ライフサイエンスコーパス: pancreatic cancer cell

1 that mechanoresponsiveness is a hallmark of pancreatic cancer cells.

2 g limits T cell recognition and clearance of pancreatic cancer cells.

3 mics or modulate Rac1 and RhoA activities in pancreatic cancer cells.

4 not detect podocalyxin-ezrin association in pancreatic cancer cells.

5 urvival signalling, preventing cell death in pancreatic cancer cells.

6 Hypoxia increased expression of KDM3A in pancreatic cancer cells.

7 oles for CAP1 and its phosphor-regulation in pancreatic cancer cells.

8 rms may limit the induction of DNA damage in pancreatic cancer cells.

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

10 juvant treatment to sensitize chemoresistant pancreatic cancer cells.

11 systematically evaluated and then applied to pancreatic cancer cells.

12 er ENT1, which reduced gemcitabine uptake by pancreatic cancer cells.

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

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

15 ment of two novel mAbs against CFPAC-1 human pancreatic cancer cells.

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

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

18 subsequent degradation of the p53 protein in pancreatic cancer cells.

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

20 NFkappaB and apoptotic signaling pathways in pancreatic cancer cells.

21 d enhanced apoptosis and chemosensitivity of pancreatic cancer cells.

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

23 inhibition creates enhanced cytotoxicity in pancreatic cancer cells.

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

25 cer, QD394, with significant cytotoxicity in pancreatic cancer cells.

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

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

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

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

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

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

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

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

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

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

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

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

38 ndent and independent proliferation of human pancreatic cancer cells.

39 hibiting IRP1 and represses proliferation in pancreatic cancer cells.

40 maximally block the tumorigenic potential of pancreatic cancer cells.

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

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

43 invasive and colony forming capabilities of pancreatic cancer cells.

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

45 xpression and inhibits cell proliferation of pancreatic cancer cells.

46 a-lapachone, another NQO1 substrate, against pancreatic cancer cells.

47 s antitumor activities, particularly against pancreatic cancer cells.

48 in combination with gemcitabine for killing pancreatic cancer cells.

49 s expressed and secreted by murine and human pancreatic cancer cells.

50 molecular mechanism leading to resistance in pancreatic cancer cells.

51 PRL increases proliferation and migration of pancreatic cancer cells.

52 n orthotopic implantation of MUC5AC-depleted pancreatic cancer cells.

53 significant change in the aggressiveness of pancreatic cancer cells.

54 onocytic cells, but not for breast, lung, or pancreatic cancer cells.

55 geted to inhibit the metastatic potential of pancreatic cancer cells.

56 ssential for the growth and tumorigenesis of pancreatic cancer cells.

57 1- and NF-kappaB-mediated signaling in human pancreatic cancer cells.

58 as a critical downstream target of PRRX1 in pancreatic cancer cells.

59 Asparagine limitation in melanoma and pancreatic cancer cells activates receptor tyrosine kina

60 egarding the role of mutant p53 and miRNA in pancreatic cancer cell adaptation to metabolic stresses.

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

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

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

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

65 mice that express oncogenic Kras in primary pancreatic cancer cells and have homozygous disruption o

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

67 The spheroids were generated by co-culturing pancreatic cancer cells and pancreatic stellate cells in

68 ved drug, as a potent inhibitor of growth in pancreatic cancer cells and patient-derived xenograft mo

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

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

71 show that KP372-1 sensitizes NQO1-expressing pancreatic cancer cells and spares immortalized normal p

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

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

74 yl CPs also reduce the metabolic activity of pancreatic cancer cells and the growth of a Panc-1 xenog

75 d whether it regulates production of sEVs in pancreatic cancer cells and their ability to form premet

76 correlated with MUC1 and MUC4 expression in pancreatic cancer cells and tumor tissue.

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

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

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

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

81 Because pancreatic cancer cells are sensitive to H2O2 generated

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

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

84 Pancreatic cancer cells break lysophosphatidic acid down

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

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

87 say and observed that exosomes isolated from pancreatic cancer cells, but not normal human cells, can

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

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

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

91 namin-2 promotes migration and metastasis of pancreatic cancer cells by regulating microtubule and fo

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

93 s in regulating pro-metastatic propensity of pancreatic cancer cells: by generating pro-metastatic en

94 ous trans-differentiation of human and mouse pancreatic cancer cells can influence the phenotype of n

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

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

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

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

99 t small extracellular vesicles secreted from pancreatic cancer cells could initiate malignant transfo

100 Pancreatic cancer cells depleted of PAF1 formed smaller

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

102 biomimetic models and 98% for aptamer-based pancreatic cancer cell detection.

