2+) influx in rat C6 glioma cells.

12 uman colonic T84 epithelial cells or U251-MG glioma cells.

13 nvasion by stimulating amoeboid migration of glioma cells.

14 revent vascular microthrombosis triggered by glioma cells.

15 lC-3 colocalize to the invading processes of glioma cells.

16 emozolomide, and irradiation induced QPRT in glioma cells.

17 l signaling proteins that are deregulated in glioma cells.

18 orescent protein (GFP) expressing human U251 glioma cells.

19 miR-145 in glial tumors and its function in glioma cells.

20 gulation of several synapse-related genes in glioma cells.

21 PD-L1-induced caspase-dependent apoptosis of glioma cells.

22 ntly decreased the migration and invasion of glioma cells.

23 rusions [tumor microtubes (TMs)] extended by glioma cells.

24 s, and fibroblasts, cortical tubers, and U87 glioma cells.

25 toma and UVW/noradrenaline transporter (NAT) glioma cells.

26 alleles are required for D-2HG production in glioma cells.

27 stin and differentiation status of malignant glioma cells.

28 silencing of CTGF decreased the migration of glioma cells.

29 C12 cells, cultured cortical neurons, and C6 glioma cells.

30 am of the PDGFRalpha-PI3K/SHP-2 signaling in glioma cells.

31 ation of prostate cancer, breast cancer, and glioma cells.

32 ibited migration and proliferation of D54-MG glioma cells.

33 at the invasive fronts in PDGF-A-stimulated glioma cells.

34 man MHC-I acts as an EHV-1 entry receptor on glioma cells.

35 nuclear exclusion of TET1 from the nuclei of glioma cells.

36 duces differentiation and autophagy of human glioma cells.

37 n of migration and cell cycle progression in glioma cells.

38 arkin expression was dramatically reduced in glioma cells.

39 come together during HuR multimerization in glioma cells.

40 potentiated the efficacy of MK-2206 against glioma cells.

41 r DNA damage and apoptotic changes in mutant glioma cells.

42 hat mediates HSP70-promoted cell survival in glioma cells.

43 3 dramatically enhanced YKL-40 expression in glioma cells.

44 omide or irradiation increases cell death in glioma cells.

45 developed a model of HuR multimerization in glioma cells.

46 on confer chemosensitization in IDH1-mutated glioma cells.

47 icrotube (TM)-mediated brain colonization by glioma cells.

48 tion for multikinase inhibitor resistance in glioma cells.

49 to promote the survival of murine proneural glioma cells.

50 ed tsA201 cells and in glial cell-derived C6 glioma cells.

51 for the in vitro and in vivo destruction of glioma cells.

52 ion of stem cell markers and self-renewal in glioma cells.

53 ive effects and triggered apoptosis of human glioma cells.

54 lly bound to cervical, lung, esophageal, and glioma cells.

55 matrix stiffness and fibronectin density in glioma cells.

56 (neuroblastoma) and UVW/NAT (NAT-transfected glioma) cells.

57 nd are associated with the transformation of glioma cells along the very aggressive mesenchymal pheno

58 rs compared to normal brain specimens and in glioma cells and glioma stem cells (GSCs) compared to no

59 s of the indirubin family reduce invasion of glioma cells and glioma-initiating cell-enriched neurosp

60 totic) functions that are reflected in human glioma cells and in a genetically defined murine model o

61 iates the prosurvival function of ATF5 in C6 glioma cells and MCF-7 breast cancer cells.

62 al activity of GPC1 expression in both human glioma cells and normal astrocytes in vitro.

