ライフサイエンスコーパス: lung cancer cell

1 the two formulations against A549 non-small lung cancer cell.

2 nies that arose from a single, EGFR-addicted lung cancer cell.

3 tion induced by femoral inoculation of Lewis lung cancer cells.

4 epa1-GFP hepatoma cells or AHR-deficient LLC lung cancer cells.

5 or invasion and metastasis of non-small cell lung cancer cells.

6 le myosin IIA-dependent trafficking in human lung cancer cells.

7 inase in maintaining survival of KRAS-mutant lung cancer cells.

8 correlated with the metastatic potential of lung cancer cells.

9 cisplatin-sensitive and cisplatin-resistant lung cancer cells.

10 rmed a genome-scale CRISPR/Cas9 screening in lung cancer cells.

11 shortened telomere length in H1299 and H920 lung cancer cells.

12 ich increased cisplatin-induced apoptosis in lung cancer cells.

13 eration in vitro and tumor growth in vivo of lung cancer cells.

14 at mediated the interactions between MFs and lung cancer cells.

15 n BRAF-, NRAS-, KRAS-, EGFR-, and ALK-mutant lung cancer cells.

16 ced growth inhibition and apoptosis in human lung cancer cells.

17 ene expression in ZEB1-activated mesenchymal lung cancer cells.

18 stem-like cells as well as therapy resistant lung cancer cells.

19 ghts into miR-155-mediated ATO resistance in lung cancer cells.

20 ay, but downregulating cellular apoptosis in lung cancer cells.

21 temporary remission, and radio-resistance in lung cancer cells.

22 tumors, as well as their functional role in lung cancer cells.

23 pendent caveolae-mediated in vitro uptake by lung cancer cells.

24 ons and inhibits transwell migration of A549 lung cancer cells.

25 d after FAM83H-AS1 knockdown using siRNAs in lung cancer cells.

26 in ovarian, prostate, pancreatic, colon, and lung cancer cells.

27 ed cellular proliferation of KRAS-associated lung cancer cells.

28 Igamma for ubiquitination and degradation in lung cancer cells.

29 , resulting in increased chemo-resistance of lung cancer cells.

30 d is elevated in mesenchymal-like metastatic lung cancer cells.

31 ase, mediates TGF-beta1-induced EMT in human lung cancer cells.

32 nes, mammalian fibroblast and pancreatic and lung cancer cells.

33 otes growth, survival, and invasion of human lung cancer cells.

34 mechanistic role of MUC5AC on metastasis of lung cancer cells.

35 sible interaction of MUC5AC and integrins in lung cancer cells.

36 ease the secreted VEGF level of the TTF-1(+) lung cancer cells.

37 proliferation, and xenograft tumor growth of lung cancer cells.

38 ted in vitro and in vivo on murine and human lung cancer cells.

39 oliferation of K-Ras-positive non-small cell lung cancer cells.

40 romotes ROS and mitochondrial dysfunction in lung cancer cells.

41 he NKX2-1 oncogene and cell proliferation in lung cancer cells.

42 rotein CP110 induced anaphase catastrophe of lung cancer cells.

43 t accompany acquired gefitinib resistance in lung cancer cells.

44 formation ability and invasion potential of lung cancer cells.

45 rasting with plasma membrane localization in lung cancer cells.

46 ased EGFR steady-state levels and sensitized lung cancer cells.

47 atment with erlotinib of PC-9 non-small cell lung cancer cells.

48 mote the proliferation and tumorigenicity of lung cancer cells.

49 , the videos of labeled EVs uptake by living lung cancer cells.

50 K-Ras-addicted pancreatic and non-small cell lung cancer cells.

51 s redundant oncogenic pathways in metastatic lung cancer cells.

52 at responds to elevated levels of GSH within lung cancer cells.

53 cancer cell lines and drug-resistant primary lung cancer cells.

54 ll molecule with activity against small cell lung cancer cells.

