ライフサイエンスコーパス: ovarian cancer cell

1 inal fluid, dendritic cells, mast cells, and ovarian cancer cells).

2 plex is critical for sustained EMT traits of ovarian cancer cells.

3 d in vitro against both multiple myeloma and ovarian cancer cells.

4 ynergistic antiproliferative effects against ovarian cancer cells.

5 2 in the regulation of TGF-beta signaling in ovarian cancer cells.

6 ing feature underlying the aggressiveness of ovarian cancer cells.

7 ociated neovasculature and on the surface of ovarian cancer cells.

8 t cell proliferation and induce apoptosis of ovarian cancer cells.

9 paB and STAT, and reduces EGFR expression in ovarian cancer cells.

10 vity of cisplatin against the drug-resistant ovarian cancer cells.

11 of action of compound 1 in A2780 epithelial ovarian cancer cells.

12 ely associated with paclitaxel resistance in ovarian cancer cells.

13 n resulted in reduced SHMT1 transcription in ovarian cancer cells.

14 ibit the growth of a stem-like population of ovarian cancer cells.

15 EGFR pathway in high-grade serous and other ovarian cancer cells.

16 novo lipogenesis, results in robust death of ovarian cancer cells.

17 nsitivity in low-grade and high-grade serous ovarian cancer cells.

18 progression, and induces apoptosis of human ovarian cancer cells.

19 and synergistically to induce cell death in ovarian cancer cells.

20 activity of cisplatin against drug-resistant ovarian cancer cells.

21 f drug-resistant ERalpha-positive breast and ovarian cancer cells.

22 interaction between DDB2 and NEDD4L in human ovarian cancer cells.

23 increases the IL-8 expression and release in ovarian cancer cells.

24 isense gene silencing effects in A2780 human ovarian cancer cells.

25 eased HIF, cell migration, and metastasis of ovarian cancer cells.

26 an important role in cisplatin resistance in ovarian cancer cells.

27 synergistically decrease the growth rate of ovarian cancer cells.

28 to silence MDR genes in cisplatin-resistant ovarian cancer cells.

29 pression induced by proteasome inhibition in ovarian cancer cells.

30 an be overcome by inhibition of autophagy in ovarian cancer cells.

31 t of STAT3 for HO-3867-mediated apoptosis in ovarian cancer cells.

32 s the proliferative and invasive behavior of ovarian cancer cells.

33 on factors and their respective promoters in ovarian cancer cells.

34 s cells and tissues but induced apoptosis in ovarian cancer cells.

35 regulator of BRK and IGF-1Rbeta signaling in ovarian cancer cells.

36 for key CRL4 substrate adaptors required for ovarian cancer cells.

37 nt in different cancers including breast and ovarian cancer cells.

38 ific roles in colonization of the omentum by ovarian cancer cells.

39 uting to the genotoxic effects of MLN4924 in ovarian cancer cells.

40 platin-resistant (NCI/ADR-RES and A2780CP20) ovarian cancer cells.

41 the molecular mechanism of proliferation in ovarian cancer cells.

42 ence of p53 on proinflammatory chemokines in ovarian cancer cells.

43 le for TR3 in cisplatin-induced apoptosis in ovarian cancer cells.

44 cid, risedronate and GGTI-2133 in a panel of ovarian cancer cells.

45 for the survival and proliferation of human ovarian cancer cells.

46 r with ERalpha/ERbeta-expressing SKOV3 human ovarian cancer cells.

47 active Rac1 leads to EMT in epithelial-like ovarian cancer cells.

48 lass I and class II molecules exclusively on ovarian cancer cells.

49 signaling mechanisms of MAGEA1 in breast and ovarian cancer cells.

50 anti-proliferative activities were tested in ovarian cancer cells.

51 nchymal traits displayed by mesenchymal-like ovarian cancer cells.

52 is essential to stem-like characteristics in ovarian cancer cells.

53 entry, shows efficacy against PTX-resistant ovarian cancer cells.

54 f PI3K involved in lamellipodia formation of ovarian cancer cells.

