ライフサイエンスコーパス: ovarian cancer cell

1 ion and epithelial-mesenchymal transition of ovarian cancer cells.

2 pha mRNA and release of TNF-alpha protein in ovarian cancer cells.

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

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

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

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

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

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

9 activates the IGF1R/STAT3 signaling axis in ovarian cancer cells.

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

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

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

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

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

15 and inducing a metabolic shift in metastatic ovarian cancer cells.

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

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

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

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

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

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

22 ynergistic antiproliferative effects against ovarian cancer cells.

23 2 in the regulation of TGF-beta signaling in ovarian cancer cells.

24 ing feature underlying the aggressiveness of ovarian cancer cells.

25 ignaling and suppressed stemness features of ovarian cancer cells.

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

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

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

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

30 ely associated with paclitaxel resistance in ovarian cancer cells.

31 ne sets regulated by miR-200 in both OSE and ovarian cancer cells.

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

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

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

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

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

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

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

39 GLS-expressing but not in low GLS-expressing ovarian cancer cells.

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

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

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

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

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

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

46 synergistically decrease the growth rate of ovarian cancer cells.

47 e a vital biomarker overexpressed in primary ovarian cancer cells.

48 inflammatory mediators in response to LPA in ovarian cancer cells.

49 n for visualization and diagnosis of primary ovarian cancer cells.

50 ion enhanced the CDDP sensitivity of hypoxic ovarian cancer cells.

51 ownregulation of p-Drp1 (Ser637) and Mfn1 in ovarian cancer cells.

52 le for the transactivation of EGFR by LPA in ovarian cancer cells.

53 tokines that stimulate glycogen breakdown in ovarian cancer cells.

54 p in monounsaturated fatty acid synthesis in ovarian cancer cells.

55 to disrupt peritoneal spread and adhesion of ovarian cancer cells.

56 uced apoptosis, and reduced proliferation of ovarian cancer cells.

57 cell death, dramatically inhibits growth of ovarian cancer cells.

58 sitivity to cisplatin (CDDP) was examined in ovarian cancer cells.

59 mitochondrial fission and CDDP resistance in ovarian cancer cells.

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

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

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

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

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

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

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

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

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

69 NETs, in turn, bound ovarian cancer cells and promoted metastasis.

70 omental niche conducive for implantation of ovarian cancer cells and raise the possibility that bloc

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

72 underlying the reciprocal interplay between ovarian cancer cells and surrounding stromal cell types

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

74 te the highly orchestrated crosstalk between ovarian cancer cells and various cancer-associated strom

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

76 target genes IL8 and HIF1A in immune cells, ovarian cancer cells, and endothelial cells.

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

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

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

80 silenced, HR+, CARM1-high, high-grade serous ovarian cancer cells become PARPi sensitive, undergo mit

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

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

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

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 that miR-450a acts as a tumor suppressor in ovarian cancer cells by modulating targets associated wi

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

89 ivity can be restored in cisplatin-resistant ovarian cancer cells by targeting the chromatin-associat

90 tential of Lyso-Gal for detection of primary ovarian cancer cells by using beta-gal as the biomarker.

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

92 , these results show that targeting FABP4 in ovarian cancer cells can inhibit their ability to adapt

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

94 depletion, led to metabolic reprogramming of ovarian cancer cells, causing decreased mitochondrial re

95 the critical regulator of lipid responses in ovarian cancer cells cocultured with adipocytes.

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

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

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

99 f the MYC oncogene in tumor cells, including ovarian cancer cells, correlates with poor responses to

100 evel is extremely low in cisplatin resistant ovarian cancer cells, correlating with higher levels of

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

102 2133 (IC50 > 25 muM) inhibited the growth of ovarian cancer cell cultures.

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

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

105 d expression transiently increased following ovarian cancer cell detachment and in tumor cells derive

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

107 Ovarian cancer cells disseminate readily within the peri

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

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

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

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

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

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

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

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

116 tes binding to its cognate receptor CCR-2 on ovarian cancer cells facilitates migration and omental m

117 pes of ovarian cancer and that SCD1 protects ovarian cancer cells from cell death.

118 Primary ovarian cancer cells from patient ascites or solid tumor

119 ibitor TMI-1 or by shRNA knockdown prevented ovarian cancer cells from releasing TNF-alpha protein in

120 olecular signature of the primary epithelial ovarian cancer cells from which they are derived.

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

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

123 in vitro inhibitor of PTP4A3 and human A2780 ovarian cancer cell growth was reduced.

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

125 Highly selective imaging of ovarian cancer cells has been achieved upon incubation w

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

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

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

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

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

131 etastasis of ovarian cancer, and survival of ovarian cancer cells in the peritoneal cavity as nonadhe

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

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

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

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

136 TGFbeta reduces MHC-I expression in ovarian cancer cells in vitro.

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

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

139 in vitro PTX efficacy in ID8-VEGF epithelial ovarian cancer cells, in vivo studies were performed upo

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

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

142 we systematically assessed in vivo growth of ovarian cancer cells, including six validated HGSC cell

143 GB3 attenuates cisplatin resistance in human ovarian cancer cells, increasing tumor cell sensitivity

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

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

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

147 TLN1 suppresses lactotransferrin's effect on ovarian cancer cell invasion potential and proliferation

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

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

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

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

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

153 Uncontrolled growth of ovarian cancer cells is the fifth leading cause of femal

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

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

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

157 ising antiproliferative effects in the human ovarian cancer cell line A2780 and the human squamous ca