55 ung cells (HFL1), A549, and H1299 (p53-null) lung cancer cells.

56 ing protein frequently deleted or mutated in lung cancer cells.

57 and restore SOX7 expression in SOX7 silenced lung cancer cells.

58 132/bortezomib at mRNA and protein levels in lung cancer cells.

59 aling, and inducing autophagic cell death in lung cancer cells.

60 egradation target of CNOT3 in non-small cell lung cancer cells.

61 lony formation in liver, but also breast and lung cancer cells.

62 the role of OPN in the aggressiveness of the lung cancer cells.

63 PH vascular cells, and in a subset of human lung cancer cells.

64 nker (P2-6R), which killed NCI-H460 and A549 lung cancer cells 100 times more effectively than the S

65 ated A(2)B(2) porphyrins were carried out in lung cancer cells (A549) to test their photodynamic ther

66 -7 enhanced the drug resistance potential of lung cancer cells against chemotherapy drugs.

67 ng cell death, XRN2-deficient fibroblast and lung cancer cells also demonstrated sensitivity to PARP1

68 or SOX9 sufficiently inhibits CSCs in human lung cancer cells and attenuates experimental lung metas

69 FBXW2 has tumour suppressor activity against lung cancer cells and blocks oncogenic function of both

70 on (EMT) and migration in both primary human lung cancer cells and cell lines.

71 ties in the cellular response to TGF-beta of lung cancer cells and discover subpopulations of cells d

72 educed OPN-induced migration and invasion of lung cancer cells and had an inhibitory effect on the OP

73 adiation-resistant and -sensitive A549 human lung cancer cells and human head and neck squamous cell

74 onal antibody against human EphA5 sensitized lung cancer cells and human lung cancer xenografts to ra

75 ted in mutant KRAS homozygous non-small-cell lung cancer cells and in vivo, in spontaneous advanced m

76 isting tumors derived from human KRAS-mutant lung cancer cells and increased the sensitivity of these

77 aling and triggered apoptosis in KRAS-mutant lung cancer cells and inhibited tumor growth in murine m

78 es cellular senescence in both A549 and H460 lung cancer cells and inhibits their transformed phenoty

79 ceptor targeted paclitaxel (PTX) delivery in lung cancer cells and its impact on normal cells.

80 ion, inhibits mitochondrial bioenergetics in lung cancer cells and mitigates lung cancer cell viabili

81 ble of delivering siRNA drugs selectively to lung cancer cells and not to normal lung cells.

82 d epithelial-mesenchymal transition (EMT) in lung cancer cells and promoted metastatic spreading.

83 wires energy homeostasis in human and murine lung cancer cells and promotes expansion of lung cancer

84 o complement-dependent cytotoxicity (CDC) in lung cancer cells and promotes tumor progression.

85 hes to specifically target PPP2R2A-deficient lung cancer cells and provides a novel biomarker that wi

86 ted the migration and invasive activities of lung cancer cells and reduced epithelial-to-mesenchymal

87 bserved enhanced S184 Bax phosphorylation in lung cancer cells and tissues that inactivates the propa

88 LOC102723729, was significantly decreased in lung cancer cells and tissues; while no association was

89 redictive biomarker pathway and re-sensitize lung cancer cells and tumors to MTI therapy.

90 ed clonogenic survival of mutant KRAS-driven lung cancer cells, and calcitriol treatment increased CY

91 isozymes in erlotinib resistance and EMT in lung cancer cells, and highlight PKCalpha as a potential

92 ne tumor models, in primary human breast and lung cancer cells, and in deposited expression data.

93 model of lung adenocarcinoma in which murine lung cancer cells are directly implanted into the left l

94 In contrast, K-Ras-dependent lung cancer cells are largely insensitive to topoisomera

95 y explain why vimentin expressing metastatic lung cancer cells are more motile and invasive.

96 ) acetate monohydrate (Ag-Phen), toward A549 lung cancer cells are presented.