55 l cancer cells, including platinum-resistant ovarian cancer cells.

56 s) and fibroblasts (CAFs) than in those from ovarian cancer cells.

57 and altered gene expression in prostate and ovarian cancer cells.

58 HIF-1alpha, which promotes proliferation of ovarian cancer cells.

59 increasing prostaglandin E2 (PGE2) levels in ovarian cancer cells.

60 In the patient derived ovarian cancer cells, a similar correlation was observed

61 tored early tumor growth of engineered human ovarian cancer cells (A2780) implanted orthotopically in

62 nti-proliferative effect on human epithelial ovarian cancer cells, A2780/WT and A2780/PTX(R), induced

63 tified Nectin-4 shedding from the surface of ovarian cancer cells after stimulation with lysophosphat

64 rian cancer cells and tissues and that human ovarian cancer cells also express the Angpt receptor Tie

65 uld effectively inhibit the proliferation of ovarian cancer cells and induce cell apoptosis.

66 rate that metastasis-associated behaviors of ovarian cancer cells and MCAs are influenced by cellular

67 Elevated levels of ErbB3 in ovarian cancer cells and NRG1 in the omentum allowed for

68 d platinum-sensitive and platinum- resistant ovarian cancer cells and ovarian cancer stem cells and (

69 9), which is upregulated in human breast and ovarian cancer cells and released from apoptotic tumor c

70 most induced microRNA by 1,25(OH)(2)D(3) in ovarian cancer cells and subsequently validated by quant

71 a synthetic lethal manner in ARID1A-mutated ovarian cancer cells and that ARID1A mutational status c

72 Angpt1, Angpt2, and Angpt4 are increased in ovarian cancer cells and tissues and that human ovarian

73 AMG655 with Apo2L/TRAIL extended to primary ovarian cancer cells and was further enhanced by combina

74 nd migration in PAK1-amplified/overexpressed ovarian cancer cells, and has no effect in cell that lac

75 stasis activate the wild type p53 pathway in ovarian cancer cells, and OGA inhibition has the potenti

76 Using ovarian cancer cells as a model, we show that mitochondr

77 r uptake of PEG(5k)-CA(8) nanoparticles into ovarian cancer cells as validated in SKOV3-luc tumor-bea

78 Notably, reintroduction of CIB2 in ovarian cancer cells blocked plasma membrane localizatio

79 uppressed the outgrowth of cisplatin-treated ovarian cancer cells both in vitro and in vivo Combinati

80 lated with autophagy induction in a panel of ovarian cancer cells but not in immortalized human ovari

81 tly labeled hormones to alphavbeta3-positive ovarian cancer cells but not to integrin-negative cells.

82 TGF-beta has limited effects on ovarian cancer cells, but its contributions to ovarian t

83 d VCAN promoted the motility and invasion of ovarian cancer cells by activating the NF-kappaB signali

84 l that EMT can be induced in epithelial-like ovarian cancer cells by co-expressing constitutively act

85 we explore the impact of VEPH1 expression in ovarian cancer cells by gene-expression profiling.

86 y controls caspase-2-dependent cell death of ovarian cancer cells by inhibiting mTOR, placing mTOR as

87 ial-to-mesenchymal transition (EMT) in human ovarian cancer cells by overexpression of key transcript

88 t p53 inhibits proinflammatory chemokines in ovarian cancer cells by reducing proteasomal degradation

89 that TGF-beta enhanced the aggressiveness of ovarian cancer cells by upregulating VCAN in CAFs.

90 t that the malignant phenotype of metastatic ovarian cancer cells can be altered by miR21 delivered b

91 patients, we find that exosomes derived from ovarian cancer cells can be identified by their expressi

92 find that ARID1B knockdown in ARID1A mutant ovarian cancer cells causes similar loss of enhancer arc

93 We also provide evidence that ovarian cancer cells classified as cisplatin-resistant c

94 on on tumor cells, we analyzed fresh primary ovarian cancer cells collected from patient ascites and

95 bition of cell proliferation was observed in ovarian cancer cells compared to CHOK1.