63 cells were analyzed in coculture with human glioma cells and normal rat astrocytes: CNS coculture ca

64 sely reflect the oxygenation status of donor glioma cells and patient tumors, and that the exosomal p

65 exchanger NHE5 is abundantly expressed in C6 glioma cells and plays an important part in regulating c

66 In vitro hypoxia experiments with glioma cells and studies with patient materials reveal t

67 aintaining high levels of ATF5 expression in glioma cells and support the conclusion that ATF5 is an

68 e differences in channel activity between C6 glioma cells and tsA201 cells expressing L166Q and A167V

69 t growth of transformed astrocytes and human glioma cells, and Akt3 loss inhibited invasion of transf

70 nant cells, larger pools of undifferentiated glioma cells, and an increase in macrophage over microgl

71 er65, protein synthesis and proliferation in glioma cells, and reduced tumor growth in an orthotopic

72 onstrated that galectin-1-deficient GL26-Cit glioma cells are approximately 3-fold more sensitive to

73 First, malignant glioma cells are stimulated to invade brain through the

74 In-vitro studies on glioma cells are used to compare the efficiency of the C

75 S2, also known as iNOS) originating from the glioma cells as a driving stimulus in the control of mic

76 dings identify human LN-229 and rodent CNS-1 glioma cells as valid systems to study the highly disper

77 relevant mouse model of glioma and find that glioma cells, as they populate the perivascular space of

78 ction in vascular smooth muscle cells and C6 glioma cells, as well as proliferation and migration.

79 This approach permits in situ analysis of glioma cells at the molecular and genomic level as well

80 as a niche supporting the growth of invasive glioma cells away from the primary tumor.

81 myelin (SM) levels, which is markedly low in glioma cells before treatment.

82 These findings suggest that glioma cells benefit from TIGAR expression by (i) improv

83 directs adenovirus to IL13Ralpha2 expressing glioma cells both in vitro and in vivo.

84 eration of chemosensitive and chemoresistant glioma cells but did not display toxicity against non-ca

85 eventually leading to necrotic death of U251 glioma cells but not primary astrocytes.

86 ated in CD133-ve glioma stem cells (GSC) and glioma cells but unmethylated in CD133+ve ones.

87 Fibulin-3 is a protein secreted by glioma cells, but absent in normal brain, that promotes

88 Human malignant glioma cells, but not nonneoplastic astrocytes, expresse

89 roliferative and nonproliferative high-grade glioma cells by programmed necrosis.

90 gs suggest that NKCC1 modulates migration of glioma cells by two distinct mechanisms: (1) through the

91 d anchorage-independent growth, and rendered glioma cells chemosensitive.

92 s, including extensive lipid droplets within glioma cells, collagen deposition in gliosarcoma, and ir

93 estigated how proliferation and dispersal of glioma cells combine to induce increasing degrees of cel

94 demonstrate that neural precursor cell (NPC):glioma cell communication underpins this propensity of g

95 s derived from microglial cells treated with glioma cell-conditioned medium to induce angiogenesis.

96 "mis-trafficking" caused by UCD38B in human glioma cells corresponds to mitochondrial depolarization

97 Conversely, galectin-1-deficient glioma cells could be eradicated by host NK cells before

98 that inhibition of annexin A2 expression in glioma cells could become a new target for glioma therap

99 thesized that disrupting iron homeostasis in glioma cells could block tumor growth, based on an acute

100 of infection was positively correlated with glioma cell death.

101 lacked PD-L1 and were defective in inducing glioma cell death; this effect was reversed on PD-L1 gen

102 er, these findings illustrate a mechanism of glioma cell defense against an incoming infection by oHS

103 Thus, indolent human glioma cells deficient for TF remain viable but permanen

104 U1242MG glioma cells depleted of NPM1 presented with altered sil

105 ry effects were associated with induction of glioma cell differentiation into mature glial cells foll

106 ic for this gBK isoform confirmed that human glioma cells displayed this protein in the cell membrane

107 uced proliferation and increased death of C6 glioma cells, effects that can be partially rescued by o

108 enograft studies show that DcR1 depletion in glioma cells enhances the efficacy of temozolomide.

109 nant progression in glioblastoma multiforme, glioma cells exhibit intrinsic resistance toward many ki

110 Glioma cells expressed both isoforms of pyruvate kinase,

111 Human glioma cells expressing both a caspase-3 sensor as a sur

112 We show that in glioma cells expressing either EGFR wild type or the mut

113 m7GTP to enrich for initiation complexes in glioma cells followed by mass spectrometry-based quantit

114 idence, malignancy, and the ability of mouse glioma cells (GC) to be cultured under stem cell conditi

115 Our work showed that ribavirin inhibits glioma cell growth and migration, and increases cell cyc

116 te of mutant IDH enzymes caused slow-down of glioma cell growth.

