ライフサイエンスコーパス: pancreatic cancer cell

1 hagy was induced by penfluridol treatment in pancreatic cancer cells.

2 antimetastatic and cytotoxic to human L3.6pl pancreatic cancer cells.

3 iggers JNK-cJUN-dependent apoptosis in human pancreatic cancer cells.

4 el target for inhibition of Shh signaling in pancreatic cancer cells.

5 juvant treatment to sensitize chemoresistant pancreatic cancer cells.

6 iogenesis, transcription factor EB (TFEB) in pancreatic cancer cells.

7 observed in vitro against AsPc-1 and BxPc-3 pancreatic cancer cells.

8 by promoting its subsequent toxic effects in pancreatic cancer cells.

9 ion experiments in human cervix, breast, and pancreatic cancer cells.

10 systematically evaluated and then applied to pancreatic cancer cells.

11 ndent and independent proliferation of human pancreatic cancer cells.

12 hibiting IRP1 and represses proliferation in pancreatic cancer cells.

13 maximally block the tumorigenic potential of pancreatic cancer cells.

14 A-7/IL-24 protein and results in toxicity in pancreatic cancer cells.

15 tin, represses tumorigenesis in K-Ras mutant pancreatic cancer cells.

16 f cell adhesion, motility, and metastasis of pancreatic cancer cells.

17 ver, gemcitabine can promote the stemness of pancreatic cancer cells.

18 xpression and inhibits cell proliferation of pancreatic cancer cells.

19 scription factors (TFs) Sp1, Sp3, and Sp4 in pancreatic cancer cells.

20 CDH17 RGD effects were also active in pancreatic cancer cells.

21 1 and caveolin-1 and their colocalization in pancreatic cancer cells.

22 rmidine (1 muM) in DFMO-treated L3.6pl human pancreatic cancer cells.

23 DNA damage signaling and radioresistance in pancreatic cancer cells.

24 tein kinase (MAPK) is highly up-regulated in pancreatic cancer cells.

25 Chinese hamster ovary (CHO) and L3.6pl human pancreatic cancer cells.

26 ies to the unmodified drug in colorectal and pancreatic cancer cells.

27 fter beta-lapachone treatment of NQO1+ human pancreatic cancer cells.

28 downstream pathways controlling survival of pancreatic cancer cells.

29 as degradation in breast, colon, glioma, and pancreatic cancer cells.

30 y in gemcitabine-sensitive versus -resistant pancreatic cancer cells.

31 related apoptosis-inducing ligand (TRAIL) in pancreatic cancer cells.

32 d the proliferation of human lung, colon and pancreatic cancer cells.

33 accumulation of tumor-suppressor proteins in pancreatic cancer cells.

34 tion of RNF43 mutant but not RNF43-wild-type pancreatic cancer cells.

35 ate migration and invasion, respectively, in pancreatic cancer cells.

36 gate the origins and evolution of metastatic pancreatic cancer cells.

37 block proliferation and induce apoptosis of pancreatic cancer cells.

38 ins; we investigated a new class of SINEs in pancreatic cancer cells.

39 zed to decrease clonogenic survival in human pancreatic cancer cells.

40 nctional roles of overexpression of EPAC1 in pancreatic cancer cells.

41 glycolytic ATP in fuelling the PMCA in human pancreatic cancer cells.

42 fficient and required for MUC1 expression in pancreatic cancer cells.

43 gic potential of pancreatic inflammation and pancreatic cancer cells.

44 gression, metastasis, and chemoresistance of pancreatic cancer cells.

45 regulates PDGFA expression and secretion in pancreatic cancer cells.

46 and thus phenocopied the effects of Snail in pancreatic cancer cells.

47 induced by novel inhibitors of TR1 in human pancreatic cancer cells.

48 the differential migration and scattering of pancreatic cancer cells.

49 n IMS-RP was established in human breast and pancreatic cancer cells.

50 ve cell migration, and CSC function in human pancreatic cancer cells.

51 1 expression enhances glycolytic activity in pancreatic cancer cells.