96 is study, we observed high HuR expression in ovarian cancer cells compared with ovarian primary cells

97 signaling events that underlie metastasis in ovarian cancer cells, consistent with a prometastatic ro

98 In vitro treatment of breast and ovarian cancer cell cultures in aqueous media by tamoxif

99 2133 (IC50 > 25 muM) inhibited the growth of ovarian cancer cell cultures.

100 Silencing GPAM in ovarian cancer cells decreased cell migration and reduce

101 approved noncancer drugs to selectively kill ovarian cancer cells derived from patients with chemothe

102 lating ST6Gal-I expression in pancreatic and ovarian cancer cells directly altered CSC spheroid growt

103 Ovarian cancer cells disseminate readily within the peri

104 ntified a novel role for AURKA in regulating ovarian cancer cell dissemination and evaluated the effi

105 Transient transfection of p53 into p53-null ovarian cancer cells downregulated proinflammatory chemo

106 ignificantly inhibited NE- and hTERT-induced ovarian cancer cell EMT and invasion.

107 active Rac1, we conclude that Rac1 sustains ovarian cancer cell EMT through simultaneous activation

108 In functional investigations in ovarian cancer cells, engineered upregulation of certain

109 ression of hTERT induced expression of Slug, ovarian cancer cell epithelial-mesenchymal transition (E

110 as localized predominantly in the nucleus of ovarian cancer cells examined, contrasting with plasma m

111 rthermore, in an ex vivo colonization assay, ovarian cancer cells exhibited increased adhesion to mes

112 we showed that acquired cisplatin-resistant ovarian cancer cells expressed high levels of MKP-1 and

113 the tumor growth and migratory phenotypes of ovarian cancer cells expressing SHMT1 shRNAs.

114 Primary ovarian cancer cells from patient ascites or solid tumor

115 In contrast, silencing of LNK decreased ovarian cancer cell growth in vitro and in vivo.

116 ellular internalization and stability of the ovarian cancer cell growth inhibitor peptide, LSCQLYQR (

117 screen to identify gene pairs that inhibited ovarian cancer cell growth when they were targeted.

118 ing Vprbp/Dcaf1 did not significantly affect ovarian cancer cell growth, even though it was expressed

119 Cytotoxicity was studied with ovarian cancer cells having high (SKOV-3), intermediate

120 y against cisplatin-resistant A2780Cis human ovarian cancer cells (IC50 74 muM, blue light) with a ph

121 In the serous ovarian cancer cells (IGROV and OVCAR-3), shPKCiota decr

122 s a major regulator of angiogenic program in ovarian cancer cells impacting HB-EGF signaling and subs

123 damage, cell cycle arrest, and apoptosis in ovarian cancer cells in a time- and dose-dependent manne

124 aneously implanted cisplatin-resistant human ovarian cancer cells in athymic nude mice.

125 ates all three arms of the UPR in breast and ovarian cancer cells in culture and in a mouse xenograft

126 ficantly decreased migration and invasion in ovarian cancer cells in the presence of NE and decreased

127 well as invasion and migration capacities of ovarian cancer cells in vitro Administration of miR-6126

128 against folate receptor 1 (FOLR1)-expressing ovarian cancer cells in vitro and in vivo Unlike convent

129 f-reinforcing loop decreases invasiveness of ovarian cancer cells in vitro and limits ovarian cancer

130 in A549 lung adenocarcinoma cells and MA148 ovarian cancer cells in vitro.

131 ratory and invasive properties of aggressive ovarian cancer cells in vitro.

132 pithelial-to-mesenchymal transition (EMT) of ovarian cancer cells in vivo, STAT4 failed to induce EMT

133 more, loss of FER impaired the metastasis of ovarian cancer cells in vivo.

134 lar biological responses on c-MET-expressing ovarian cancer cells including increase of cell prolifer

135 produced marked changes in the phenotype of ovarian cancer cells, including an increase in resistanc

136 ted the secretion of several chemokines from ovarian cancer cells, including CXCL1, CXCL2 and CXCL8.