117 pathway is a central regulator of glial and glioma cell growth.

118 GC expression also correlated inversely with glioma cells growth.

119 mpact on patient survival, primarily because glioma cells have an inherent propensity to invade into

120 Most therapeutic approaches targeting glioma cells have failed.

121 Therapies aimed at mechanisms intrinsic to glioma cells have translated to only limited success; ef

122 ify a functional role for SOX1 in regulating glioma cell heterogeneity and plasticity, and suggest SO

123 tion of chemoattractant signals toward which glioma cells home.

124 OPCs and highly proliferative Olig2-positive glioma cells identified all the transcripts associated w

125 e study of the in vivo radiation response of glioma cells in a mouse model of proneural glioblastoma.

126 ells efficiently killed HLA-A2(+)H3.3K27M(+) glioma cells in an antigen- and HLA-specific manner.

127 roach has been used to assess the density of glioma cells in murine orthotopic xenografts models and

128 y reduce TM-associated brain colonization by glioma cells in patients.SIGNIFICANCE STATEMENT In this

129 I efficiently inhibited the proliferation of glioma cells in the presence of serum by activating the

130 rest and mitigated the proliferation rate of glioma cells in vitro and in vivo.

131 le of NKCC1 in the invasion of human primary glioma cells in vitro and in vivo.

132 nti-tumoral effects in vivo, despite killing glioma cells in vitro, suggesting a TME-mediated resista

133 glioblastoma cell lines and patient-derived glioma cells in vitro.

134 inhibited the tumorigenicity and invasion of glioma cells in vivo.

135 th factor (EGF), which promotes migration of glioma cells, increased the phosphorylation of NKCC1 thr

136 e peptides colocalizes with GIP within human glioma cells, indicating that GIP might be a potential t

137 gliosis in peritumoral area; and (4) reduces glioma cell infiltration in healthy parenchyma.

138 Collectively, our findings show how glioma cells influence the tumor microenvironment to rec

139 Overexpression of IGFBP3 in glioma cells inhibited cell proliferation in vitro and i

140 Dock180(WT), protein in EGFRvIII-expressing glioma cells inhibited receptor-stimulated cell prolifer

141 seizure etiology, we implanted human-derived glioma cells into severe combined immunodeficient mice.

142 In vivo, we injected the glioma cells into the rodent brain and followed glioma p

143 These findings were corroborated in GL261 glioma cells intracranially transplanted in mice express

144 Glioma cells invade in distinct patterns, possibly deter

145 tatively assess cell volume changes of human glioma cells invading within the brain's extracellular s

146 ic acid (NA), an essential vitamin, inhibits glioma cell invasion in vitro and in vivo.

147 d miR-124 expression significantly inhibited glioma cell invasion in vitro.

148 (matrix metalloproteinase 1) expression and glioma cell invasion in vitro.

149 oliferation, overexpression of GBP1 enhanced glioma cell invasion through MMP1 induction, which requi

150 ts its function from inhibiting to promoting glioma cell invasion.

151 Functionally, miR-491-3p inhibited glioma cell invasion; overexpression of both miR-491-5p

152 egulates Id-1 gene expression and associated glioma cell invasiveness and self-renewal.

153 expression levels positively correlate with glioma cell invasiveness in culture and with histopathol

154 ose that oncogenic activation of EGFRvIII in glioma cells is driven by co-expressed activated EGFR wi

155 ced variant initially described within human glioma cells is the glioma BK (gBK) channel.

156 the contrary, the overexpression of IL-8 in glioma cells lacking DeltaEGFR potently enhanced their t

157 ing of CIC protein to the nucleus in a human glioma cell line expressing IDH1(R132H) and overexpressi

158 sts were found to inhibit proliferation of a glioma cell line in vitro.

159 low EC(50) value (500 nM against the C6 rat glioma cell line), compound 3.1a was selected for furthe

160 FIA axis suppresses tumorigenesis in a human glioma cell line.

161 rase activity and CD133 levels in GSC and in glioma cell line.

162 ll gliomas or robust 53BP1 gene silencing in glioma cell lines (but not 53BP1 heterozygous tumors or

163 ects of VP without light activation on human glioma cell lines (LN229 and SNB19).