52 ovel selectin ligand expressed by metastatic pancreatic cancer cells.

53 sion was significantly increased in PSCs and pancreatic cancer cells.

54 and migration of Snail- and Slug-expressing pancreatic cancer cells.

55 - and time-dependent up-regulation of SHH in pancreatic cancer cells.

56 tein synthesis, and cell size in ovarian and pancreatic cancer cells.

57 ants in human and genetically defined murine pancreatic cancer cells.

58 NFkappaB and apoptotic signaling pathways in pancreatic cancer cells.

59 d enhanced apoptosis and chemosensitivity of pancreatic cancer cells.

60 val in response to IR exposure of breast and pancreatic cancer cells.

61 id analog BA145 on cell cycle progression in pancreatic cancer cells.

62 d 2, which activate insulin/IGF receptors on pancreatic cancer cells.

63 a gemcitabine-resistance mechanism found in pancreatic cancer cells.

64 ated Mcl-1, and up-regulated Bim and Puma in pancreatic cancer cells.

65 dent and cap-independent mRNA translation in pancreatic cancer cells.

66 species (ROS) in Panc1, MiaPaCa2, and L3.6pL pancreatic cancer cells.

67 ctivation approach, it is possible to detect pancreatic cancer cells accurately and specifically impa

68 E-selectin-mediated rolling facilitates pancreatic cancer cell adhesion to hyaluronic acid.

69 in phosphorylation and signaling pathways in pancreatic cancer cells after gemcitabine treatment usin

70 therapeutic target, clearly interfering with pancreatic cancer cells' aggressiveness.

71 esion assays using MUC16 immunopurified from pancreatic cancer cells and found that it efficiently bi

72 escent properties - to inhibit the growth of pancreatic cancer cells and further investigated the mol

73 We demonstrated that pancreatic cancer cells and glioblastoma cells were spec

74 and of the sigma-2 receptor, SV119, binds to pancreatic cancer cells and induces target cell death in

75 significant decrease in the proliferation of pancreatic cancer cells and induction of apoptosis.

76 KIAA1199 is specifically expressed in human pancreatic cancer cells and pancreatic intraepithelial n

77 clax and minocycline was highly cytotoxic to pancreatic cancer cells and safely efficacious in vivo.

78 study, we investigated whether exosomes from pancreatic cancer cells and serum from patients with pan

79 se epsilon (IKBKE) and NF-kappaB activity in pancreatic cancer cells and show that this activity is a

80 nstrate the interaction of tRNA with MEK2 in pancreatic cancer cells and suggest that tRNA may impact

81 oclax induced growth arrest and apoptosis in pancreatic cancer cells and synergized with minocycline

82 CHD5 expression with DDR activation in human pancreatic cancer cells and the association of CHD5 expr

83 be recent studies on the interaction between pancreatic cancer cells and tumor stroma, and potential

84 scription factors (TFs) Sp1, Sp3, and Sp4 in pancreatic cancer cells and tumors, and this was accompa

85 ne sets related to cell cycle progression in pancreatic cancer cells and tumors.

86 l pancreas cells, as well as in KRAS mutated pancreatic cancer cells and was essential for ER homoeos

87 IFN-gamma activated the p38-MAPK pathway in pancreatic cancer cells, and both played an important ro

88 on complex of the translational machinery in pancreatic cancer cells, and culminates in mda-7/IL-24-m

89 layer in-vitro cytotoxicity experiments with pancreatic cancer cells, and simulating the effects of s

90 guanides to reduce viability in melanoma and pancreatic cancer cells, and to extend C. elegans lifesp

91 We further demonstrated that invasive pancreatic cancer cells are more deformable than normal

92 Because pancreatic cancer cells are sensitive to H2O2 generated

93 ctivity and the molecular targets of CCN1 in pancreatic cancer cells are unknown.

94 lencing of YAP in Sk-Hep1, SNU182, HepG2, or pancreatic cancer cells, as well as incubation with thio

95 ng MUC16 expression by RNAi markedly reduces pancreatic cancer cell binding to E- and L-selectin unde

96 neurotensin receptor 1 (NTR)-overexpressing pancreatic cancer cells, both in vitro and in vivo.