97 Lung cancer cells are rendered sensitive to MEK inhibito

98 Lung cancer cells are sensitive to 5-aza-2'-deoxycytidin

99 Non-neuroendocrine Notch-active small-cell lung cancer cells are slow growing, consistent with a tu

100 profound effects of tobacco on the genome of lung cancer cells are well-documented(6-10), but equival

101 and integrin beta4 was observed both in A549 lung cancer cells as well as genetically engineered mous

102 studies (using paclitaxel as cargo) in A549 lung cancer cells at pH 6.6.

103 eferentially impedes tumorigenicity of human lung cancer cells bearing KMT2D-inactivating mutations.

104 stemness and adherence independent growth of lung cancer cells but these inhibitors could also effici

105 pithelial-to-mesenchymal transition (EMT) of lung cancer cells by directly repressing the expression

106 he naive-like B cells suppress the growth of lung cancer cells by secreting four factors negatively r

107 tumor migration, invasion and metastasis in lung cancer cells by targeting beta-catenin for degradat

108 FBXW2 inhibits proliferation of lung cancer cells by targeting SKP2 for degradation.

109 Metastatic lung cancer cells can undergo an epithelial-to-mesenchym

110 Two lung cancer cells, CL1-0 and CL1-5, were selected as the

111 KRAS-mutated lung cancer cell clones were stably silenced for LSD1 ex

112 nes and effectively suppressed the growth of lung cancer cells compared with the corresponding negati

113 1 expression by shRNA in both pancreatic and lung cancer cells containing dominant active KRAS (mt) c

114 t bind a CSC subpopulation of non-small cell lung cancer cells (defined by Aldefluor positivity), but

115 Surprisingly, the EDM of TTF-1(+) lung cancer cells (designated EDM-TTF-1(+)) displayed an

116 TKI treatment favored selection of lung cancer cells displaying mesenchymal morphology with

117 conclusion, Th9 and Th17 lymphocytes induce lung cancer cell EMT, thereby promoting migration and me

118 -PTX was approximately 2.3 nM for A549 human lung cancer cells, equipotent with PTX in vitro.

119 Together, our data suggest that lung cancer cells escape oncogene-induced premature sene

120 SOX2-positive lung cancer cells exhibited a lower dissemination capaci

121 or xenografts generated from FGFR1-dependent lung cancer cells exhibited only modest sensitivity to m

122 Knockdown of USP10 in lung cancer cells exhibits increased cell survival and d

123 We show that human and mouse breast and lung cancer cells express protocadherin 7 (PCDH7), which

124 Lung cancer cells expressing oncogenic K-Ras have bypass

125 hrough genomic analysis of 1,122 EGFR-mutant lung cancer cell-free DNA samples and whole-exome analys

126 Herein, we report that lung cancer cells grown on a 3D fibrous scaffold form tu

127 nal transduction takes a significant part in lung cancer cell growth and in vivo tumorigenesis.

128 ased Akt activity, leading to suppression of lung cancer cell growth in vitro and in xenografts.

129 hese results indicated that PL could inhibit lung cancer cell growth via inhibition of NF-kappaB sign

130 ross-talk between Mcl-1 and Akt in promoting lung cancer cell growth.

131 Lung cancer cells H1975 treated with 5a could induce mic

132 ficantly suppressed the growth of small-cell lung cancer cell (H526) xenografts in mice.

133 ociated with smoking in normal and precursor lung cancer cells have been reported, yet their role in

134 8.4 mug/mL) at a lower concentration than to lung cancer cells (IC50 = 59.1 mug/mL), and L-PTX demons

135 growth factor-beta (TGF-beta)-induced EMT in lung cancer cells identified complement cascade as one o

136 Abolishing the expression of TNFR1 on lung cancer cells impaired the antitumor efficacy of MEK

137 vely prevented the metastatic progression of lung cancer cells in an orthotopic animal model.

