ライフサイエンスコーパス: melanoma cell

1 crophages and high uptake by SPARC(+) B16F10 melanoma cells).

2 umulation of gallium corroles was fastest in melanoma cells).

3 y are potent against endogenous AC in intact melanoma cells.

4 uine, also induced the expression of CCL5 in melanoma cells.

5 Indeed, AC expression is abnormally high in melanoma cells.

6 dherin disassembly in response to metastatic melanoma cells.

7 apoptotic pathways and induces cell death in melanoma cells.

8 cathepsin B in MDA-MB-435S, A375, and C8161 melanoma cells.

9 bly important for the malignant phenotype of melanoma cells.

10 for the MSX1-induced migratory phenotype in melanoma cells.

11 nd relatively selective cytotoxicity against melanoma cells.

12 We first examined its role in established melanoma cells.

13 croM of ascorbate induced apoptosis in A2058 melanoma cells.

14 s, particularly a loss of PTEN in aggressive melanoma cells.

15 stress, and necrotic death also in B16 mouse melanoma cells.

16 esulted in reduced proliferative capacity of melanoma cells.

17 he establishment of drug resistance in human melanoma cells.

18 metastases in response to challenge with B16 melanoma cells.

19 resses invasion and the growth of aggressive melanoma cells.

20 DR5 levels in both human thyroid cancer and melanoma cells.

21 at CD147 regulates MMP-2 expression in uveal melanoma cells.

22 astrocytes in facilitating initial growth of melanoma cells.

23 l migration and invasion in human and murine melanoma cells.

24 ules for direct CD4(+) T cell recognition of melanoma cells.

25 11 was ectopically expressed in nonpigmented melanoma cells.

26 growth or survival properties of mutant NRAS melanoma cells.

27 e of adipocyte exosomes, FAO is increased in melanoma cells.

28 nase signaling and growth of N-Ras-dependent melanoma cells.

29 cantly attenuated the malignant phenotype of melanoma cells.

30 augment both angiogenesis and metastasis of melanoma cells.

31 from subsequent challenge by unmodified B16 melanoma cells.

32 ed that T-oligo can form G4 in the nuclei of melanoma cells.

33 e myeloid attractant CCL2 in BRAFi-resistant melanoma cells.

34 diate resistance to BRAF inhibitors in human melanoma cells.

35 cal circadian clock in mouse melanocytes and melanoma cells.

36 e gene encoding for AC, ASAH1, in human A375 melanoma cells.

37 igenetic modulators against human metastatic melanoma cells.

38 molecule anle138b, we explored its effect on melanoma cells.

39 7 activities and promoted apoptosis in human melanoma cells.

40 of the tumorigenic phenotype of B16F10-Nex2 melanoma cells.

41 osis and inhibited proliferation of cultured melanoma cells.

42 ning malignancy and self-renewal of invasive melanoma cells.

43 e show that Src-induced invadosomes in human melanoma cells (A375M and MDA-MB-435) undergo rapid remo

44 al cell contractility abrogates migration of melanoma cells across endothelial monolayers.

45 The mechanisms by which some melanoma cells adapt to Serine/threonine-protein kinase

46 upregulated by tumor blood vessels, of which melanoma cell adhesion molecule (MCAM) and its extracell

47 We further identify the melanoma cell adhesion molecule (MCAM) as a novel KDM3A

48 cted four cell membrane glycoproteins, CD146/melanoma cell adhesion molecule (MCAM)/MUC18, CD31/plate

49 o-survival role of mitochondrial function in melanoma cells after oncogenic MAPK inhibition.

50 Results have shown a striking spread of melanoma cells along preexisting microvascular channels

51 itor of invasion differentially expressed in melanoma cells and healthy melanocytes.