97 dant on the surface and vicinity of cultured pancreatic cancer cells but absent from normal pancreas

98 ited proliferation and promoted apoptosis of pancreatic cancer cells, but did not affect human pancre

99 acropinocytosis can be a nutrient source for pancreatic cancer cells, but it is not fully understood

100 ed in some cells, e.g. C3H10T1/2, MC3T3, and pancreatic cancer cells, but not all cells.

101 n catabolism and macropinocytosis in situ by pancreatic cancer cells, but not by adjacent, non-cancer

102 the effect of erlotinib in ErbB3-expressing pancreatic cancer cells by directly suppressing ErbB3 ac

103 IL8 and TNF, and promotes cell migration in pancreatic cancer cells by enhancing Ca(2+) responses.

104 t with TRAIL-R2 initially were identified in pancreatic cancer cells by immunoprecipitation, mass spe

105 a strategy to suppress the KRAS oncogene in pancreatic cancer cells by means of small molecules bind

106 ts as a modulator of the hypoxic response in pancreatic cancer cells by regulating the expression/sta

107 roblasts directly support chemoresistance of pancreatic cancer cells by secreting insulin-like growth

108 ux through the sialic acid pathway in SW1990 pancreatic cancer cells by using a colabeling strategy w

109 and tumorigenicity of the side population of pancreatic cancer cells (cancer stem cells) in a xenogra

110 cription is activated up to 30-fold in human pancreatic cancer cells compared to normal pancreatic du

111 pha (PPP2R2A), a PP2A regulatory subunit, in pancreatic cancer cells compared with normal pancreatic

112 onstrating an expanded function of HOTAIR in pancreatic cancer cells compared with other cancer cell

113 Upon exposure of TAS to pancreatic cancer cell-conditioned media, we documented

114 Taken together, these data suggest that pancreatic cancer cells consume extracellular protein, i

115 Moreover, this association in pancreatic cancer cells correlated with functional cross

116 hRNA-mediated silencing had little effect on pancreatic cancer cells cultured in high glucose, but le

117 Mice injected with metastatic human L3.6pl pancreatic cancer cells demonstrated significant reducti

118 UN-KC-6141 cells (pancreatic cancer cells derived from Pdx1-Cre;LSL-Kras(G

119 rmore, the culture medium from PAR-2-treated pancreatic cancer cells enhanced human umbilical vein en

120 riptolide, HIF-1alpha protein accumulated in pancreatic cancer cells even though hypoxic response was

121 ocarcinoma signaling pathway in MYB-silenced pancreatic cancer cells exhibiting suppression of EGFR a

122 nograft model established by implantation of pancreatic cancer cells expressing firefly luciferase.

123 criptome of MYB-overexpressing and -silenced pancreatic cancer cells, followed by in silico pathway a

124 f Usp9x enhances transformation and protects pancreatic cancer cells from anoikis.

125 We isolated pancreatic cancer cells from multiple independent tumor

126 hypoxia increases the "glycolytic" switch of pancreatic cancer cells from oxydative phosphorylation t

127 pecific knockdown of PKD1 in PKD2-expressing pancreatic cancer cells further enhanced the invasive pr

128 eracts with the wild-type and mutant MEK2 in pancreatic cancer cells; furthermore, the MEK2 inhibitor

129 ater emerged as the most potent inhibitor of pancreatic cancer cells grown as tumors in animals.

130 ference also induced apoptosis and decreased pancreatic cancer cell growth and invasion, indicating t

131 y showed that extracellular lumican inhibits pancreatic cancer cell growth and is associated with pro

132 ition of PLAC8 expression strongly inhibited pancreatic cancer cell growth by attenuating cell-cycle

133 preferentially inhibits glioma, breast, and pancreatic cancer cell growth, with IC50 values of 6-19

134 te for the first time that FSTL-1 suppresses pancreatic cancer cell growth.