138 t FSP1 mediates resistance to ferroptosis in lung cancer cells in culture and in mouse tumour xenogra

139 immune rejection and allows growth of human lung cancer cells in lal(-/-) mice.

140 , secreted peptide by epithelial ovarian and lung cancer cells in situ This finding prompted us to st

141 red for survival and outgrowth by metastatic lung cancer cells in the brain parenchyma.

142 HIP1 significantly repressed the mobility of lung cancer cells in vitro and in vivo and regulated the

143 rotein diminished the metastatic capacity of lung cancer cells in vitro and in vivo.

144 s the migratory and invasive capabilities of lung cancer cells in vitro and in vivo.

145 ntrodia cinnamomea ethanol extract (ACEE) on lung cancer cells in vitro and tumor growth in vivo.

146 RT2's protective effects were not evident in lung cancer cells in vitro or in tumors in vivo.

147 d F10 efficiently inhibited proliferation of lung cancer cells in vitro while being nontoxic to endot

148 ted proliferation, migration and invasion of lung cancer cells in vitro, and repressed tumor growth i

149 18 was involved in the metastatic process of lung cancer cells in vivo by suppressing local invasion

150 ophagy is sufficient to trigger apoptosis in lung cancer cells, including cells lacking p53.

151 3 overexpression in noninvasive melanoma and lung cancer cells increased anchorage-independent growth

152 le ectopic expression of OPN in the SK-MES-1 lung cancer cells increased levels of cellular invasion

153 ressor gene in TUSC2 deficient EGFR wildtype lung cancer cells increased sensitivity to erlotinib.

154 Of note, TXNDC5 knockdown in lung cancer cells inhibited cell proliferation and repre

155 TGF-beta and IL-6 in myofibroblasts (MFs) - lung cancer cell interactions, lung cancer cells (Lewis

156 dly decreased the proliferative potential of lung cancer cells, leading to improved survival of tumou

157 lasts (MFs) - lung cancer cell interactions, lung cancer cells (Lewis and CTM-167 cell lines) were st

158 RNA-seq analysis in human lung cancer cell line H1299 reveals that downregulated g

159 significant dose-dependent inhibition of the lung cancer cell line H157, which suggests potential for

160 R predictions of FGFR and MTOR dependence in lung cancer cell line H1581, showing synergistic reducti

161 selected and MRP1 overexpressing small cell lung cancer cell line H69 AR in a calcein AM and daunoru

162 rated by injection of a LH2-expressing human lung cancer cell line into nude mice.

163 Finally, by establishing an in vitro EMT lung cancer cell line model, an attempt was made to subs

164 ncluding breast cancer cell line MDA-MB-231, lung cancer cell line PC-9, and leukemia cell line K-562

165 FSTL1 attenuated nicotine-induced BEAS2B and lung cancer cell line proliferation.

166 of alpha-tubulin instead of histones in the lung cancer cell line, LL2.

167 DeltaN-LKB1 is expressed solely in the lung cancer cell line, NCI-H460.

168 npointed proteins in vitro using an invasive lung cancer cell line.

169 in significantly decreased migration in two lung cancer cell lines (A549 and H1437) as compared with

170 lung carcinoma (LLC1) and 10 different human lung cancer cell lines (adenocarcinoma, squamous cell ca

171 sumption and use it to screen non-small-cell lung cancer cell lines against bioactive small molecules

172 n proliferation assays using patient-derived lung cancer cell lines and by analyzing downstream kinas

173 ylamine (EMD), in targeting c-Myc in several lung cancer cell lines and drug-resistant primary lung c

174 protein levels of eight atypical cyclins in lung cancer cell lines and formalin-fixed and paraffin-e

175 lly, we overexpressed ts-46 and ts-47 in two lung cancer cell lines and performed a clonogenic assay

176 ylated, but was silenced or downregulated in lung cancer cell lines and primary lung tumor tissues ha

177 significantly co-repressed in non-small cell lung cancer cell lines and primary tumors from multiple