52 le anti-cancer characteristics in A375 human melanoma cells and in a metastatic melanoma model in mic

53 nificantly reduced or absent in nonpigmented melanoma cells and lost during human melanoma progressio

54 HPR is effective in killing both the bulk of melanoma cells and MICs.

55 ncrease in proliferative potential of Hs294T melanoma cells and normal immortalized Mel-ST melanocyte

56 of Ino80, the SWI/SNF ATPase, is elevated in melanoma cells and patient melanomas compared with norma

57 Using brain-seeking patient-derived melanoma cells and real-time in vivo imaging, we show a

58 ession induced by MAPK pathway inhibition in melanoma cells and sensitizes melanoma cells with NRAS o

59 e brain metastasis of human lung, breast and melanoma cells and their therapeutic responses to chemot

60 AMIGO2 is upregulated in melanoma cells and tissues compared to human melanocytes

61 of MITF in vemurafenib-resistant BRAF(V600E)-melanoma cells and underlies the increased invasion in t

62 reased sensitivity of BRAF(Val600Glu)-mutant melanoma cells and xenograft tumors to BRAFi.

63 ival and motility of RAC1(P29S)-mutant human melanoma cells, and on tumor formation and progression f

64 y identified a large population of apoptotic melanoma cells, and single-cell electrophoresis indicate

65 proach is not curative, as some BRAF-mutated melanoma cells are intrinsically resistant to MAPK inhib

66 We have studied whether melanoma cells are phenotypically distinct and hierarchi

67 We also found and that RAC1-mutant human melanoma cells are resistant to clinical inhibitors of B

68 ostaglandin E synthases in Braf(V600E) mouse melanoma cells, as well as in Nras(G12D) melanoma or in

69 ignificantly overexpressed in multiple human melanoma cells at mRNA and protein levels.

70 Cranial neural crest and metastatic melanoma cells avoid DAN protein stripes in vitro.

71 ssociated with melanocyte proliferation, and melanoma cells bearing this mutation are insensitive to

72 aging demonstrates that after extravasation, melanoma cells become pigmented and enact a gene express

73 l calcium dysregulation and ATP depletion in melanoma cells but not in normal cells.

74 ficantly (P < 0.001) inhibited the growth of melanoma cells but not normal melanocytes.

75 ll viability in a subset of glucose-deprived melanoma cells, but synergizes with acetate to support c

76 Induction of matrix metalloproteinases in melanoma cells by longwave UVA radiation, possibly via a

77 t of NK cells and TRAIL-dependent killing of melanoma cells by macrophages.

78 r the enhanced killing of ganetespib treated melanoma cells by T cells.

79 ll-mediated killing of patient-derived human melanoma cells by their autologous T cells in vitro and

80 Melanoma cells can adopt two functionally distinct forms

81 Here we show that human melanoma cells can display profound transcriptional vari

82 we show that exosomes from poorly metastatic melanoma cells can potently inhibit metastasis to the lu

83 a highly tumorigenic subpopulation of mouse melanoma cells, can be selected by being cultured and gr

84 loped and validated with perfused human DB-1 melanoma cells carrying the BRAF V600E mutation, which p

85 matically accelerated syncytium formation in melanoma cells caused by fusion of infected cells with m

86 support the hypothesis that miR-211 loss in melanoma cells causes abnormal regulation of energy meta

87 f miR-211-mediated downregulation of PDK4 in melanoma cells causes inhibition of invasion by nonpigme

88 We show a clear dependence of melanoma cell-cell adhesion on pHe and NHE1 as a modulat

89 e cells, but could reverse the resistance of melanoma cells chronically treated with vemurafenib.

90 of the SPRY4 gene, is up-regulated in human melanoma cells compared to melanocytes.