135 We observed that TRAIL-resistant pancreatic cancer cells had higher levels of HOTAIR expr

136 f HOTAIR expression, whereas TRAIL-sensitive pancreatic cancer cells had lower HOTAIR levels.

137 ere we report a systematic definition of how pancreatic cancer cells harboring mutant p53 respond to

138 Furthermore, we demonstrate that pancreatic cancer cells have a specific motility respons

139 itro proliferation caused by GLS inhibition, pancreatic cancer cells have adaptive metabolic networks

140 In one case, reprogrammed human pancreatic cancer cells have been shown to recapitulate

141 Pancreatic cancer cells have extensively reprogrammed me

142 In human pancreatic cancer cells, IER3 expression efficiently sus

143 ted cell viability, and induced apoptosis of pancreatic cancer cells in a concentration and incubatio

144 FATc1 drives EMT reprogramming and maintains pancreatic cancer cells in a stem cell-like state throug

145 r new functions under the control of GSK3 in pancreatic cancer cells in addition to providing key ins

146 ffect of FASN inhibitors with gemcitabine in pancreatic cancer cells in culture and orthotopic implan

147 MT1-MMP)- and ERK1/2-dependent scattering of pancreatic cancer cells in three-dimensional type I coll

148 Overexpression of CLPTM1L enhanced growth of pancreatic cancer cells in vitro (1.3-1.5-fold; PDAY7 <

149 55A/T159A/S280A) suppressed tumorigenesis in pancreatic cancer cells in vitro and in vivo to a greate

150 and promoted invasiveness and metastasis of pancreatic cancer cells in vitro and in vivo.

151 es as an important source of amino acids for pancreatic cancer cells in vivo.

152 de and haloperidol) reduced proliferation of pancreatic cancer cells, induced endoplasmic reticulum s

153 ated LDH-A short hairpin RNA knockdown Pan02 pancreatic cancer cells injected in C57BL/6 mice develop

154 rthotopic implantation of PR55alpha-depleted pancreatic cancer cells into nude mice resulted in marke

155 time PKD1 and 2 isoform-selective effects on pancreatic cancer cell invasion and angiogenesis, in vit

156 ce or by small molecule inhibitors prevented pancreatic cancer cell invasion in vitro and metastasis

157 e shows that HOTAIR has an important role in pancreatic cancer cell invasion, as reported in other ca

158 Pancreatic cancer cell invasion, metastasis, and angioge

159 We report that both kinases control pancreatic cancer cell invasive properties in an isoform

160 formation of non-adherent tumour spheres by pancreatic cancer cells is associated with upregulation

161 d that caveolin-1-enhanced aggressiveness of pancreatic cancer cells is dependent on the presence of

162 SHh regulation by CCN1 in pancreatic cancer cells is mediated through the active N

163 Moreover, pancreatic cancer cells isolated from the tumors of GPC1

164 5 depletion and low CHD5 expression in human pancreatic cancer cells lead to increased H2AX-Ser139 an

165 rn, influences proliferation and invasion of pancreatic cancer cells leading to higher tumor burden i

166 rthermore, PARP-1 mutant overexpression in a pancreatic cancer cell line (MIA PaCa-2) increased sensi

167 examined by methylation-specific PCR using a pancreatic cancer cell line (Panc-1).

168 normal PZ-HPV-7 prostate cells) and for the pancreatic cancer cell line BxPC-3 (but not for normal S

169 potent antitumor activity against the human pancreatic cancer cell line MIA PaCa-2 with growth inhib

170 BA145 induced robust autophagy in pancreatic cancer cell line PANC-1 and exhibited cell pr

171 As a proof-of-principle, the pancreatic cancer cell line Panc-1 was investigated for

172 salivary biomarkers by implanting the mouse pancreatic cancer cell line Panc02 into the pancreas of

173 stance, we generated a gemcitabine-resistant pancreatic cancer cell line using stepwise selection and

174 schistosome parasitic flatworm larvae and a pancreatic cancer cell line were deconvoluted in a subtr

175 itivity responses in a poorly differentiated pancreatic cancer cell line, MIA PaCa-2.