178 tributes to the proliferation of a subset of lung cancer cell lines by supporting oncogenic RAS trans

179 We have analyzed a panel of 17 KRAS mutant lung cancer cell lines classified as K-Ras-dependent or

180 y hypermethylated in lung cancer tissues and lung cancer cell lines compared with normal lung tissues

181 ve-like B cells from NSCLC patients with two lung cancer cell lines demonstrate that the naive-like B

182 Analyses of lung cancer cell lines demonstrated that LH2 is present

183 diotherapy exposures, we screened a panel of lung cancer cell lines for cholesterol levels following

184 t antiproliferative effects in nonsmall cell lung cancer cell lines harboring SRC activation, thus pr

185 of ALDOA increased migration and invasion of lung cancer cell lines in vitro and formation of metasta

186 is, modulation of SASH1 levels in a panel of lung cancer cell lines mediated changes in cellular prol

187 Whole genome RNAi screening of lung cancer cell lines provides an ideal source for dete

188 It was discovered that some lung cancer cell lines release surfactants only when pla

189 R) by antibody or CRISPR knockout of IL37 in lung cancer cell lines repolarized TAMs, resulting in re

190 ncer activity and therapeutic index, we used lung cancer cell lines that are naturally sensitive or r

191 f transcription factors, is downregulated in lung cancer cell lines that have been selected to grow i

192 normal epithelial cells, EGF stimulation of lung cancer cell lines that lack DUOX1 promotes EGF-indu

193 th our Kras/p53 mutant mouse model and human lung cancer cell lines to demonstrate that upon miR-200

194 tance of additional EGFR-dependent HNSCC and lung cancer cell lines to EGFR blockade, they are unable

195 atterns of differential vulnerability across lung cancer cell lines to loss of functionally related g

196 ive form of STAT3 was expressed in colon and lung cancer cell lines to replicate IL6R signaling.

197 kinase, CHK1, in a variety of non-small cell lung cancer cell lines using CRISPR-mediated genetic app

198 n human lung cancer tissues and immortalized lung cancer cell lines via indirect immunofluorescence a

199 king effect on FSTL1, normal cell BEAS2B and lung cancer cell lines was treated with nicotine and the

200 tabolites along the gluconeogenesis pathway, lung cancer cell lines were incubated with (13)C(3)-lact

201 an normal lung epithelial cell line and four lung cancer cell lines were treated with TGF-beta.

202 atively measure glutamine-derived ammonia in lung cancer cell lines with differential expression of g

203 , LGR4 or their signaling mediator IQGAP1 in lung cancer cell lines with Keap1 deficiency and high RS

204 of HKlincR1 affected cell growth in multiple lung cancer cell lines, and led to disruption of genes i

205 ted strong cytotoxicity toward various human lung cancer cell lines, as well as chemotherapeutic-resi

206 t, esophageal, colorectal, and nonsmall cell lung cancer cell lines, as well as heterogeneity within

207 After knockdown of LINC00152 using siRNAs in lung cancer cell lines, both cell proliferation and colo

208 ere, we confirm that H1299 and A549 cells, 2 lung cancer cell lines, relay on aerobic glycolysis as m

209 Here, using several human lung cancer cell lines, siRNA-mediated gene silencing, i

210 In lung cancer cell lines, SMURF2 overexpression increased

211 educed mitogenic signaling in non-small cell lung cancer cell lines, suggesting that targeting TACC3

212 approach, utilizing 106 human non-small-cell lung cancer cell lines, was used to interrogate 4,725 bi

213 t phosphorylation of EGFR protein in several lung cancer cell lines.

214 GFR) inhibitor, erlotinib, in Non-Small Cell Lung Cancer cell lines.

215 r formation in vivo and induced apoptosis in lung cancer cell lines.

216 d with the USP10 protein level in a panel of lung cancer cell lines.

217 l-cell lung cancers and in Ras-mutated human lung cancer cell lines.