103 Loss of Rab27a in pancreatic cancer cells did not decrease tumor growth in

104 is a cancer vaccine consisting of allogeneic pancreatic cancer cells engineered to express the murine

105 MUC1 knockdown in pancreatic cancer cells enhanced unfolded protein respon

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

107 Pancreatic cancer cells exhibited increased pyruvate car

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

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

110 Pancreatic cancer cells from KPC mice were subcutaneousl

111 We isolated pancreatic cancer cells from multiple independent tumor

112 Pancreatic cancer cells from these tumors had higher inv

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

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

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

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

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

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

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

120 HIF1A-knockout pancreatic cancer cells had increased expression of prot

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

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

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

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

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

126 Pancreatic cancer cells have extensively reprogrammed me

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

128 reduces metastases derived from prostate and pancreatic cancer cells in a FBXL7-dependent manner.

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

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

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

132 e (HDAC) inhibitors are effective in killing pancreatic cancer cells in in vitro PDAC studies, and al

133 eir ability to form premetastatic niches for pancreatic cancer cells in mice.

134 55A/T159A/S280A) suppressed tumorigenesis in pancreatic cancer cells in vitro and in vivo to a greate

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

136 signaling impacted the growth of Wnt-driven pancreatic cancer cells in vivo.

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

138 ns of intracellular zinc and is increased in pancreatic cancer cells, in cell lines and mice.

139 antly reduced accumulation of gemcitabine in pancreatic cancer cells, increased growth of xenograft t

140 Loss of HIF1A from pancreatic cancer cells increases their invasive and met

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

142 Similarly, Ptf1a re-expression in human pancreatic cancer cells inhibits their growth and colony

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

144 rates that the actin architecture of TMTs in pancreatic cancer cells is fundamentally different from

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

146 ave equivalent potency to gemcitabine in the pancreatic cancer cell line MIA PaCa-2.

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

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

149 protrusions, which we classify as TMTs, in a pancreatic cancer cell line, Dartmouth-Hitchcock Pancrea

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

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

152 mesenchymal transition (EMT) using the Suit2 pancreatic cancer cell line, which has low endogenous ST

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

154 Pancreatic cancer cell lines (PD2560) were orthotopicall

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

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

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

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

159 We investigated its activities in pancreatic cancer cell lines and its regulation of the g

160 release and remarkable cytotoxicity in human pancreatic cancer cell lines and Kras(G12D); Trp52(R172H

161 In studies of pancreatic cancer cell lines and mice, we found that ZIP

162 methylation of 11 KRAS-mutant and dependent pancreatic cancer cell lines and observed strikingly sim

163 e knocked down KDM3A in MiaPaCa-2 and S2-007 pancreatic cancer cell lines and overexpressed KDM3A in

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

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

166 trate that UBAP2 is highly expressed in both pancreatic cancer cell lines and tumor tissues of PDAC p

167 Expression of USP27X in breast and pancreatic cancer cell lines and tumors positively corre

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

169 lyzed pancreatic tumor tissues from mice and pancreatic cancer cell lines by immunohistochemistry and

170 was knocked down in primary cancer cells and pancreatic cancer cell lines by using small hairpin RNAs

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

172 alyzed a panel of KRAS mutant colorectal and pancreatic cancer cell lines for their dependency on 28

173 Metastatic human pancreatic cancer cell lines had increased levels of PPP

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

175 Knockdown of Atg5 in pancreatic cancer cell lines increased their migratory a

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

177 We performed studies with the human pancreatic cancer cell lines PATU-8988T, BxPC-3, PANC-1,

178 Knockdown of KDM3A in pancreatic cancer cell lines reduced their invasive and

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

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

181 We found human PDAC samples and pancreatic cancer cell lines to overexpress KDM3A.

182 ological perturbation of Mcl-1 and Bcl-xL in pancreatic cancer cell lines using a CDK5 inhibitor anal

183 Atg5 was knocked down in pancreatic cancer cell lines using small hairpin RNAs; c

184 Downregulation of Dab2 expression in pancreatic cancer cell lines was found to trigger induct

185 Pancreatic cancer cell lines were analyzed by gene-expre

186 Three different human pancreatic cancer cell lines were compared to normal pan

187 Pancreatic cancer cell lines were engineered to knockdow

188 Pancreatic cancer cell lines were genetically manipulate

189 WM-266-4 melanoma and AsPC-1 pancreatic cancer cell lines were treated with LMWH (Tin

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

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

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

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

194 atic cancer epithelial cells, human or mouse pancreatic cancer cell lines, or immune cells.

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

196 s in reduced phosphorylation of cortactin in pancreatic cancer cell lines, resulting in increased in

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

198 Using a panel of colon and pancreatic cancer cell lines, we now report the inductio

199 In pancreatic cancer cell lines, we show that either CDK5 k

200 s that possess selective bioactivity against pancreatic cancer cell lines.