176 Cells of a pancreatic cancer cell line, Panc-1, up-regulate MMP act

177 ine pancreatic cancer model, using the human pancreatic cancer cell line, Suit-2.

178 e 10-fold more potent against the MIA PaCa-2 pancreatic cancer cell line, with IC50 values of ~10 nM.

179 was overexpressed ectopically in a MYB-null pancreatic cancer cell line.

180 Pancreatic cancer cell lines (PsPC-1 and BXPC-3) and a n

181 Additionally, six pancreatic cancer cell lines and a spleen subcapsular in

182 interference or pharmacologic inhibitors in pancreatic cancer cell lines and analyses of xenograft t

183 inhibits maturation of the microRNA let-7 in pancreatic cancer cell lines and increases their prolife

184 ed the effects of SINE analogs in a panel of pancreatic cancer cell lines and nontransformed human pa

185 using genomic DNA from exosomes derived from pancreatic cancer cell lines and serum from patients wit

186 ressed the growth of a subset of KRAS-mutant pancreatic cancer cell lines and that concurrent phospha

187 ted directly with high cavin-1 expression in pancreatic cancer cell lines and tumor specimens (P < 0.

188 The system was validated in three model pancreatic cancer cell lines before being applied to pri

189 Pancreatic cancer cell lines derived from these mice exp

190 ell viability and clonogenic survival in all pancreatic cancer cell lines examined, but not in nontum

191 over 50% when tested against a panel of four pancreatic cancer cell lines in vitro.

192 STAT3 transcription factor at Tyr705 in the pancreatic cancer cell lines PANC-1 and MIAPaCa-2 as wel

193 e-expression of SMARCA4 in SMARCA4-deficient pancreatic cancer cell lines reduced cell growth and pro

194 RNAi-mediated depletion of PR55alpha in pancreatic cancer cell lines resulted in diminished phos

195 ited sub-micromolar IC(50) values in all the pancreatic cancer cell lines tested using MTT and colony

196 cement of cell kill in a panel of breast and pancreatic cancer cell lines that are insensitive to the

197 ility, we analyzed the proteomes of 10 human pancreatic cancer cell lines to a depth of >8,700 quanti

198 A panel of 39 pancreatic cancer cell lines was tested for Wnt dependen

199 Pancreatic cancer cell lines were genetically manipulate

200 , flow cytometry analysis was performed in 3 pancreatic cancer cell lines with different expression l

201 metry assays in BXPC-3 and PANC-1 cells, two pancreatic cancer cell lines with high and low TF expres

202 We studied CD44v6 signaling in several pancreatic cancer cell lines, and its role in tumor grow

203 ombinant immunotoxin) is highly cytotoxic to pancreatic cancer cell lines, but with limited activity

204 beit attenuated, responses are seen in other pancreatic cancer cell lines, BxPC-3 and AsPC-1.

205 Adrenomedullin was up-regulated in pancreatic cancer cell lines, in which supernatants redu

206 eal was conducted in a cohort of low-passage pancreatic cancer cell lines, primary patient-derived xe

207 In Ras mutant pancreatic cancer cell lines, the phosphorylation and di

208 Using mouse models and human pancreatic cancer cell lines, we investigated whether pr

209 ancreatic adenocarcinoma patients and 71% of pancreatic cancer cell lines.

210 fect of PDEdelta knockdown in a set of human pancreatic cancer cell lines.

211 d photodynamic therapy on a variety of human pancreatic cancer cell lines.

212 tive (BxPC3) and -negative (MIAPaCa-2) human pancreatic cancer cell lines.

213 s of loss or gain of S100A4 were examined in pancreatic cancer cell lines.

214 identified in innately gemcitabine-resistant pancreatic cancer cell lines.

215 n PanINs, pancreatic cancers, and in several pancreatic cancer cell lines.

216 l cycle progression and apoptosis in several pancreatic cancer cell lines.

217 T5C) as favoring the mesenchymal identity in pancreatic cancer cell lines.

218 of the interaction between tRNA and MEK2 in pancreatic cancer cell lines.

219 ent inhibitor of brain, breast, ovarian, and pancreatic cancer cell lines.