137 or caspase-2 is required for robust death of ovarian cancer cells induced by FASN inhibitors.

138 induction is mostly tumor-type-specific with ovarian cancer cells inducing primarily ovarian TVMs, wh

139 on of GAB2 by inducible small hairpin RNA in ovarian cancer cells inhibited tumor cell proliferation,

140 hormone-dependent, cisplatin-resistant human ovarian cancer cells, inhibiting IDO by transcriptional

141 Ce (0.1 mg/kg body weigh) treatment of A2780 ovarian cancer cells injected intra-peritoneally in nude

142 ing of hTERT expression abrogated NE-induced ovarian cancer cell invasion, EMT and Slug expression.

143 Suppressing KDM4B inhibits ovarian cancer cell invasion, migration and spheroid for

144 ipt and protein expression, and subsequently ovarian cancer cell invasion.

145 of MLK3 is required for suppression of SKOV3 ovarian cancer cell invasion.

146 namido ethyleneamine complexes towards human ovarian cancer cells is enhanced by up to 50 x in the pr

147 erstanding of the mechanism of metastasis in ovarian cancer cells is essential to the design of effec

148 n-125, which is found on the surface of many ovarian cancer cells is known to be a gold standard clin

149 mined by the expression of HS6ST isoforms in ovarian cancer cells, is a major regulator of angiogenic

150 Furthermore, in primary human ovarian cancer cells isolated from patient ascites, HO-3

151 ient mice than did ROR1-negative (ROR1(Neg)) ovarian cancer cells isolated from the same tumor popula

152 d depletion of endogenous RNase L in a human ovarian cancer cell line (Hey1b) increased the levels of

153 motifs were identified and validated from an ovarian cancer cell line (OVCAR-3).

154 Following infection of a human ovarian cancer cell line (OVCAR3) with a recombinant low

155 ration/survival of both an established human ovarian cancer cell line (OVCAR8) and a subset of primar

156 The mutation frequency of the ovarian cancer cell line A2780, analyzed at the HPRT loc

157 ts and HDAC inhibitory activity in the human ovarian cancer cell line A2780, the human squamous carci

158 NVs) as small as 30 kb in single cells of an ovarian cancer cell line and as small as 9 Mb in two hig

159 pic implantation of the human drug-resistant ovarian cancer cell line HeyA8-MDR, followed by porous s

160 an invasive variant of the murine epithelial ovarian cancer cell line ID8-T.

161 atin's ability to induce tumor cell death in ovarian cancer cell line in vitro and in vivo.

162 tors PP242 or rapamycin-sensitized DOV13, an ovarian cancer cell line incapable of inducing REDD1, to

163 d colorectal cancer cells and the unexplored ovarian cancer cell line NIH:OVCAR-3, with respective PN

164 ne fusions missed by other algorithms in the ovarian cancer cell line OVCAR3.

165 Using an UNG2-deficient ovarian cancer cell line that is hypersensitive to floxu

166 multi-isoform genes in a stem cell line, an ovarian cancer cell line, and a breast cancer cell line

167 vaccine using whole cell lysate of a murine ovarian cancer cell line, ID8 was prepared by spray dryi

168 As such, an ovarian cancer cell line, OV-90, was cultured in adheren

169 el supported by in vitro experiments with an ovarian cancer cell line.

170 H1 variants, H1.3, in the OVCAR-3 epithelial ovarian cancer cell line.

171 cell death and DNA damage was studied in two ovarian cancer cell lines (OVCAR3 and A2780), normal ham

172 with elevated expression in the majority of ovarian cancer cell lines (three SDs above the mean of n

173 minescence signals from ES-2 and SKOV3 human ovarian cancer cell lines after IP injection.

174 DH1-bright (ALDH1(br)) cells from epithelial ovarian cancer cell lines and characterized the properti

175 APOBEC3B is active in the nucleus of several ovarian cancer cell lines and elicits a biochemical pref

176 in molecular profiles between commonly used ovarian cancer cell lines and high-grade serous ovarian

177 Here we analyse a panel of 47 ovarian cancer cell lines and identify those that have t

178 purification and culture of PGCCs from human ovarian cancer cell lines and primary ovarian cancer.