91 Human melanoma cells constitutively produce the growth factor

92 hat cytoplasmic transfer from macrophages to melanoma cells correlates with melanoma invasion and ari

93 interaction increases ER stress, leading to melanoma cell death by concomitant induction of autophag

94 hat treatment with anle138b leads to massive melanoma cell death due to a major dysregulation of auto

95 Glucose-deprived melanoma cells depend on both oxidative phosphorylation

96 (FTIR) spectra of intact hydrated B16 mouse melanoma cells deprived of RNA and to highlight the in-c

97 ometry, that Hsp90 or BRAF inhibitor-induced melanoma cell differentiation resulted in an upregulatio

98 rophage cytoplasmic transfer correlated with melanoma cell dissemination.

99 pathways of immunosuppression elaborated by melanoma cells dominate the tumor microenvironment and h

100 In BRAF mutant melanoma cells, ectopic CK2alpha decreased sensitivity t

101 rong efficacy in xenograft mouse models with melanoma cells either sensitive or resistant to BRAF inh

102 the cells are drug-addicted, suggesting that melanoma cells evolve a 'just right' level of mitogen-ac

103 Significance: These findings show that human melanoma cells express high levels of the immune checkpo

104 ith prominent nuclear localization of NLRP1, melanoma cells expressed NLRP1 mainly in the cytoplasm.

105 ptide biosensor to quantify CDK4 activity in melanoma cell extracts, skin biopsies and melanoma xenog

106 tance and contribute to suboptimal growth of melanoma cells following the withdrawal of BRAF inhibiti

107 to detect melanin induction in SKMEL28 human melanoma cells, following inhibition of Hsp90 and BRAF s

108 sing via endocytosis, sensitized neighboring melanoma cells for CD4(+) T cell recognition.

109 microenvironment regulate the transition of melanoma cells from actin-driven protrusion to blebbing,

110 e that facilitates the therapeutic escape of melanoma cells from BRAF inhibition.

111 We found that CD271(-) and CD271(+) melanoma cells from each of seven patients were similarl

112 Melanoma cells from two of three late recurrent metastas

113 In addition to having high AC levels, melanoma cells generate lower amounts of ceramides than

114 the secreted flavoprotein RNLS in promoting melanoma cell growth and CD163(+) TAM in the tumor micro

115 cing MEK1/2 and ERK1/2 signaling, inhibiting melanoma cell growth and inducing apoptosis.

116 In addition, GV affects melanoma cell growth by promoting mitochondrial apoptosi

117 m the roots of Cryptolepis sanguinolenta, on melanoma cell growth.

118 tumor effects both in vitro and in vivo in a melanoma cells harboring the BRAF fusion.

119 E5) expression increases the invasiveness of melanoma cells; hence, pharmacological inhibition of PDE

120 PGC1alpha silencing makes poorly metastatic melanoma cells highly invasive and, conversely, PGC1alph

121 eres, elicits potent DNA-damage responses in melanoma cells; however, its mechanism of action is larg

122 , downregulation of MITF induces invasion in melanoma cells; however, little is known about the under

123 the photoacoustic signal from a circulating melanoma cell immediately hardware-triggers a lethal pin

124 with\ Pin1 in BRAF(V600E)-driven metastatic melanoma cells impaired both FOXM1 activity and cell sur

125 itor Gant61 led to decreased invasion of the melanoma cells in a three-dimensional skin reconstruct m

126 abel-free imaging of rare single circulating melanoma cells in both arteries and veins of mice.

127 s are validated by analyzing the invasion of melanoma cells in collagen matrices of varying concentra

128 owed significant anticancer activity against melanoma cells in cytotoxicity, colony formation, and ce

129 king peptides repressed the proliferation of melanoma cells in freshly isolated human metastatic mela

130 icient to decrease lung colonization by A375 melanoma cells in NSG mice, relative to control cells.

131 10 (PTEN), alters the invasive potential of melanoma cells in response to WNT/beta-catenin signaling

132 cular expression of Serpin B2 by angiotropic melanoma cells in the murine brain and in human melanoma

133 nhibit ATX-dependent invasion of A2058 human melanoma cells in vitro.

134 increased after TET2 overexpression in human melanoma cells in vitro.