164 eutic target in a panel of diverse pediatric glioma cell lines (SF188, KNS42, UW479 and RES186) using

165 y and late endosomes in four different human glioma cell lines after UCD38B treatment, followed by ca

166 ntration of alpha-ketoglutarate substrate in glioma cell lines and could be suppressed by ectopic ove

167 ents and GICs derived from xenografted human glioma cell lines and determined that miR-33a promotes G

168 or this inserted region confirmed that human glioma cell lines and freshly resected surgical tissues

169 In glioma cell lines and glioma-stem-like cells, HDAC6 inhi

170 It replicated well in human glioma cell lines and GSCs, effectively killing cells in

171 iR-491-5p and -3p inhibited proliferation of glioma cell lines and impaired the propagation of glioma

172 Glioma cell lines and low passage primary cultures were

173 prone H-Ras(12V) knock-in mice as well as in glioma cell lines and patient-derived GBM specimens exhi

174 In multiple glioma cell lines and patient-derived glioma stem cells

175 ha-driven glioma EMT, invasion and growth in glioma cell lines and patient-derived glioma stem cells

176 ted glioma EMT, tumor growth and invasion in glioma cell lines and patient-derived GSCs.

177 sed on malignant glioma and are cytotoxic to glioma cell lines and primary GBM explants.

178 We then used human glioma cell lines as model astroglial cells to represent

179 Suppression of BCAT1 in glioma cell lines blocked the excretion of glutamate and

180 ectopic expression of DeltaEGFR in different glioma cell lines caused up to 60-fold increases in the

181 GBMs and glioma cell lines had low levels of NPTX2 transcripts, w

182 GBM and glioma cell lines had low levels of ULK2 transcripts, wh

183 g HLA-G gene expression were investigated in glioma cell lines U251MG, D247MG, and U138MG.

184 es of glioma tissues and in all of the human glioma cell lines we examined.

185 By treating glioma cell lines with the polyclonal N-20 antibody agai

186 th and migration of several human and murine glioma cell lines, as well as human glioblastoma stem-li

187 tured murine (GL261) and human (U251, U87MG) glioma cell lines, increased by approximately 25% when t

188 In this study, we used two glioma cell lines, mouse GL261-EGFP and rat C6/LacZ, as

189 ts target, Topoisomerase 2 alpha (TOP2A), in glioma cell lines, resulting in decreased cell prolifera

190 induces cell death and apoptosis in several glioma cell lines, targets HIF-1alpha-mediated pathways,

191 Functional analysis of ECONEXIN in glioma cell lines, U87 and U251, showed it was dominantl

192 oma line, while infection of the susceptible glioma cell lines, which expressed human MHC-I, were blo

193 esses c-Myc expression and activity in human glioma cell lines.

194 osis in otherwise highly apoptosis-resistant glioma cell lines.

195 n of CD133 promoter in glioma stem cells and glioma cell lines.

196 tial flow promotes cell invasion in multiple glioma cell lines.

197 face of CHO and HEK cells as well as several glioma cell lines.

198 tion of GSCs and their progeny in a panel of glioma cell lines.

199 GRP78 as a target for suppressing high-grade glioma cell lines.

200 face GRP78 to the survival and growth of the glioma cell lines.

201 urface-localized GRP78 in diverse high-grade glioma cell lines.

202 In rat 9L glioma cells loaded with nanoemulsion, the local pH of n

203 ith the maximal levels found in the invading glioma cells located within normal brain tissue; and (ii

204 strated that the unedited miR-376a* promoted glioma cell migration and invasion, while the edited miR

205 n of Akt, Erk1/2, Rac1 and Cdc42 activities, glioma cell migration and survival in vitro and tumor gr

206 In addition miR-145 regulates glioma cell migration by targeting CTGF which downregula

207 ckdown of SGEF expression by shRNA decreases glioma cell migration in vitro and invasion ex vivo.