158 RNA-seq analysis of the ovarian cancer cell line A2780 revealed that overexpress

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

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

161 In vitro chemotherapy treatment increased ovarian cancer cell line capacity to activate prosurviva

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

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

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

165 MDR1 inhibition in a fusion positive ovarian cancer cell line increased sensitivity to paclit

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

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

168 studies performed in uMUC1-expressing human ovarian cancer cell line SKOV3/Luc and control uMUC1(low

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

170 er agents, we developed and characterized an ovarian cancer cell line that is resistant to a previous

171 This TRIP-resistant ovarian cancer cell line, A2780TR, was found to be 9 tim

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

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

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

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

176 tive to TRIP compared to the wild-type A2780 ovarian cancer cell line.

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

178 tumor effect of ferroptosis inducers in both ovarian cancer cell lines and a mouse orthotopic xenogra

179 ent-derived xenografts and high-grade serous ovarian cancer cell lines and discover clone-specific dy

180 Here, we show that a subset of ovarian cancer cell lines and ex vivo models derived fro

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

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

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

184 CDK9 was highly expressed in human ovarian cancer cell lines and was also elevated in metas

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

186 tivity against sensitive and resistant A2780 ovarian cancer cell lines but is only marginally active

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

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

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

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

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

192 as shown that many of the most commonly used ovarian cancer cell lines have been mischaracterised, le

193 In this study, we cultured ovarian cancer cell lines in adherent and nonadherent co

194 the proliferation of a subset of clear cell ovarian cancer cell lines in vitro.

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

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

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

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

199 itro chemotherapy response across a panel of ovarian cancer cell lines revealed that increased IGF-1R

200 Here, we use 10 epithelial ovarian cancer cell lines to investigate 2D migration, c

201 s9-mediated deletion of DAB2IP in epithelial ovarian cancer cell lines upregulated expression of stem

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

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

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

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

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

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

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

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

210 igen presentation complex in human and mouse ovarian cancer cell lines.

211 AR-3, SKOV-3, and TYKNu) and one mouse (ID8) ovarian cancer cell lines.

212 viability, characteristics of less invasive ovarian cancer cell lines.

213 ns in BRCA1 from samples of human breast and ovarian cancer cell lines.

214 istant cell lines were established using two ovarian cancer cell lines: SKOV3ip1 and HeyA8.

215 the growth, survival or apoptosis in several ovarian cancer cells lines.

216 Here we report that ovarian cancer cells manifest a spectrum of tumorigenic

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

218 ination with anti-PD-L1, in two novel murine ovarian cancer cell models.

219 tor) reduced growth and peritoneal spread of ovarian cancer cells more effectively than either single

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

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

222 monstrate that antiproliferative activity in ovarian cancer cells (OVCAR8) depends on CDK2 degradatio

223 Ovarian cancer cells overexpressing GAB2 are dependent o

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

225 Here we report that ovarian cancer cells overexpressing glutaminase (GLS), a

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

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

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

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

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

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

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

233 iated knockout of FABP4 in high-grade serous ovarian cancer cells reduced metastatic tumor burden in

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

235 nisms that govern this metastatic process in ovarian cancer cells remain poorly understood.

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

237 s study describes the mechanism exhibited by ovarian cancer cells required for adherent cell transiti

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

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

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

241 Ovarian cancer cells retained intrinsic sensitivity to p

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

243 ivo models we show that secondary epithelial ovarian cancer cells (sEOC) do not fully reacquire the m

244 e effects of dual IGF-1R/ErbB3 inhibition on ovarian cancer cell signaling, growth, and in vivo effic

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

246 lysosomal beta-gal detection and imaging in ovarian cancer cells (SKOV-3 cells).

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

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

249 Inhibition of CDK9 also suppressed ovarian cancer cell spheroid growth, clonogenicity forma

250 Invasive ovarian cancer cells spontaneously formed protrusions, s

251 In conclusion, CA-MSC activate ovarian cancer cell STAT3 signaling via IL6 and LIF and

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

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

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

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

256 In ovarian cancer cells that have developed acquired cispla

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

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

259 chymal transition is required for epithelial ovarian cancer cells to acquire metastatic potential, th

260 1 depletion and NNMT upregulation sensitized ovarian cancer cells to agents that inhibit mitochondria

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

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

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

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

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

266 Adipocytes are critical for ovarian cancer cells to home to the omentum, but the met

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

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

269 on of lysyl oxidase (LOX) in mesothelial and ovarian cancer cells to promote collagen crosslinking an

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

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

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

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

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

275 d differences in the resistance responses of ovarian cancer cells to TRIP and conventional drugs.

276 1 transfection increased CDDP sensitivity of ovarian cancer cells under hypoxia.

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

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

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

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

281 PIK3R1 loss renders ovarian cancer cells vulnerable to inhibition of AKT or

282 Therapeutically, p85beta expression renders ovarian cancer cells vulnerable to inhibitors of AXL, p1

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

284 Downregulation of ACP6 in ovarian cancer cells was necessary and sufficient to sup

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

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

287 FZD7(+) platinum-tolerant ovarian cancer cells were more sensitive and underwent f

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

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

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

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

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

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

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

295 Here, we show that ovarian cancer cells with higher level of NADP(+), an NA

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

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

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.