135 nchronized by medium changes, and in B16-F10 melanoma cells, in the presence of the selective OPN4 an

136 significantly reduced the viability of other melanoma cells, including those resistant to mono-treatm

137 ly, overexpression of miR-200a in metastatic melanoma cells induces cell cycle arrest by targeting CD

138 elanocytes and nevi, and AMIGO2 silencing in melanoma cells induces G1/S arrest followed by apoptosis

139 gulated fusion was investigated by comparing melanoma cells infected with wild-type-like VZV or hyper

140 and showed that disruption of FMN2 in mouse melanoma cells inhibits their extravasation and metastas

141 del to analyze the interactions of GFP human melanoma cells injected into the mouse brain with red fl

142 t be improved by taking the Wnt signature of melanoma cells into account.

143 le mitochondria, we injected B16rho(0) mouse melanoma cells into syngeneic C57BL/6N(su9-DsRed2) mice

144 that AR can have positive roles to increase melanoma cell invasion in multiple cell lines in vitro a

145 chanism dissection suggest that AR increases melanoma cell invasion via modulating the MITF-AXL signa

146 novel tumor suppressive microRNA that blocks melanoma cell invasion without affecting cell survival.

147 p by an antagomiR was sufficient to increase melanoma cell invasion, an effect that could be phenocop

148 s required for MITF-dependent suppression of melanoma cell invasion, tumorigenicity and lung coloniza

149 Restoring MITF can reverse AR-enhanced melanoma cell invasion.

150 We demonstrate that G1-arrested melanoma cells, irrespective of the underlying cause med

151 wn-regulation of microRNA-200a expression in melanoma cells is associated with disease progression an

152 finavir is effective in BRAF and NRAS mutant melanoma cells isolated from patients progressed on MAPK

153 he formulated lipoplexes to internalize into melanoma cells, knockdown the expression of the BRAF pro

154 Knockdown of endogenous RNF157 in melanoma cells leads to late S phase and G2/M arrest and

155 le genome sequencing of a matched metastatic melanoma cell line (COLO829) and normal across three lin

156 co-culture experiment with human metastatic melanoma cell line (SKMEL- 147) and immortalized keratin

157 ry in a cell-based assay for invasion by the melanoma cell line A375.

158 Restoration of 5-hmC, as assessed in a human melanoma cell line by introducing full-length TET2 and T

159 We established a melanoma cell line from a tumor with none of the common

160 A murine melanoma cell line highly metastatic to lymph nodes (B16

161 onducted a microarray on a highly metastatic melanoma cell line in which NFAT1 expression was stably

162 A transplantable mouse MPNST-like melanoma cell line recapitulated mast cell recruitment i

163 blocked ERK phosphorylation and growth in a melanoma cell line, suggesting that it may provide a hig

164 n primary melanocytes and a highly pigmented melanoma cell line, we demonstrate that reduced expressi

165 ghly expressing alphavbeta3 human metastatic melanoma cell line.

166 ted cell response to UV radiations also in a melanoma cell line.

167 II, which reduced the viability of the DB-1 melanoma cell line.

168 way activation in a BRAF(V600E)-mutant human melanoma cell line.

169 Treatment of human melanoma cell lines (A375, Hs294t, SK-Mel28 and SK-Mel11

170 y knocking down of NLRP1 in human metastatic melanoma cell lines 1205Lu and HS294T, indicating that N

171 anti-proliferative activity against various melanoma cell lines and could induce G2/M phase arrest a

172 of comparing CDK4 activity between different melanoma cell lines and further responds to CDK4 downreg

173 In multiple human melanoma cell lines and in melanoma patient-derived xeno

174 the related inhibitor cystatin E/M occur in melanoma cell lines and to evaluate to what extent the u

175 NFAT1 expression and metastatic potential in melanoma cell lines and tumor specimens.

176 e found that CK2alpha protein is elevated in melanoma cell lines compared with normal human melanocyt

177 oma-associated marker tyrosinase in adherent melanoma cell lines corresponding to different cancer pr

178 ort that TTM inhibited transformed growth of melanoma cell lines resistant to BRAF or MEK1/2 inhibito

179 erences were found in human NRAS(Q61) mutant melanoma cell lines that were also more sensitive to pha

180 nhibition remodeled the signaling network of melanoma cell lines that were BRAF mutant and PTEN null.