220 ted from chronic pancreatitis tissues and in pancreatic cancer cells metastasized to the liver.

221 s show that EPAC1 plays an important role in pancreatic cancer cell migration and invasion, and thus

222 ght be necessary for CCN1-dependent in vitro pancreatic cancer cell migration and tumorigenicity of t

223 knockdown of Cad-11 in cancer cells reduced pancreatic cancer cell migration.

224 Using ovarian and pancreatic cancer cell models with ST6Gal-I overexpressi

225 d the contribution made by HGF signalling to pancreatic cancer cell motility remain to be elucidated.

226 es, the pair did significantly colocalize in pancreatic cancer cells, multicellular tumor spheroids,

227 inhibits two major pro-oncogenic pathways in pancreatic cancer cells, namely mammalian target of rapa

228 PARI upregulation in pancreatic cancer cells or avian DT40 cells conferred DN

229 The in vitro therapeutic studies in pancreatic cancer cells (PANC-1 and CAPAN-1) demonstrate

230 an cancer cells of epithelial origin such as pancreatic cancer cells (PANC-1) was covalently attached

231 Moreover, miR-10b overexpression accelerated pancreatic cancer cell (PCC) proliferation and tumor gro

232 Here, we found that proliferating pancreatic cancer cells (PCCs) from human PDAC patients

233 Here, we report that pancreatic cancer cell phenotype was altered in response

234 tion factor NFATc1 as a central regulator of pancreatic cancer cell plasticity.

235 osphorylate AKT Furthermore, USP49 inhibited pancreatic cancer cell proliferation and enhanced cellul

236 hat recently developed by our group, reduced pancreatic cancer cell proliferation and Gli-1 activatio

237 ied from Spirulina, effectively inhibits the pancreatic cancer cell proliferation in vitro and xenogr

238 ule inhibitor of Hhat can successfully block pancreatic cancer cell proliferation.

239 nd that CUL7/Fbxw8 ubiquitin ligase promotes pancreatic cancer cell proliferation.

240 Consistent with this, FSTL-1 inhibited pancreatic cancer cell proliferation.

241 the local control of pancreatic cancer, but pancreatic cancer cell radioresistance remains a serious

242 Inhibition of DRD2 in pancreatic cancer cells reduced proliferation and migrat

243 al, and CRISPR-mediated knockout of GCNT3 in pancreatic cancer cells reduced proliferation and sphero

244 nd that NRP2 depletion in human prostate and pancreatic cancer cells resulted in the accumulation of

245 lar signal-regulated kinase 1/2 signaling in pancreatic cancer cells reverses the translational block

246 amine the role of Slug (Snai2) in regulating pancreatic cancer cell scattering in three-dimensional t

247 Our results show that pancreatic cancer cells secrete high levels of sAPPalpha

248 y reducing the membrane level of Frizzled in pancreatic cancer cells, serving as a negative feedback

249 Both breast and pancreatic cancer cells showed higher basal apoptotic ra

250 Cell viability studies in pancreatic cancer cells showed that carbamate functional

251 and STAT3 These results demonstrate that in pancreatic cancer cells, STAT3 is an Sp-regulated gene t

252 lysis of mRNA time course data from lung and pancreatic cancer cells stimulated to undergo TGF-beta1-

253 Expression of WNT2 in pancreatic cancer cells suppresses anoikis, enhances anc

254 re we sought to determine the role of APP in pancreatic cancer cell survival and proliferation.

255 CDF decreased pancreatic cancer cell survival, clonogenicity, formatio

256 f proteins is a process required for hypoxic pancreatic cancer cell survival.

257 ed more liver metastases after injections of pancreatic cancer cells than mice without increased leve

258 ntrast, HOTAIR knockdown in Panc1 and L3.6pL pancreatic cancer cells that overexpress this lincRNA de

259 lation of embryonal, melanoma, prostate, and pancreatic cancer cells that possess stem-like character

260 d by flow cytometry of MIA PaCa-2 and PANC-1 pancreatic cancer cells that possess the properties of C

261 We then used microraft arrays to select pancreatic cancer cells that proliferate in spite of cyt

262 n-regulate the expression of this protein in pancreatic cancer cells, thereby causing cell death.

