ライフサイエンスコーパス: cancer cell growth

1 a, among other small molecules, also impairs cancer cell growth.

2 ive kinase signaling, which is essential for cancer cell growth.

3 litates lung cancer progression by promoting cancer cell growth.

4 ne and vitamin D to suppress KSHV-associated cancer cell growth.

5 NRG1, in turn, activates YAP and stimulates cancer cell growth.

6 because androgens are essential for prostate cancer cell growth.

7 ion, attenuated Wnt signaling, and repressed cancer cell growth.

8 t MSI2 loss-of-function abrogates colorectal cancer cell growth.

9 es AR-dependent gene expression and prostate cancer cell growth.

10 t protein kinase 4 (CaMKIV) to control liver cancer cell growth.

11 nucleotides and are indispensable for human cancer cell growth.

12 ecific HIF-dependent expression and prostate cancer cell growth.

13 inhibit CREB-mediated gene transcription and cancer cell growth.

14 ced AR transcriptional activity and prostate cancer cell growth.

15 al to the tumor microenvironment and promote cancer cell growth.

16 nced genes that encode negative mediators of cancer cell growth.

17 simulated to predict their ability to reduce cancer cell growth.

18 rone, which might be repositioned to control cancer cell growth.

19 homeostatic mechanism, to increase prostate cancer cell growth.

20 stem cell niche factor, and an inhibitor of cancer cell growth.

21 ed by AR, which in turn facilitates prostate cancer cell growth.

22 ation, binding of colchicine to tubulin, and cancer cell growth.

23 ologically restoring BRM and thereby inhibit cancer cell growth.

24 treated with fatty acid, E2 promoted breast cancer cell growth.

25 ted degradation of DHFR and to inhibition of cancer cell growth.

26 ntly decreases FOXA1 expression and prostate cancer cell growth.

27 loid cells is sufficient to inhibit prostate cancer cell growth.

28 other tumors and are required for efficient cancer cell growth.

29 n of OGT was sufficient to decrease prostate cancer cell growth.

30 r the deleterious effects of MMP-8 on breast cancer cell growth.

31 main eliminated suppression of PC-3 prostate cancer cell growth.

32 anscriptional activity and promotes prostate cancer cell growth.

33 ase activity and thereby selectively inhibit cancer cell growth.

34 r and has a role in the regulation of breast cancer cell growth.

35 rogression by secreting factors that mediate cancer cell growth.

36 d expression of AR target genes and prostate cancer cell growth.

37 of SOCS3 and SOCS4 and this is essential for cancer cell growth.

38 to identify 3D-specific effectors of breast cancer cell growth.

39 at LIN28A functions as an oncogene promoting cancer cell growth.

40 ed in most human cancers and is critical for cancer cell growth.

41 d eEF2 phosphorylation with little effect on cancer cell growth.

42 was reported to correlate with inhibition of cancer cell growth.

43 Like siRNA, A-484954 had little effect on cancer cell growth.

44 rectly affect anti-tumor immune function and cancer cell growth.

45 ogen-dependent gene transcription and breast cancer cell growth.

46 olism and support a role for ASAH1 in breast cancer cell growth.

47 ctivation and anchorage-independent prostate cancer cell growth.

48 l mechanism for CYP3A4 involvement in breast cancer cell growth.

49 ng the effects of the Reptin-AGR2 complex in cancer cell growth.

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

51 egradation by miR-934 promotes human bladder cancer cell growth.

52 ated proteins and plays an important role in cancer cell growth.

53 for exercise-dependent suppression of breast cancer cell growth.

54 erases that function in pathways critical to cancer cell growth.

55 breast cancer cells, selectively suppresses cancer cell growth.

56 called the Warburg effect, is important for cancer cell growth.

57 f the metabolic reprogramming that underlies cancer cell growth.

58 synergize with DNA-damaging agent to inhibit cancer cell growth.

59 other mitogens to enter the CSF and promote cancer cell growth.

60 can positively or negatively regulate human cancer cell growth.

61 racellular asparagine levels is critical for cancer cell growth.

62 first time that FSTL-1 suppresses pancreatic cancer cell growth.

63 ignaling networks, resulting in reduction of cancer cell growth.