181 tin limited the responses of these PTEN-null melanoma cell lines to vemurafenib, with enhanced cytoto

182 Accordingly, NFAT1 depletion in metastatic melanoma cell lines was associated with reduced IL8 and

183 A subset of acquired drug-resistant melanoma cell lines was sensitive to Gamitrinib.

184 ensitivity profiling revealed that PTEN(LOF) melanoma cell lines were sensitive to PI3Kbeta inhibitor

185 To develop this approach, melanoma cell lines were treated with AKT inhibitor AZD5

186 produce robust calcium mobilization in human melanoma cell lines which can be blocked by the CXCR4-se

187 ion and protein synthesis in patient-derived melanoma cell lines with acquired resistance to combined

188 is study, we demonstrate that in BRAF(V600E) melanoma cell lines, activating MEK mutations drive resi

189 as verified at transcript level in different melanoma cell lines, and at protein level in A2058 cells

190 CTLA4 is also highly expressed by most human melanoma cell lines, as well as in normal human melanocy

191 n normal human melanocytes and proliferative melanoma cell lines, compared with other skin cells (ker

192 TF transcriptional and oncogenic activity in melanoma cell lines, derived from human melanoma patient

193 first presented here in two human amelanotic melanoma cell lines, derived from vertical growth phase

194 In melanoma cell lines, elevated baseline expression relied

195 n isoform 2 was overexpressed in BRAF mutant melanoma cell lines, melanoma cell proliferation and in

196 ing siRNA-mediated knockdown across multiple melanoma cell lines, we determined that loss of GABPA re

197 In this study, across 60 melanoma cell lines, we find bimodal expression patterns

198 Specifically, we demonstrate that melanoma cell lines, with acquired in vitro-induced vemu

199 25W was enriched to MAF = 0.65 in the NCI-60 melanoma cell lines.

200 d resistance to BRAFi and in BRAFi-resistant melanoma cell lines.

201 panel of patient-derived BRAF(V600) -mutant melanoma cell lines.

202 analysis of 216 melanoma tumors and 13 human melanoma cell lines.

203 Motivated by experimental observations on melanoma cells lines (1205Lu and SBcl2) migrating on fib

204 fibroblasts in close contact with PEDF-null melanoma cells lost PEDF expression and tumor-suppressiv

205 aise the possibility that CTLA4 targeting on melanoma cells may contribute to the clinical immunobiol

206 in vitro binding was performed using B16F1 (melanoma cells), MCF-10A (breast epithelial cells), and

207 n a series of experiments, using human uveal melanoma cells (MEL 270), human embryonic kidney cells (

208 -activated protein kinase pathways abolishes melanoma cell migration and angiogenesis.

209 Moreover, nifuroxazide markedly impaired melanoma cell migration and invasion by down-regulating

210 We found that FOSL1 is involved in melanoma cell migration as well as cell proliferation an

211 increased expression of these genes promotes melanoma cell motility and early steps in metastasis.