179 (Pol eta) in ovarian CSCs isolated from both ovarian cancer cell lines and primary tumors, indicating

180 ow that MICU1 is overexpressed in a panel of ovarian cancer cell lines and that MICU1 overexpression

181 and quantitative (phospho-)proteomes of five ovarian cancer cell lines and the global cancer genome r

182 Using human ovarian cancer cell lines as well as malignant epithelia

183 and carboplatin on 10 different cervical and ovarian cancer cell lines as well as on the ability of t

184 ere are approximately 100 publicly available ovarian cancer cell lines but their cellular and molecul

185 The bioenergetics phenotype of ovarian cancer cell lines correlated with functional phe

186 We generated several novel murine ovarian cancer cell lines derived from the ovarian surfa

187 MGCR), was found to be over-expressed in all ovarian cancer cell lines examined and upregulated by mu

188 portantly, we found that cisplatin-resistant ovarian cancer cell lines exhibit lower levels of MOAP-1

189 in the peritoneal cavity, whereas aggressive ovarian cancer cell lines failed to form tumors or metas

190 spheroids compared to monolayer cultures of ovarian cancer cell lines or primary cells.

191 ated that the levels of FER were elevated in ovarian cancer cell lines relative to those in immortali

192 wn-regulation of HS6ST-1 or HS6ST-2 in human ovarian cancer cell lines results in 30-50% reduction in

193 ing of 13 established and 12 patient derived ovarian cancer cell lines revealed significant bioenerge

194 B gene silencing restored the sensitivity of ovarian cancer cell lines to cisplatin in vitro.

195 Comprehensive profiling of 39 ovarian cancer cell lines under controlled, uniform cond

196 We have characterized 39 ovarian cancer cell lines under uniform conditions for g

197 Downregulation of CtBP2 expression in ovarian cancer cell lines using short-hairpin RNA strate

198 in the MDA-MB-231 breast cancer and SK-OV-3 ovarian cancer cell lines with IC50 values of 11.0 and 2

199 and ZEB1 attenuated mesothelial clearance in ovarian cancer cell lines with strong activity.

200 ncing of HSulf-1 in OV202 and TOV2223 cells (ovarian cancer cell lines) resulted in increased lipid d

201 Of the 39 ovarian cancer cell lines, 14 were assigned as high-grad

202 These loops operate in several ovarian cancer cell lines, and BRCA1-IRIS silencing or i

203 port the integrated proteomic analysis of 26 ovarian cancer cell lines, HGSOC tumours, immortalized o

204 either overexpressed or silenced in several ovarian cancer cell lines.

205 as induced by Wee1 inhibition in breast and ovarian cancer cell lines.

206 ormal ovary and tumor samples and epithelial ovarian cancer cell lines.

207 mples and with cisplatin resistance in human ovarian cancer cell lines.

208 etween PKCiota and cyclin E in a panel of 19 ovarian cancer cell lines.

209 e of origin and histopathology of epithelial ovarian cancer cell lines.

210 a tumor-associated antigen overexpressed in ovarian cancer cells, making it a potential target for i

211 PET imaging of CA125 expression by ovarian cancer cells may enhance the evaluation of the e

212 not a phospho-inhibitory mutant, stimulated ovarian cancer cell migration and invasion, correlating

213 enhance lysophosphatidic acid (LPA)-induced ovarian cancer cell migration.

214 n tumors, and showed how TGF-beta stimulates ovarian cancer cell motility and invasion by upregulatin

215 ling pathways mediate the effect of MFAP5 on ovarian cancer cell motility and invasion potential.

216 In the current study, culture of epithelial ovarian cancer cells on three-dimensional collagen I gel

217 TSC2 RNAi protected FASN inhibitor-sensitive ovarian cancer cells (OVCA420 cells) from orlistat-induc

218 Ovarian cancer cells overexpressing GAB2 are dependent o

219 ry epithelial cells and clonogenic growth of ovarian cancer cells overexpressing GAB2.

