ライフサイエンスコーパス: lung cancer cell

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

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

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

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

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

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

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

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

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

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

11 romotes ROS and mitochondrial dysfunction in lung cancer cells.

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

13 rotein CP110 induced anaphase catastrophe of lung cancer cells.

14 t accompany acquired gefitinib resistance in lung cancer cells.

15 formation ability and invasion potential of lung cancer cells.

16 rasting with plasma membrane localization in lung cancer cells.

17 context-specific metabolic vulnerability in lung cancer cells.

18 acked proliferative or clonogenic effects on lung cancer cells.

19 nd neck tumor cells, and H358 non-small cell lung cancer cells.

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

21 by Akt/GSK3beta signaling in H1299 non-small lung cancer cells.

22 ing protein that suppresses RhoA activity in lung cancer cells.

23 esistance to ALK inhibition in ALK-dependent lung cancer cells.

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

25 uce broad changes in the kinome signature of lung cancer cells.

26 , TrkB activated Akt signaling in metastatic lung cancer cells.

27 tion of aberrant signaling in non-small cell lung cancer cells.

28 an endogenous suppressor of the SP in human lung cancer cells.

29 ty may involve regulation of the SP in human lung cancer cells.

30 n efficiency, in a dose-dependent manner, of lung cancer cells.

31 s upregulated during TGF-beta1-driven EMT in lung cancer cells.

32 chanism of neferine in inducing autophagy in lung cancer cells.

33 duce radioresistance of human non-small cell lung cancer cells.

34 ic phosphorylation of PLK1 in TBK1-sensitive lung cancer cells.

35 ell growth and is enriched in drug-resistant lung cancer cells.

36 are overexpressed in the plasma membrane of lung cancer cells.

37 ways, and results in specific killing of the lung cancer cells.

38 h inhibition and apoptosis in TBK1-sensitive lung cancer cells.

39 nd an IC(50) of 25.82 microM in H-1299 human lung cancer cells.

40 CLC and the role of CXCR2 and its ligands in lung cancer cells.

41 stimulated proliferation and growth of Lewis lung cancer cells.

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

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

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

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

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

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

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

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

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

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

52 Igamma for ubiquitination and degradation in lung cancer cells.

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

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

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

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

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

58 -7 enhanced the drug resistance potential of lung cancer cells against chemotherapy drugs.

59 iRNA) of endogenous LKB1 expression in H1792 lung cancer cells also correlated with increased pRTK.

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

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

62 Recent reports indicate that most human lung cancer cells and cell lines express CD22, making it

63 o vimentin-positive focal adhesions (FAs) in lung cancer cells and complexes with vimentin and FA kin

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

65 tial cytotoxicity and genotoxicity upon A549 lung cancer cells and Human Umbilical Vein Endothelial C

66 The NLCS was tested in vitro using human lung cancer cells and in vivo utilizing mouse orthotopic

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

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

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

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

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

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

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

74 eration and transformation potential of A549 lung cancer cells and suppresses the tumorigenicity of A

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

76 mTOR inhibition upregulates Bcl2 in lung cancer cells and tumor tissues from clinical trial

77 ed with mesenchymal attributes of breast and lung cancer cells and with poor differentiation in clini

78 drugs and mixture of siRNAs specifically to lung cancer cells and, as a result, efficient suppressio

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

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

81 essed at measurable levels on the surface of lung cancer cells, and that these cells cannot be killed

82 pression of miR-33a inhibits the motility of lung cancer cells, and this inhibition can be rescued by

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

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

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

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

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

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

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

90 Tid1-L overexpression in lung cancer cells attenuated EGFR signaling and inhibite

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

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

93 knockout lungs, depletion of Fam13a in human lung cancer cells causes an obvious reduction in Wnt sig

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

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

96 -72) that exhibit selective toxicity against lung cancer cells compared with normal human bronchial e

97 1 expression by shRNA in both pancreatic and lung cancer cells containing dominant active KRAS (mt) c

98 on in normal human respiratory epithelia and lung cancer cells cultured in the presence or absence of

99 ing CK2-, MAPK- and EGFR-targeting assays in lung cancer cells demonstrate the advantage of kinase-ta

100 ative breast cancer cells and non-small cell lung cancer cells depleted of ERCC1 exhibited increased

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

102 ect evidence that following CDK2 inhibition, lung cancer cells develop multipolar anaphase and underg

103 In the absence of EphA5, lung cancer cells displayed a defective G1/S cell cycle

104 , anchorage-independent growth in vitro, and lung cancer cell dissemination in mice after tail vein i

105 c detection of ZEB1 in lysates from NCI-H358 lung cancer cells down to an estimated concentration of

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

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

108 pound suppressed Aurora B kinase activity in lung cancer cells, evidenced by the inhibition of the ph