212 highlighting pigment-producing cells as the melanoma cell of origin, and indicate that regional vari

213 mouse models to define the role of MCSCs as melanoma cells of origin, demonstrate that MCSC quiescen

214 icle hybrids presented here comprised either melanoma cells or prostate cancer cells stably adorned w

215 se type glycans in melanocytes (HEMa-LP) and melanoma cells originating from the radial growth phase

216 ontain a high level of HDAC1/2 and malignant melanoma cells overexpress HDAC1/2/3 compared with nonca

217 etween tumor and stromal cells revealed that melanoma cells produced PDGF-BB and TGFbeta, which block

218 xpressed in BRAF mutant melanoma cell lines, melanoma cell proliferation and in vivo tumor growth wer

219 ith a small-molecule inhibitor reduces uveal melanoma cell proliferation and tumorigenesis in a mouse

220 ermore, Ino80 silencing selectively inhibits melanoma cell proliferation, anchorage-independent growt

221 To test whether AC might contribute to melanoma cell proliferation, we blocked AC activity usin

222 gether with its unusual metabolic effects in melanoma cells provide evidence that mensacarcin targets

223 is a molecular switch that is turned off in melanoma cells, raising the hope that in the future we m

224 e and macroautophagy targeting could improve melanoma cell recognition by CD4(+) T cells and should b

225 OO(-), and Ca(2+) ions, and more than 50% of melanoma cells remain viable in the presence of millimol

226 Whether and how GV affects melanoma cells remains unknown.

227 NA to the basal epidermis/upper dermis where melanoma cells reside.

228 o counteract HDAC- and RAD51/FANCD2-mediated melanoma cell resistance.

229 demonstrate that CRAF overexpression renders melanoma cells resistant to BRAF-targeting agents.

230 We generated A375 melanoma cells resistant to vemurafenib with the goal of

231 We studied melanoma cell responses to transient exposure to the cyt

232 pin RNA-mediated knockdown of SIRT3 in human melanoma cells resulted in (i) a decrease in cellular pr

233 , low microRNA-200a expression in metastatic melanoma cells results in higher levels of CDK6 and a mo

234 h encode subunits of the cohesin complex, in melanoma cells results in resistance to BRAFi.

235 Melanoma cells share many biological properties with neu

236 Internalization studies using B16F1 melanoma cells show 60.7% of the cell-bound activity was

237 At an early stage, melanoma cells showed a dedifferentiated c-Jun(high)/MIT

238 rsion and illustrate the mechanisms by which melanoma cells silence stromal PEDF to promote malignanc

239 of the human CTLA4 gene in a melanocyte and melanoma cell-specific manner.

240 pes and confirmed very high toxicity against melanoma cells, specifically the LOX IMVI and SK-MEL-28

241 nt and full activation of a mesenchymal-like melanoma cell state program.

242 r level for cultured healthy melanocytes and melanoma cells, suggesting a limit of pharmacological as

243 ovided protection against apoptosis in human melanoma cells, suggesting a suppressive role of NLRP1 i

244 haracterized by the formation of clusters of melanoma cells surrounded by keratinocytes constraining

245 r supporting its important role in promoting melanoma cell survival and progression.

246 multaneous treatment synergistically reduced melanoma cell survival and tumor growth.

247 Thus, we conclude that IFN-gamma promotes melanoma cell survival by regulating CD74-MIF signaling,

248 an RNLS-derived inhibitory peptide decreased melanoma cell survival, and anti-RNLS therapy blocked tu

249 molecule, as a BET target gene essential for melanoma cell survival.

250 es, displayed anti-cancerous activity on all melanoma cells tested, including cells isolated from pat

251 goxin, are significantly more toxic to human melanoma cells than normal human cells.

252 sis and metastatic colonization than control melanoma cells that are grown on rigid plastic.

253 relationships between CD271(-) and CD271(+) melanoma cells that are inconsistent with classical, epi

254 ic drug resistance is an escape mechanism of melanoma cells that has implications on the choice and t

255 activates a multi-step signalling cascade in melanoma cells that results in a decrease in beta-cateni

256 Within populations of melanoma cells, there is a marked heterogeneity in PGC1a

257 upts the interaction between PHB and CRAF in melanoma cells, thus reducing MEK1/2 and ERK1/2 signalin

258 bition of class I HDACs sensitizes malignant melanoma cells to apoptosis following exposure to alkyla

259 -mediated model of vemurafenib resistance in melanoma cells to assess the importance of the interacti

260 Loss of APE1 attenuates the response of melanoma cells to DNA damage induced by reactive oxygen

261 We tested 2,368 genes expressed by melanoma cells to identify those that synergize with or

262 r profoundly sensitizes BRAF and NRAS mutant melanoma cells to MAPK-pathway inhibitors.