64 ch drugs to inhibit KRAS(G12C) signaling and cancer cell growth.

65 rs, and its inhibition can result in reduced cancer cell growth.

66 androgen-dependent AR program, and prostate cancer cell growth, acting, at least in part, by functio

67 Silencing Stat3 blocks breast cancer cell growth and abrogates (+/-)-14,15-EET-induced

68 Stromal SOD3 had a stimulatory effect on cancer cell growth and an inhibitory effect on cancer ce

69 Significantly, kaempferol inhibits cancer cell growth and angiogenesis and induces cancer c

70 lular screens reveal compounds that modulate cancer cell growth and angiogenesis in vitro.

71 ppaB/miR-148a/152 feedback loop can regulate cancer cell growth and angiogenesis, and is also associa

72 ins, an effect associated with inhibition of cancer cell growth and apoptosis.

73 ansduction pathways for inhibition of breast cancer cell growth and can be used as a dietary suppleme

74 ptional activity, and also promoted prostate cancer cell growth and castration resistance.

75 ession of miR-502 inhibited autophagy, colon cancer cell growth and cell-cycle progression of colon c

76 Knock-down of plectin inhibits prostate cancer cell growth and colony formation in vitro, and gr

77 sion, and biologically Ajuba promotes breast cancer cell growth and contributes to tamoxifen resistan

78 uggesting a role for purinergic signaling in cancer cell growth and death.

79 models through two mechanisms: inhibition of cancer cell growth and deregulation of angiogenesis.

80 umor microenvironment and actively stimulate cancer cell growth and dissemination.

81 icroenvironment, and are often used to study cancer cell growth and drug efficacy.

82 that high DAPK1 expression causes increased cancer cell growth and enhanced signaling through the mT

83 in cellular microenvironment for inhibiting cancer cell growth and even metastasis.

84 the presence of DPP, resulting in attenuated cancer cell growth and eventually cell death.

85 Tailoring siRNAs to silence genes vital for cancer cell growth and function could be an effective tr

86 of enzymatic activity of PRP4 in regulating cancer cell growth and identified an array of potential

87 ransduction takes a significant part in lung cancer cell growth and in vivo tumorigenesis.

88 XL2 stabilized cyclin D3 levels, accelerated cancer cell growth and increased cell viability after vi

89 of TR3 by RNA interference (siTR3) inhibited cancer cell growth and induced apoptosis.

90 suppressed MDA-MB231 triple negative breast cancer cell growth and induced apoptosis.

91 4a inhibited cancer cell growth and induced cell death by various mec

92 adopt a secretory phenotype that facilitates cancer cell growth and invasion when they become senesce

93 ispensable for CAF-mediated ECM remodelling, cancer cell growth and invasion, DKK3-driven YAP/TAZ act

94 o induced apoptosis and decreased pancreatic cancer cell growth and invasion, indicating that downreg

95 ARA70 isoform, ARA70beta, promotes prostate cancer cell growth and invasion.

96 tor tyrosine kinase that plays a key role in cancer cell growth and invasion.

97 y cytokines favoring a permissive milieu for cancer cell growth and invasive behavior.

98 ases C-MYC stability, resulting in increased cancer cell growth and invasiveness.

99 at extracellular lumican inhibits pancreatic cancer cell growth and is associated with prolonged surv

100 a histone demethylase that promotes gastric cancer cell growth and is enriched in drug-resistant lun

101 DBeQ also potently inhibits cancer cell growth and is more rapid than a proteasome i

102 -metabolizing enzyme that also has a role in cancer cell growth and metabolism.

103 kt is a critical protein kinase that governs cancer cell growth and metabolism.

104 ms through which CXCR4 contributes to breast cancer cell growth and metastases are poorly understood.

105 Increased PRSS8 expression inhibited cancer cell growth and metastasis in nude mice and inhib

106 The elevated mTORC2 promotes cancer cell growth and metastasis via Akt(S437) phosphor

107 ng the translation of proteins implicated in cancer cell growth and metastasis.

108 lectin is an important regulator of prostate cancer cell growth and metastasis.

109 motes MYC degradation, and markedly inhibits cancer cell growth and metastasis.