263 ctor vascular endothelial growth factor C in pancreatic cancer cells through an NF-kappaB-independent

264 nd S100A4 promotes tumorigenic phenotypes of pancreatic cancer cells through the Src-FAK mediated dua

265 assess agonist properties, and in AR42J rat pancreatic cancer cells to determine receptor binding ch

266 ntial targets and strategies for sensitizing pancreatic cancer cells to gemcitabine.

267 ras-driven mouse pancreatic tumors and human pancreatic cancer cells to identify the novel core mucin

268 inhibited cullin neddylation and sensitized pancreatic cancer cells to ionizing radiation in vitro w

269 MMAE sensitized colorectal and pancreatic cancer cells to IR in a schedule- and dose-de

270 RAS-E2F1-ILK-hnRNPA1 regulatory loop enables pancreatic cancer cells to promote oncogenic KRAS signal

271 ivation by its agonist clofibrate sensitizes pancreatic cancer cells to radiation by modulating cell

272 ate-mediated PPARalpha activation sensitizes pancreatic cancer cells to radiation through the Wnt/bet

273 of an ILK-KRAS regulatory loop that enables pancreatic cancer cells to regulate KRAS expression.

274 igh HOTAIR levels increase the resistance of pancreatic cancer cells to TRAIL-induced apoptosis via e

275 We also highlight the high dependence of pancreatic cancer cells upon cholesterol uptake, and ide

276 on of changes in abundance of metabolites in pancreatic cancer cells upon treatment with 17-DMAG.

277 sing CD44 protein levels in human breast and pancreatic cancer cells via lysosomal degradation of CD4

278 ly regulates growth and genomic stability of pancreatic cancer cells via targeting complex gene netwo

279 n of TLR4 by IFN-gamma in BxPC-3 and CFPAC-1 pancreatic cancer cells was augmented by LPS, resulting

280 formation of liver metastases from injected pancreatic cancer cells was not observed in TIMP1 or CD6

281 Using pancreatic cancer cells, we demonstrate that inhibition

282 Using a siRNA screen in human pancreatic cancer cells, we identified the CHD5 tumor su

283 mice; the effects of conditioned media from pancreatic cancer cells were reduced by small hairpin RN

284 ate buffer saline spiked with low numbers of pancreatic cancer cells were successfully detected by sp

285 I (PARPBP), is overexpressed specifically in pancreatic cancer cells where it is an appealing candida

286 port that exDNA is present on the surface of pancreatic cancer cells where it is critical for driving

287 to the inner face of the plasma membrane in pancreatic cancer cells, where it interacts with specifi

288 ocalization of TFEB is unveiled in fully fed pancreatic cancer cells, whereas a reduction in TFEB exp

289 s and inhibits proliferation and invasion in pancreatic cancer cells, whereas silencing of FOXL1 by s

290 ion inhibited the invasion and metastasis of pancreatic cancer cells, which could not be restored by

291 Pancreatic cancer cells, which use macropinocytosed prot

292 tor-beta (TGF-beta)-responsive gene in human pancreatic cancer cells, whose downregulation is SMAD4 d

293 vitro was confirmed by preincubation of the pancreatic cancer cells with C225 as well as Nitrobenzyl

294 rmacological ascorbate induced cell death in pancreatic cancer cells with diverse mutational backgrou

295 Here, we describe small subpopulations of pancreatic cancer cells with high intrinsic Wnt activity

296 ted the growth of Panc-1, BxPC-3 and AsPC-1, pancreatic cancer cells with IC50 ranging between 6-7 mu

297 Accordingly, pancreatic cancer cells with reduced PR55alpha expressio

298 ain driving forces behind the development of pancreatic cancer cells with stem-cell-like properties a

299 which leads to higher production of exDNA by pancreatic cancer cells, with a significant reduction in

300 ctivation of the prodrug is expected to kill pancreatic cancer cells without harming normal pancreati