220 fferentiation capacity of four heterogeneous ovarian cancer cell populations defined by the expressio

221 We demonstrated that ALDH(+) ovarian cancer cells possess multiple stem cell characte

222 cancer microenvironment, as well as enhance ovarian cancer cell proliferation and invasion in vivo.

223 mones as potent alphavbeta3-ligands, driving ovarian cancer cell proliferation and suggest that disru

224 expression, ultimately mediating FSH-driven ovarian cancer cell proliferation.

225 e uniquely and directly capable of promoting ovarian cancer cell proliferation.

226 Overexpression of SIK2 in ovarian cancer cells promotes abdominal metastasis while

227 dings suggest that overexpression of GAB2 in ovarian cancer cells promotes tumor growth and angiogene

228 growth and metastasis, specifically blocking ovarian cancer cell recruitment to the ovary.

229 re, we show that disabling CDK12 function in ovarian cancer cells reduces BRCA1 levels, disrupts HR r

230 wever, molecular mechanism sustaining EMT of ovarian cancer cells remains elusive.

231 parib) while overexpression of USP13 renders ovarian cancer cells resistant to chemotherapy.

232 ntiproliferative behavior against epithelial ovarian cancer cells resistant to cisplatin.

233 that this property is maintained in vivo in ovarian cancer cells resistant to paclitaxel.

234 diminish nuclear accumulation of platinum in ovarian cancer cells, resulting in resistance to platinu

235 Thus, ovarian cancer cells seem to display heterogeneity in us

236 their antiproliferative properties in human ovarian cancer cells sensitive and resistant to cisplati

237 ALDH(-) ovarian cancer cells showed no engraftment in the hESCT

238 RNAi-mediated silencing of HuR in ovarian cancer cells significantly decreased cell prolif

239 2, Cul4a, and DDB1 had inhibitory effects on ovarian cancer cells similar to MLN4924 treatment, which

240 noncanonical, or other pathways in the human ovarian cancer cell SKOV-3.

241 combination index analysis studies in human ovarian cancer cells (SKOV-3) and rat cardiomyocytes (H9

242 platform for the automated quantification of ovarian cancer cells (SKOV3) from whole blood is reporte

243 Ovarian cancer cells, SKOV3, have been immobilized onto

244 Invasive ovarian cancer cells spontaneously formed protrusions, s

245 HOXA9 expression in ovarian cancer cells stimulated chemotaxis of peritoneal

246 ession of matrix metalloprotease (MMP)-14 on ovarian cancer cells stimulates a tumor-stromal signalin

247 line (OVCAR8) and a subset of primary serous ovarian cancer cell strains (DFs).

248 However, CRL roles in ovarian cancer cell survival and the ovarian tumor repre

249 me-dependent manner, with greater effects in ovarian cancer cells than in breast cancer cells.

250 REDD1 induction is compromised in ovarian cancer cells that do not respond to FASN inhibit

251 gulation of metastasis-associated behaviors, ovarian cancer cells that express low endogenous levels

252 In ovarian cancer cells that have developed acquired cispla

253 s and reverses multi-drug resistance against ovarian cancer cells through downregulation of survivin.

254 d migration, invasion, and tumorigenicity of ovarian cancer cells through NF-kappaB activation, which

255 light, the prodrug effectively killed SKOV-3 ovarian cancer cells through the combined effects of PDT

256 ed depletion or inhibition of ATR sensitized ovarian cancer cells to all four agents.

257 loss of Pak1 function causes 11q13-amplified ovarian cancer cells to arrest in the G2/M phase of the

258 apeutics, expression of CIB2 also sensitized ovarian cancer cells to carboplatin.

259 Depleting or inhibiting USP13 sensitizes ovarian cancer cells to cisplatin and PARP inhibitor (ol

260 ance (MDR) genes and resensitizing resistant ovarian cancer cells to cisplatin treatment.