110 erleukin (IL)-6 and TNF-alpha, which promote cancer cell growth and metastasization.

111 -MYC and SRC-3 oncoproteins, FBXL16 promoted cancer cell growth and migration and colony formation in

112 R)-dependent manner to influence both breast cancer cell growth and migration.

113 of HGF/MET in beta-catenin-mediated prostate cancer cell growth and progression and implicate a molec

114 in multiple anabolic processes that support cancer cell growth and proliferation (reviewed in ref.

115 rder to tackle the major hurdle of increased cancer cell growth and proliferation.

116 consolidates metabolic programs that sustain cancer cell growth and proliferation.

117 E235Q) promotes anchorage-independent breast cancer cell growth and resistance to gefitinib, U0126, a

118 he oncogenic REGgamma-proteasome, attenuates cancer cell growth and sensitizes p53-compromised cells

119 We then showed GATA2 promotes breast cancer cell growth and stimulates AKT phosphorylation by

120 ands for Fyn-related kinase), which inhibits cancer cell growth and suppresses tumorigenesis.

121 mportant role in tumorigenesis by supporting cancer cell growth and suppressing oncogene-induced sene

122 bolic pathway reprogramming is a hallmark of cancer cell growth and survival and supports the anaboli

123 downstream AREG-EGFR signaling in human MEC cancer cell growth and survival in vitro and in vivo usi

124 Metastasis depends upon cancer cell growth and survival within the metastatic ni

125 cited a substantially stronger inhibition of cancer cell growth and survival, protein synthesis, cell

126 nd that fibroblasts confer effects on breast cancer cell growth and survival.

127 nal coactivator BRD4, a protein critical for cancer cell growth and survival.

128 ds to the loss of Mst1 functions, supporting cancer cell growth and survival.

129 a protein homeostatic pathway essential for cancer cell growth and survival.

130 cell lung cancer (NSCLC) and is required for cancer cell growth and survival.

131 cylate induced apoptosis and decreased colon cancer cell growth and the sodium salt of aspirin also i

132 bility to inhibit hormone-independent breast cancer cell growth and to regulate ERalpha and cyclin D1

133 that arsenic trioxide (ATO) suppresses human cancer cell growth and tumor development in mice by inhi

134 hibited TNFalpha-induced NF-kappaB activity, cancer cell growth and tumor growth in an ovarian cancer

135 tiple targets, they elicit potent effects on cancer cell growth and tumorigenesis.

136 pathway has an important regulatory role in cancer cell growth and tumorigenesis.

137 lighted miRNAs, substantially repressed lung cancer cell growth and tumorigenicity in a dose-dependen

138 ith LARGE overexpression is shown to inhibit cancer cell growth and tumorigenicity.

139 in an enzymatic assay, while also inhibiting cancer cell growth and viability and activating p53-depe

140 we find that loss of SREBP activity inhibits cancer cell growth and viability by uncoupling fatty aci

141 nes, called E6 and E7, that are required for cancer cell growth and viability.

142 ion prevents the hypoxia-induced human colon cancer cells growth and invasion.

143 sion has an important role in promoting lung cancer cell growth, and that its oncogenic function is p

144 Genetic knockdown of G9a inhibits cancer cell growth, and the dimethylation of p53 K373 re

145 MKK2 function is sufficient to inhibit liver cancer cell growth, and the growth defect resulting from

146 s many cardinal features of cancer including cancer cell growth, apoptosis resistance, DNA damage res

147 against specific signaling pathways driving cancer cell growth, are needed to pave the way for the d

148 Furthermore, immune dormancy promotes cancer cell growth arrest and angiogenic control.

149 Curcumin induces cancer cell growth arrest and apoptosis in vitro, but it

150 nthesis, leading to inhibition of mTORC1 and cancer cell growth arrest.

151 cancer cells, autophagy is as essential for cancer cell growth as mRNA transcription or translation

152 ylation offers much potential for inhibiting cancer cell growth, as does disruption of interactions b

153 BET bromodomain inhibitors block prostate cancer cell growth at least in part through c-Myc and an

154 -38 at 1 microM, FL118 effectively inhibited cancer cell growth at less than nM levels in a p53 statu

155 6-methoxybenzo[b]furan (3g), which inhibited cancer cell growth at nanomolar concentrations (IC50 val

156 -3 protein degradation and was able to block cancer cell growth at nanomolar concentrations.