109 As a result, EGFR-mutant lung cancer cells exhibited olaparib sensitivity in vitr

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

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

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

113 Lung cancer cells expressing oncogenic K-Ras have bypass

114 established YAP as an essential barrier for lung cancer cell fate conversion and provided a mechanis

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

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

117 K-Ras oncogenic stress, whereas it promoted lung cancer cell growth through inducing the cell prolif

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

119 xpression has an important role in promoting lung cancer cell growth, and that its oncogenic function

120 e induction of MCP-1 was also found in other lung cancer cells H157 and H460 that express relatively

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

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

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

124 duced after TBK1 knockdown in TBK1-sensitive lung cancer cells, implicating that TBK1 mediates unknow

125 nib treatment increases the clonogenicity of lung cancer cells in a sphere-forming assay, suggesting

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

127 s a novel mechanism of action of neferine on lung cancer cells in the induction of autophagy.

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

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

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

131 increased liposomal delivery and toxicity to lung cancer cells in vitro.

132 18 was involved in the metastatic process of lung cancer cells in vivo by suppressing local invasion

133 y) significantly blocks growth of A549 human lung cancer cells in vivo.

134 nd also the metastatic potential of invasive lung cancer cells in vivo.

135 decreased growth and metastatic potential of lung cancer cells in vivo.

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

137 3 overexpression in noninvasive melanoma and lung cancer cells increased anchorage-independent growth

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

139 Hmga2 can promote the transformation of lung cancer cells independent of protein-coding function

140 gnificantly inhibits cell growth in cultured lung cancer cells, indicating its potent tumor suppresso

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

142 In this report, we found that, in human lung cancer cells, knockdown of RIP1 substantially incre

143 In this study, we revealed that CD133(+) lung cancer cells labeled by a human CD133 promoter-driv

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

145 NLCS effectively delivered its payload into lung cancer cells leaving healthy lung tissues intact an

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

147 both C-Raf and B-Raf isoforms, including the lung cancer cell line H1299 cells.

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

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

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

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

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

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

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

155 e chemoresistance in the A549 non-small-cell lung cancer cell line to CDDP is associated with the het

156 We tested the hypothesis that the lung cancer cell line, H460 stably transfected with hCD6

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

158 X30 hypermethylation was detected in 100% of lung cancer cell lines (9/9) and 70.83% (85/120) of prim

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

160 Four lung cancer cell lines (A549, HTB56, EBC1, and H1975) we

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

162 d show selective cytotoxicity to DDR2 mutant lung cancer cell lines (IC50 120-400 nM).

163 plied KAR to predict kinase dependency of 21 lung cancer cell lines and 151 leukemia patient samples

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

165 EPCK (PCK2) is expressed and active in three lung cancer cell lines and in non-small cell lung cancer

166 MARCKS and phospho-MARCKS in highly invasive lung cancer cell lines and lung cancer specimens from no

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

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

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

170 The side population (SP) in human lung cancer cell lines and tumors is enriched with cance

171 ) and its receptor (IL6R) in human colon and lung cancer cell lines by flow cytometry and enzyme-link

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

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

174 h proteins are expressed more highly in many lung cancer cell lines compared to normal tissue.

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

176 levels of GSK3 activity in a panel of human lung cancer cell lines correlated with more efficacious

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

178 proteasomal proteases in multiple breast and lung cancer cell lines exceeds the activity of the prote

179 d in-depth membrane proteome profiling of 11 lung cancer cell lines harboring different EGFR mutation

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

181 f MARCKS expression in these highly invasive lung cancer cell lines reduced cell migration and suppre

182 ctopic expression of miR-4423 in a subset of lung cancer cell lines reduces their anchorage-independe

183 ckdown decreased the metastatic potential of lung cancer cell lines resembling TPCs.

184 s between Gefitinib-resistant and -sensitive lung cancer cell lines revealed several up-regulated mem

185 ith IC50 values of 1-2 nM in four small-cell lung cancer cell lines sensitive to potent and specific

186 Knockdown of TrkB in human lung cancer cell lines significantly decreased their mig

187 Knocking down FUT8 in aggressive lung cancer cell lines significantly inhibits their mali

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

189 inker sensitivity in a subset of EGFR-mutant lung cancer cell lines that is reminiscent of the defect

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

191 used an unbiased phosphoproteomics screen in lung cancer cell lines to discover cell motility protein

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

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

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

195 ly, both compounds sensitized non-small cell lung cancer cell lines toward the induction of apoptosis

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

197 that levels of CD22 mRNA in a panel of human lung cancer cell lines were 200 to 60,000-fold lower tha

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

199 microarray expression analysis performed on lung cancer cell lines with ChIP-Seq data designed to id

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

201 re, we report that treatment of EGFR-mutated lung cancer cell lines with erlotinib, while showing rob

202 Incubation of colon and lung cancer cell lines with IL6, but not other cytokines

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

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

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

206 an breast, head and neck, and non-small cell lung cancer cell lines, in cell lines that were either w

207 e, we show that overexpression of miR-194 in lung cancer cell lines, results in suppressing metastasi

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

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

210 show that BMP signaling is basally active in lung cancer cell lines, which can be effectively inhibit

211 ells from Kras/Tp53-mutant animals and human lung cancer cell lines, ZEB1 activated PI3K by derepress

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

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

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

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

216 ative activity using human breast cancer and lung cancer cell lines.