263 Here we perturbed genes in human melanoma cells to mimic loss-of-function mutations invol

264 xpression, which is known to be critical for melanoma cells to shift between differentiated and invas

265 ibition of HDAC1/2/3 caused sensitization of melanoma cells to temozolomide in vitro and in melanoma

266 ease progression, reprograms melanocytes and melanoma cells toward a neural crest precursor-like stat

267 l level (100 muM) increased 5 hmC content in melanoma cells toward the level of healthy melanocytes.

268 Melanoma cells transduced to express FIST15 failed to es

269 Melanoma cells treated using these agents are known to e

270 Applying our approach to human melanoma cells treated with a panel of cancer therapeuti

271 f class I HDACs on the response of malignant melanoma cells treated with alkylating agents.

272 d the proliferative kinetics of BRAF-mutated melanoma cells treated with the BRAF inhibitor PLX4720 f

273 ve intracellular domain of Notch4 (N4ICD) in melanoma cells triggered a switch from a mesenchymal-lik

274 etic potential and mitochondrial activity of melanoma cells, triggered through regulation of pro-surv

275 Loss of STING function rendered melanoma cells unable to produce type I IFN and other im

276 Deletion of p205 in B16 melanoma cells using CRISPR/Cas9 showed a similar loss o

277 n demonstrate refined clonal trackability of melanoma cells using this scheme.

278 shRNA-mediated down-regulation of MITF in melanoma cells was accompanied by down-regulation of BPT

279 arising from intradermal injection of B16 F1 melanoma cells was also reduced in comparison to control

280 of the BRAF protein and induce cell death in melanoma cells was studied by fluorescent microscopy, in

281 expression of both miRNA in drug-naive human melanoma cells was sufficient to confer vemurafenib resi

282 11, a known metabolic switch in nonpigmented melanoma cells, was severely down-regulated in vitiligo

283 c optical absorption contrast of circulating melanoma cells, we developed dual-wavelength photoacoust

284 respectively, while that of drug-susceptible melanoma cells were 40,197+/-222 Omega and 4069+/-79 Ome

285 These melanoma cells were highly sensitive to CRAF, but not BR

286 it is found in both cytosol and nucleus) and melanoma cells (where it is primarily localized to cytos

287 STING signaling is recurrently suppressed in melanoma cells, where this event may enable immune escap

288 known as JARID1B)-positive subpopulation of melanoma cells, which are slow-cycling and treatment-res

289 mensacarcin exposure, SK-Mel-28 and SK-Mel-5 melanoma cells, which have the BRAF(V600E) mutation asso

290 motes the survival of primary and metastatic melanoma cells, which is the exact opposite of the effec

291 Murine B16 melanoma cells, which overproduce TGFbeta, were lysed by

292 wn that intrinsically resistant BRAF-mutated melanoma cells with a low basal level of mitochondrial b

293 Of clinical relevance, pretreatment of melanoma cells with a mitogen-activated protein kinase p

294 fine the physiologic relevance of this loop, melanoma cells with different Wnt status were treated in

295 Melanoma cells with high Wnt5A and low beta-catenin disp

296 Treatment of melanoma cells with HSP70 inhibitors decreased levels of

297 inhibition in melanoma cells and sensitizes melanoma cells with NRAS or BRAF plus NRAS mutations to

298 by Hsp90 and BRAF-MEK-targeted therapies in melanoma cells with potential significance for in vivo i

299 An RNA microarray analysis of B16F10-Nex2 melanoma cells with SOCS1 silenced by shRNAi-SOCS1 was u

300 addition, we observed that the proportion of melanoma cells within the total population has increased