208 as well as Fn14 overexpression can stimulate glioma cell migration, invasion and resistance to chemot

209 confirm, that the stiffness optimum of U251 glioma cell migration, morphology and F-actin retrograde

210 P-2 C459S mutant inhibited PDGF-A-stimulated glioma cell migration, phosphorylation of Dyn2 and conco

211 ) cotransporter 1 (NKCC1) can play a role in glioma cell migration, the precise mechanism by which th

212 PDGFRalpha activation of Rac1 and Cdc42, and glioma cell migration, thereby establishing a link betwe

213 n of Dock180, stimulates Rac1 activation and glioma cell migration.

214 brogated the inhibitory effect of miR-145 on glioma cell migration.

215 imulated phosphorylation of Akt and Dyn2 and glioma cell migration.

216 Here we analyze rat C6 and patient-derived glioma cell motility in vitro using micropatterned linea

217 it did the growth of differentiated non-stem glioma cells (NSGCs).

218 ECFNs; optimum approximately 1 kPa) and U251 glioma cells (optimum approximately 100 kPa).

219 efficient replication and oncolysis in MO59J gliomas cells; other gliomas tested required the entire

220 LuIII selectively infected glioma cells over normal glial cells in vitro.

221 Glioma cells overexpressing DeltaEGFR showed constitutiv

222 Chemical screening of patient-derived glioma cells (PDCs) shows that therapeutic response is a

223 f therapy on these tumors has focused on the glioma cells per se.

224 ss-associated NKG2D ligands on TMZ-resistant glioma cells, potentially rendering them vulnerable to g

225 In contrast, silencing expression of MCSF in glioma cells prevented tube formation of human umbilical

226 PCL nanoparticles could efficiently suppress glioma cell proliferation and induce cell apoptosis in v

227 r, these results suggested netrin-1 promotes glioma cell proliferation by activating NF-kappaB signal

228 stant tumor cell conditioned media increased glioma cell proliferation compared with media from macro

229 regulation of GBP1 expression did not affect glioma cell proliferation, overexpression of GBP1 enhanc

230 ncanonical Wnt ligand, was also required for glioma cell proliferation.

231 uction had no effect on in vitro IDH1 mutant glioma cell proliferation.

232 Glioma cells recruit and exploit microglia (the resident

233 endothelial cell motility and association to glioma cells, reduced endothelial cell sprouting, and in

234 molecular consequences of NLGN3 secretion in glioma cells remain unknown.

235 as a way to deliver cytotoxic agents to the glioma cells remaining after surgical resection while sp

236 ectively, our results suggest that stem-like glioma cells reprogram their metabolism to self-renew an

237 Stem-like glioma cells reside within a perivascular niche and disp

238 ype; (ii) Fn14 expression can be detected in glioma cells residing in both the tumor core and invasiv

239 Surprisingly, knockdown of NKCC1 in glioma cells resulted in the formation of significantly

240 hat primary resistance to EGFR inhibition in glioma cells results from a rapid compensatory response

241 arison to 2-dimensional bulk cultures of U87 glioma cells revealed 3 groups of genes essential for th

242 In vitro uptake assays in mouse DBT gliomas cells revealed that (S)-[(18)F]FAMPe enters cell

243 -mediated gliovascular coupling is lost, and glioma cells seize control over the regulation of vascul

244 therefore be a valuable strategy to enhance glioma cell sensitivity toward spontaneously occurring o

245 n of NP-DOX efficacy using drug-resistant C6 glioma cells showed a 300% increase in cellular internal

246 Notably, parkin-expressing glioma cells showed a reduction in levels of cyclin D1,

247 In BDNF-deficient mice (bdnftm1Jae/J) and in glioma cells silenced for TrkB receptor expression, olea

248 omoting inhibition of adenylyl cyclase in C6 glioma cells stably expressing the P2Y14-R was shifted t

249 e examined the roles of miR-124 and SNAI2 in glioma cell stem-like traits.

250 el and targetable molecular circuit by which glioma cell stemness and tumor-propagating capacity are

251 in part by altering mevalonate metabolism in glioma cells, suggesting a therapeutic strategy in this

252 Here we show that malignant glioma cells suppress NK immune surveillance by overexpr

253 g 2 (ID2), which we found to be required for glioma cell survival.

254 significant impact against the infiltrative glioma cells that are a major source of recurrence.