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

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

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

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

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

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

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

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

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

210 molar concentration in MIA PaCa-2 and PANC-1 pancreatic cancer cell lines.

211 using a classical clonogenic assay in murine pancreatic cancer cell lines.

212 short hairpin RNAs in AsPC-1 and MIA PaCa-2 pancreatic cancer cells lines, and in pancreatic cells f

213 increase DUOX2 expression in both colon and pancreatic cancer cells mediated, at least in part, by s

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

215 l mechanism by which podocalyxin facilitates pancreatic cancer cell migration and metastasis.

216 n dynamics and ultimately promoted efficient pancreatic cancer cell migration via microtubule- and Sr

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

218 d store-operated calcium entry essential for pancreatic cancer cell migration.

219 itor treatment of small cell lung cancer and pancreatic cancer cell models have a synergistic effect.

220 Taking advantage of prostate and pancreatic cancer cell models known to have high basal R

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

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

223 Pancreatic cancer cells (mT3) from KPC mice (C57BL/6), w

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

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

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

227 The reciprocal interplay between PSCs and pancreatic cancer cells (PCCs) not only enhances tumour

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

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

230 CSCs were isolated from pancreatic cancer cell populations using flow cytometry

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

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

233 h the small molecule inhibitor FDI6 suppress pancreatic cancer cell proliferation and induces their a

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

235 show that knockout (KO) of LINC00346 impairs pancreatic cancer cell proliferation, tumorigenesis, mig

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

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

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

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

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

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

242 urthermore, the silencing of MUC5AC in human pancreatic cancer cells reduced their tumorigenic propen

243 cause for resistance to STAT3 inhibitors in pancreatic cancer cells, regardless of KRAS mutation sta

244 or subsequent utilization during invasion of pancreatic cancer cells, representing a potential target

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

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

247 ned media experiments revealed that squamous pancreatic cancer cells secrete factors that recruit neu

248 PRKD1-deficient pancreatic cancer cells showed increased loading of inte

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

250 The resulting devices captured pancreatic cancer cells spiked in blood samples with (98

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

252 HSP70-BCL2 signaling axis that is crucial to pancreatic cancer cell survival and therapeutic resistan

253 hagy, which is thought to be responsible for pancreatic cancer cell survival.

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

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

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

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

258 le for exploiting metabolic reprogramming in pancreatic cancer cells to confer therapeutic opportunit

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

260 FDI6 sensitizes pancreatic cancer cells to Etoposide and Gemcitabine ind

261 PPP1R1B significantly reduced the ability of pancreatic cancer cells to form lung metastases in mice.

262 e whereas down-regulation of SOX2 sensitizes pancreatic cancer cells to gemcitabine treatment.

263 tion factors may be effective in sensitizing pancreatic cancer cells to gemcitabine treatment.

264 aminase inhibitors sensitized chemoresistant pancreatic cancer cells to gemcitabine, thereby improvin

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

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

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

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

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

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

271 such as penfluridol, block PRL signaling in pancreatic cancer cells to reduce their proliferation, i

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

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

274 CXCL10 as proteins that promote migration of pancreatic cancer cells toward sensory neurons.

275 AXL from the plasma membrane to endosomes in pancreatic cancer cells treated with the AXL ligand grow

276 Glutamine-deficient pancreatic cancer cells up-regulate classic EMT regulato

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

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

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

280 The increased sortilin level in pancreatic cancer cells was confirmed by immunohistochem

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

282 Using pancreatic cancer cells, we demonstrate that inhibition

283 LOAd713-infected pancreatic cancer cells were killed by oncolysis, wherea

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

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

286 atment increases the release of sVCAM-1 from pancreatic cancer cells, which attracts macrophages into

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

288 f H(2)O(2) to tumor cells, activates DUOX in pancreatic cancer cells, which provide sustained product

289 Pancreatic cancer cells, which use macropinocytosed prot

290 In KRAS-mutant Pa16C pancreatic cancer cells, while KRAS knockdown resulted i

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

292 Combined treatment of pancreatic cancer cells with EGFR and STAT3 inhibitors p

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

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

295 Pancreatic cancer cells with ITGA3 or ITGB1 knockdown ha

296 Pancreatic cancer cells with loss or inhibition of PRKD1

297 Pancreatic cancer cells with PRLR knockdown formed signi

298 Accordingly, pancreatic cancer cells with reduced PR55alpha expressio

299 ed PRL-induced JAK2 signaling; incubation of pancreatic cancer cells with these compounds reduced the

300 trongly reduced the adhesion and invasion of pancreatic cancer cells without affecting cell survival