261 nduced autophagy and subsequently sensitizes ovarian cancer cells to cisplatin-induced apoptosis.

262 and Chk1 inhibitors differentially sensitize ovarian cancer cells to commonly used chemotherapy agent

263 eatment with UC-961 impaired the capacity of ovarian cancer cells to form spheroids or tumor xenograf

264 cumulation and sensitized HE4-overexpressing ovarian cancer cells to fulvestrant and tamoxifen.

265 In addition, MLN4924 sensitized ovarian cancer cells to other chemotherapeutic drug trea

266 To evaluate whether the response of ovarian cancer cells to pitavastatin is potentiated by f

267 how inhibiting DNA methylation can sensitize ovarian cancer cells to platinum drugs, in large part by

268 itaxel (PTX) and doxorubicin (DOX) resistant ovarian cancer cells to PTX and DOX by inhibiting surviv

269 ition promoted oncogenic behavior by leading ovarian cancer cells to release more exosomes.

270 wever, the tumor-specific factors that allow ovarian cancer cells to spread are unclear.

271 sduction and increases the responsiveness of ovarian cancer cells to TGF-beta-induced growth inhibiti

272 at CLDN3 and CLDN4 affect sensitivity of the ovarian cancer cells to the cytotoxic effect of cDDP by

273 e in vivo hTERT expression and metastasis of ovarian cancer cells to the lung.

274 RCP was sufficient to enhance metastasis of ovarian cancer cells to the lung.

275 indicate that OvCa429 and SKOV3ip epithelial ovarian cancer cells undergo similar morphological and c

276 pective roles of the ATR and Chk1 kinases in ovarian cancer cells using genetic and pharmacologic inh

277 ectivity of organo-Os complex FY26 for human ovarian cancer cells versus normal lung fibroblasts to 6

278 from both chemosensitive and chemoresistant ovarian cancer cells via exosomes.

279 tes underwent selective internalization into ovarian cancer cells via PRLR-mediated endocytosis.

280 nduced reduction in E-cadherin expression in ovarian cancer cells was mediated by C3a and is Kruppel-

281 detection in serum samples and measuring of ovarian-cancer cells was also investigated.

282 cisplatin-sensitive and cisplatin resistant ovarian cancer cells, was observed.

283 To investigate the role of histone H1 in ovarian cancer cells, we characterize individual H1 vari

284 get ODNs specific to Homo sapiens Breast and ovarian cancer cells were detected at femtomolar concent

285 st of mesenchymal traits in mesenchymal-like ovarian cancer cells, whereas expressing constitutively

286 its clonal growth, migration and invasion of ovarian cancer cells, whereas silencing in vivo inhibits

287 is and suppressing migration and invasion in ovarian cancer cells, which indicates its therapeutic po

288 rogen receptor-alpha (ERalpha) activation in ovarian cancer cells, which was suppressed by 1alpha,25-

289 Co-incubation of ovarian cancer cells with ascites fluid significantly in

290 the activities of Erk and Src are higher in ovarian cancer cells with constitutively active Rac1, we

291 hibition in suppressing clonogenic growth of ovarian cancer cells with GAB2 overexpression.

292 asion, and promotes E-cadherin expression in ovarian cancer cells with high-Gab2 expression.

293 array of the chemokine network revealed that ovarian cancer cells with low or mutated p53 expression

294 , and downregulates E-cadherin expression in ovarian cancer cells with low-Gab2 expression.

295 rt-chain C6-ceramide decreased the number of ovarian cancer cells with PI3KC2beta-driven lamellipodia

296 Using pancreatic and ovarian cancer cells with ST6Gal-I knockdown or overexpr

297 Ovarian cancer cells with stable shRNA- or transient siR

298 ic activity of MEK inhibitors in KRAS-mutant ovarian cancer cells, with reciprocal downregulation of

299 evealed the presence of grossly metastasized ovarian cancer cells within the lymphoid tissues.

300 n and cell death whose modulation might kill ovarian cancer cells without the attendant side effects.