255 In contrast, neither causes changes in glioma cells that have higher cholesterol content.

256 tern blot analysis, we identified that human glioma cells that were exposed to VP without light activ

257 hin (PTN)-containing complex, which attracts glioma cells through ROCK/Rho activation.

258 entry oHSVs are preferentially taken up into glioma cells through the endosomal pathway rather than v

259 LX5-WNT5A axis governs the diffuse spread of glioma cells throughout the brain parenchyma, contributi

260 r the response of three different subsets of glioma cells to a clinically relevant chemotherapeutic a

261 F-2 kinase could modulate the sensitivity of glioma cells to Akt inhibition.

262 aggressive growth and the ability of single glioma cells to disperse throughout the brain.

263 Ms have been associated with the capacity of glioma cells to effectively invade the brain and prolife

264 Olig2 deletion further sensitizes glioma cells to EGFR inhibitors and extends the lifespan

265 We engineered glioma cells to express this reporter and showed that br

266 tumors or partial gene knockdown) sensitizes glioma cells to ionizing radiation (IR), both in vitro a

267 ully repair the damaged DNA upon exposure of glioma cells to IR with a consequent prolonged cell-cycl

268 smallest achievable cell volume and require glioma cells to release all free unbound cytoplasmic wat

269 We also demonstrate that exposing glioma cells to the HuR inhibitor tanshinone group compo

270 teracting Ser/Thr kinase 1 (MNK1) sensitizes glioma cells to the mTORC1 inhibitor rapamycin through a

271 pathway extensively sensitized IDH1-mutated glioma cells to TMZ.

272 The underlying molecular mechanism used by glioma cells to transform microglia into a tumor-support

273 and consequently restores the sensitivity of glioma cells to tyrosine kinase inhibitors in vivo in pr

274 inhibitor protein PME-1 drives resistance of glioma cells to various multikinase inhibitors.

275 ic antidepressant treatment of rats or of C6 glioma cells, tracks with the delayed onset of therapeut

276 actor (CTGF) as a novel target of miR-145 in glioma cells; transfection of the cells with this miRNA

277 These effects were also observed in glioma cells treated with the Aurora-A inhibitor TC-A231

278 Hence, invading glioma cells use hydrodynamic volume changes to meet the

279 Treatments of glioma cells using the PKA inhibitors H-89 and KT5720, o

280 NDI/2DG-induced death of glioma cells was partly prevented by lysosomal cathepsin

281 multiforme (GBM) cell line, highly malignant glioma cells, was first injected into 5-week-old athymic

282 Glioma cells were evaluated for CXCR4 expression and pol

283 Finally, mice bearing subcutaneous C6 glioma cells were injected intravenously with (18)F-FDG

284 In contrast, differentiated glioma cells were unaffected by the targeting of purine

285 rom neonatal rats and cultures of the C6 rat glioma cells were used as models.

286 Sustained treatment of C6 glioma cells, which lack 5-hydroxytryptamine transporter

287 ULK2 also inhibited the growth of glioma cells, which required autophagy induction as kina

288 significant radiosensitization of malignant glioma cells, which will guide the development of combin

289 Here, we demonstrate that human glioma cells whose migration is guided by bradykinin gen

290 Infection of glioma cells with Delta68H-6 and 1716-6 induced autophag

291 Transfection of glioma cells with miR-145 mimic or transduction with a l

292 Treatment of the U251 glioma cells with NA in vitro results in reduced invasio

293 Glioma cells with one or two TMs were mainly responsible

294 his adaptive axis at multiple nodes rendered glioma cells with primary resistance sensitive to EGFR i

295 Glioma cells with stem cell traits are thought to be res

296 role in balancing the division properties of glioma cells with stemness properties.

297 ctive activity (EC50 = 0.26-1.8 muM) against glioma cells with the IDH1 R132H mutation.

298 a relatively quiescent subset of endogenous glioma cells, with properties similar to those proposed

299 llular Ca(2+) concentration in 1321N1 and C6 glioma cells without altering TRAP-6 and carbachol Ca(2+

300 owth of IDH1-mutant--but not IDH1-wild-type--glioma cells without appreciable changes in genome-wide