218 ession reduced SMARCD1 protein expression in lung cancer cell lines.

219 selective anticancer effects on STK11 mutant lung cancer cell lines.

220 d MET or c-Src signaling, including in human lung cancer cell lines.

221 rough aberrant methylation in non-small-cell lung cancer cell lines.

222 ltimately apoptotic cell death in breast and lung cancer cell lines.

223 e to polyploid growth and multinucleation in lung cancer cell lines.

224 The results of this study suggest that lung cancer cells may utilize at least some steps of glu

225 In both melanoma and lung cancer cells, MEKi increased cell-surface expressio

226 MUC5AC/integrin beta4/FAK-mediated lung cancer cell migration was confirmed through experim

227 -67 intensity and clonogenicity and promoted lung cancer cell migration.

228 es phosphorylation of FAK at Y397 leading to lung cancer cell migration.

229 demonstrate that expressing TbetaRIII-SS in lung cancer cell models induces epithelial-to-mesenchyma

230 dditional mechanisms in gene fusion-positive lung cancer cells, mouse models, and human clinical spec

231 as assessed in H1299 and A549 non-small cell lung cancer cells, normal MRC9 lung fibroblasts, and Dox

232 Breast and lung cancer cells of murine and human origin induced IL-

233 k between SOX2 and TGFbeta signaling affects lung cancer cell plasticity and TKI tolerance.

234 ermine how compromised LKB1 function affects lung cancer cell polarity and invasion.

235 In vitro studies subsequently showed that lung cancer cells polarized macrophages to express MARCO

236 Here, we report that lung cancer cell populations generate phenotypic and onc

237 to delineate their effects on non-small cell lung cancer cell proliferation and apoptosis.

238 hereas dual inactivation of them suppresses, lung cancer cell proliferation and metastatic growth in

239 reducing cell cycle pathways and inhibiting lung cancer cell proliferation and migration.

240 24 subfamily A member 1 (CYP24A1) increases lung cancer cell proliferation by activating RAS signali

241 ues and its expression level is critical for lung cancer cell proliferation, which may serve as a pro

242 FSTL1 may prevent nicotine-induced lung cancer cell proliferation.

243 romoted and reduced PRR14 expression impeded lung cancer cell proliferation.

244 is approach to model different mechanisms of lung cancer cell resistance to EGFR inhibitors and to as

245 Lung cancer cells resistant to MEK inhibition become hig

246 64%, and 8% of human colon, pancreatic, and lung cancer cells, respectively, overexpressed SHH at tr

247 acilitates CK2alpha binding to histone H4 in lung cancer cells, resulting in increased H4S1ph and epi

248 ition, depletion of SMYD5 in human colon and lung cancer cells results in increased tumor growth and

249 Ectopic GATA4 expression results in lung cancer cell senescence.

250 rmore, in vitro studies performed using A549 lung cancer cells, showed effective intracellular delive

251 In lung cancer cells, SOX2 bound the EPCAM promoter to indu

252 duction of specific eicosanoids critical for lung cancer cell survival and proliferation, with possib

253 onary games in co-cultures of non-small cell lung cancer cells that are sensitive and resistant to th

254 We have previously shown in lung cancer cells that GSK3alpha and to a lesser extent

255 o TNFalpha and IFNgamma-induced apoptosis in lung cancer cells that were refractory to MEKi killing a

256 heterozygous mouse embryonic fibroblasts and lung cancer cells, that these genotypes are phenotypical

257 omoting migration and invasion properties of lung cancer cells through its phosphorylation activation

258 e to increase the dissemination potential of lung cancer cells through the generation of the CD133(+)

259 s chemotherapeutic-resistant patient-derived lung cancer cells, through apoptosis induction in compar

260 hermore, activated KRAS mutations sensitized lung cancer cells to CDK2 inhibition by deregulating CP1