157 mor-associated macrophages inhibits prostate cancer cell growth, at least in part, by derepressing th

158 , PIM-1 kinase isoforms may promote prostate cancer cell growth, at least in part, through modulating

159 cells reduces E7 protein levels and inhibits cancer cell growth both in vitro and in tumor xenografts

160 howed that in prostate cancer, JQ1 inhibited cancer cell growth but promoted invasion and metastasis

161 antagonizes estradiol (E2) -dependent breast cancer cell growth, but exerts partial agonist/antagonis

162 e report that UNC45A is essential for breast cancer cell growth, but is dispensable for normal cell p

163 mTOR is a central mediator of cancer cell growth, but it also directs immune cell diff

164 0 inhibitor geldanamycin, Disruptin inhibits cancer cell growth by a nonapoptotic mechanism.

165 Rhophilin suppresses cancer cell growth by activating the Hippo pathway.

166 s citrate across cell membranes, halts liver cancer cell growth by altering both energy production an

167 MSI2 influenced breast cancer cell growth by altering ESR1 function.

168 AC8 expression strongly inhibited pancreatic cancer cell growth by attenuating cell-cycle progression

169 Treatment with C3 ablated prostate cancer cell growth by disruption of both beta-catenin/T-

170 s support the new notion that INZ suppresses cancer cell growth by dually targeting SIRT1 and IMPDH2.

171 igen-specific IgEs were reported to restrict cancer cell growth by engaging high-affinity Fc receptor

172 t PRMT5 may function as an oncogene to drive cancer cell growth by epigenetic inactivation of several

173 rovide evidence that PRMT5 promotes prostate cancer cell growth by epigenetically activating transcri

174 re examples of RNAa-based drugs that inhibit cancer cell growth by inducing expression of tumor suppr

175 PARP inhibitors (PARPi) prevent cancer cell growth by inducing synthetic lethality with

176 aradoxical role that GPC-1 plays in prostate cancer cell growth by interacting with stromal cells and

177 ent ubiquinone coenzyme Q(10.) Inhibition of cancer cell growth by MitoQ was associated with G(1)/S c

178 We found that KD of E6AP attenuates cancer cell growth by promoting cellular senescence in v

179 d anchorage-dependent and -independent colon cancer cell growth by reducing ERK-RSK phosphorylation a

180 We also provide evidence that SNHG1 promotes cancer cell growth by regulating gene expression both in

181 findings indicate that HIF-2alpha increases cancer cell growth by up-regulating YAP1 activity, sugge

182 er intrinsic properties of metastatic breast cancer cell growth can be regulated through an extrinsic

183 Depletion of hSETD1A inhibits colorectal cancer cell growth, colony formation, and tumor engraftm

184 at Toll-like receptor 4 (TLR4) drives breast cancer cell growth differentially based on the presence

185 These potent GSTO1 inhibitors suppress cancer cell growth, enhance the cytotoxic effects of cis

186 Schweinfurthins are potent inhibitors of cancer cell growth, especially against human central ner

187 p/Dcaf1 did not significantly affect ovarian cancer cell growth, even though it was expressed by ovar

188 tion by PLD2 determines the output of ERK in cancer cell growth factor signaling.

189 modifications important to tumorigenesis and cancer cell growth, here we report a chemoproteomic anal

190 ing, metabolic homeostasis, inflammation and cancer cell growth highlighting its potential as a thera

191 , GADD45, and PUMA expression and inhibiting cancer cell growth in a p53-dependent manner.

192 onstrate a novel mechanism of YHL-14 against cancer cell growth in bladder and colon cancer cell line

193 required for ERbeta-dependent inhibition of cancer cell growth in culture and in murine xenografts.

194 glutathione conjugates, prevents human colon cancer cell growth in culture as well as in nude mouse x

195 lso potently inhibits triple-negative breast cancer cell growth in human cells and in animal models b

196 As expected, loss of LATS1/2 promotes cancer cell growth in most cell lines.

197 d ATF mRNA resulted in inhibition of ovarian cancer cell growth in nude mice accompanied with Maspin

198 xygenase that promotes Stat3-mediated breast cancer cell growth in part through (+/-)-14,15-EET biosy

199 promising new therapeutic target to inhibit cancer cell growth in solid tumor types.