217 lar expression of CD22 protein in a panel of lung cancer cell lines.

218 with SP fraction size in six non-small cell lung cancer cell lines.

219 ing the efficacy of our CD22 immunotoxins on lung cancer cell lines.

220 or was required to decrease BMP signaling in lung cancer cell lines.

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

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

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

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

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

226 bited in vitro proliferation and invasion of lung cancer cells mediated by CSC or overexpression of m

227 expression of ARHGAP5 considerably inhibited lung cancer cell migration and invasion, resembling that

228 em designed to discover factors critical for lung cancer cell migration identified brain-derived neur

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

230 -67 intensity and clonogenicity and promoted lung cancer cell migration.

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

232 lly its phosphorylated form, in potentiating lung cancer cell migration/metastasis and suggest a pote

233 e results demonstrate that ANGPTL1 represses lung cancer cell motility by abrogating the expression o

234 V2 pathway as a potential novel regulator of lung cancer cell motility.

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

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

237 By screening 40 non-small cell lung cancer cell (NSCLC) lines, we established a surpris

238 or its anti-cancer effects against non-small lung cancer cells (NSCLC).

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

240 ally suppresses growth and tumorigenicity of lung cancer cells, our findings may open an avenue for d

241 monstrate that the TGF-beta1-induced EMT for lung cancer cells, particularly during the maturation st

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

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

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

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

246 cal role of JNK signaling in EPHA2-dependent lung cancer cell proliferation and motility and a role f

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

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

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

250 RNAi-mediated attenuation of YEATS4 in human lung cancer cells reduced their proliferation and tumor

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

252 Lung cancer cells resistant to MEK inhibition become hig

253 p65-Sema3C, but not FR-sema3C, rendered A549 lung cancer cells resistant to serum deprivation, sugges

254 well as H1975 activating-EGF receptor mutant lung cancer cell resulted in dephosphorylation of severa

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

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

257 BRAF(V600E)/PIK3CA(H1047R)-expressing mouse lung cancer cells revealed mechanistic clues about coope

258 Furthermore, lung cancer cell sensitivity to TBK1 was highly correlat

259 Cytotoxicity assays using A549 and H596 lung cancer cells showed that both micelle formulations

260 e free energy changes during the EMT for the lung cancer cells shows a stable intermediate state.

261 In a murine model, compared with control lung cancer cells, SLIT-expressing cells had a decreased

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

263 AF1 inhibition and activity in nonsmall cell lung cancer cells, specifically increased monoubiquitina

264 Hk2 deletion in lung cancer cells suppressed glucose-derived ribonucleot

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

266 utative TBK1 downstream effector involved in lung cancer cell survival.

267 rexpression is more widely observed in human lung cancer cells than that of Bcl-2, suggesting that Bc

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

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

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

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

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

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

274 his peptide also enhanced the sensitivity of lung cancer cells to erlotinib treatment, especially tho

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

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

277 d an unbiased siRNA screen in non-small-cell lung cancer cells to identify deubiquitylases (DUBs) tha

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

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

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

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

282 E)/TP53(Null) or BRAF(V600E)/INK4A-ARF(Null) lung cancer cells triggered a G1 cell-cycle arrest regar

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

284 date somatic variants that are essential for lung cancer cell viability.

285 rker characteristic of stem-like behavior in lung cancer cells was also identified in the isolated su

286 n line, enhanced metastasis of NME2-depleted lung cancer cells was found in zebrafish and nude mice t

287 egulated overexpression of PKCbetaII in A549 lung cancer cells was necessary for the enhanced prolife

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

289 Comparing drug-resistant and sensitive lung cancer cells, we reveal that post-translational pho

290 Using cultured lung cancer cells, we showed that SAG knockdown suppress

291 1 exerts the opposite effect in EGFR-mutated lung cancer cells, where it suppresses growth by increas

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

293 gnaling promotes cell growth and survival of lung cancer cells, which is mediated through its regulat

294 cytochrome c release and apoptosis in human lung cancer cells, which occurs in a Bax- but not Bak-de

295 lines, results in suppressing metastasis of lung cancer cells, while inhibiting its expression throu

296 Co-culture of lung cancer cells with astrocytes - the most abundant ce

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

298 Coimplantation of lung cancer cells with wild-type Mmp1a(+/+) fibroblasts

299 ed in other adenocarcinoma and squamous cell lung cancer cells, with validation rates of 80% to 95% a

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