261 P110 plays a mechanistic role in response of lung cancer cells to CDK2 inhibition, especially in the

262 We found that although SMARCD1 sensitized lung cancer cells to chemotherapy drug-induced apoptosis

263 ensitizes the KRAS-mutated A549 and NCI-H460 lung cancer cells to cisplatin, a common chemotherapy us

264 kappaB and Akt signaling pathways sensitizes lung cancer cells to cisplatin-induced apoptosis, we for

265 ATA6 can modulate the chromatin landscape of lung cancer cells to control their proliferation and div

266 tudy, we found that Srx knockdown sensitizes lung cancer cells to endoplasmic reticulum (ER) stress-i

267 els of KLF12 results in increased ability of lung cancer cells to form tumours in vivo and is associa

268 e sensitivity of the corresponding resistant lung cancer cells to gefitinib was reduced by desialylat

269 Nanosheets reduced the ability of lung cancer cells to generate three-dimensional tumor sp

270 that suppressing S100A4 signaling sensitizes lung cancer cells to glycolysis inhibition.

271 nces the sensitivity of KRAS- or BRAF-mutant lung cancer cells to MEK inhibition.

272 mous addiction of KRAS-mutant non-small-cell lung cancer cells to receptor-dependent nuclear export.

273 A 10-min exposure of A549 human lung cancer cells to sequential 50- and 385-Hz oscillati

274 strated that a senescence-like state enables lung cancer cells to survive dual inhibition of EGFR and

275 serve enhanced sensitivity of STK11-silenced lung cancer cells to the FDA-approved CDK4 inhibitor pal

276 mRNA expression analysis of TUSC2 inducible lung cancer cells treated with erlotinib uncovered defec

277 e discovered that a subset of non-small cell lung cancer cells underwent a gradually progressing epit

278 When Aurora kinases were inhibited together, lung cancer cells uniformly grew into multinucleated PGC

279 Collectively, our data suggest that lung cancer cells use caveolin-2 expressed in bone marro

280 Depletion of endogenous Mcl-1 from human lung cancer cells using CRISPR/Cas9 or Mcl-1 shRNA signi

281 nergetics in lung cancer cells and mitigates lung cancer cell viability, growth, progression, and met

282 CNTD2 overexpression increased lung cancer cell viability, Ki-67 intensity and clonogen

283 The IC(50) of EMD against lung cancer cells was approximately 60 uM.

284 nuclear EGFR localization in DUOX1-deficient lung cancer cells was associated with altered dynamics o

285 uction in in vitro survival fraction of A549 lung cancer cells was observed compared to free cisplati

286 quine (CQ) and quinacrine (Q) on KRAS mutant lung cancer cells, we demonstrate that inhibition of the

287 cellular erythritol production in human A549 lung cancer cells, where ADH1 is minimally expressed.

288 1 exerts the opposite effect in EGFR-mutated lung cancer cells, where it suppresses growth by increas

289 t EMT, migration, invasion and metastasis in lung cancer cells, whereas Foxf2 inhibition significantl

290 of PKCalpha in regulating mTORC1 activity in lung cancer cells, whereby a primary switching occurs fr

291 migration and invasion abilities of the A549 lung cancer cells which endogenously expresses OPN.

292 rative activity in autophagy-deficient H1650 lung cancer cells, which have a biallelic deletion of At

293 Transformed non-small-cell lung cancer cells, which maintain high glycolytic rates

294 The treatment of lung cancer cells with chloropyramine, a compound that i

295 s proliferation of A549 human non-small cell lung cancer cells with enhanced mRNA stability and subse

296 ously discovered that CDK2 inhibition causes lung cancer cells with more than two centrosomes to unde

297 We find that lung cancer cells with RASSF1A promoter methylation disp

298 Coculturing lung cancer cells with Th9/Th17 cells or exposing them t

299 Preselection of EGFR-mutant lung cancer cells with the mesenchymal phenotype diminis

300 A to undruggable KRAS mutated non-small cell lung cancer cells would sensitize the cells to TKI drugs