200 nstrate that the plasma-like B cells inhibit cancer cell growth in the early stage of NSCLC, but prom

201 ere found to be very effective inhibitors of cancer cell growth in the HupT3 (IC(50) = 50 nM) and Mia

202 on of Bcl-xL expression, followed by reduced cancer cell growth in the presence of Met-targeting drug

203 ate production and synergistically inhibited cancer cell growth in vitro (HepG2) and in vivo (H22).

204 tate resulted in a synergistic inhibition of cancer cell growth in vitro and an enhanced reduction of

205 which we found is able to potently suppress cancer cell growth in vitro and in vivo by binding beta-

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

207 of Wnt target genes as well as in colorectal cancer cell growth in vitro and in vivo.

208 Functionally, NOV inhibits prostate cancer cell growth in vitro and in vivo.

209 wild-type NADK in PDAC cell lines attenuates cancer cell growth in vitro and in vivo.

210 A-knockdown cells partially rescued prostate cancer cell growth in vitro and in vivo.

211 stically relieve gene silencing and suppress cancer cell growth in vitro and in xenografts.

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

213 hown that loss of SALL4 inhibits endometrial cancer cell growth in vitro and tumorigenicity in vivo,

214 tently, overexpression of ZMYND11 suppresses cancer cell growth in vitro and tumour formation in mice

215 As such, BMP2 suppressed bulk cancer cell growth in vitro but increased tumor initiati

216 xhibited greater inhibition of BT-474 breast cancer cell growth in vitro to a level that could not be

217 -yl)phenyl]amide (4a), suppresses pancreatic cancer cell growth in vitro with the lowest IC(50) value

218 4(nrb) and SREBP-1a were required for breast cancer cell growth in vitro, and p54(nrb) binding to nuc

219 I have been found to synergistically inhibit cancer cell growth in vitro, yet clinical studies of the

220 cancer and that miR-32 can improve prostate cancer cell growth in vitro.

221 nhibitor proteins and to suppress pancreatic cancer cell growth in vivo.

222 (PI3K) beta signaling is required to sustain cancer cell growth in which the tumor suppressor phospha

223 h the role of lipids as an energy source for cancer cell growth, in vivo time-course studies revealed

224 otently inhibited tubulin polymerization and cancer cell growth, including stimulation of natural kil

225 ng that this snoRNA-PAR partnership promotes cancer cell growth independent of DNA repair pathways.

226 am effects on client protein degradation and cancer cell growth inhibition has not been thoroughly in

227 Colon cancer cell growth inhibition was accompanied by downreg

228 Cancer cell growth inhibition was also demonstrated eith

229 edominant type II PRMT, produces synergistic cancer cell growth inhibition when combined with GSK3368

230 th low micromolar IC(50) in PAD activity and cancer cell growth inhibition.

231 ne products were derivatized and show potent cancer cell-growth inhibition.

232 internalization and stability of the ovarian cancer cell growth inhibitor peptide, LSCQLYQR (LR), is

233 Pladienolide B (PB) is a potent cancer cell growth inhibitor that targets the SF3B1 subu

234 w potent class of tubulin polymerization and cancer cell growth inhibitors with the potential to inhi

235 f multitudes of anchorage-independent breast cancer cell growth inhibitors.

236 ure of nanomolar PLK4 inhibitors with potent cancer cell growth inhibitory activity.

237 iple signal transduction pathways regulating cancer cell growth, invasion, metastasis, survival, and

238 molecular markers and pathways implicated in cancer cell growth is a promising avenue for developing

239 In mouse models of LM, cancer cell growth is supported by the LCN2/SLC22A17 sys

240 ism and protein synthesis, crosstalk to fuel cancer cell growth is unknown.

241 or overexpressed oncogenic proteins driving cancer cell growth, leading to the acceptance of Hsp90 a

242 ntify signaling pathways regulating prostate cancer cell growth led to our discovery that checkpoint

243 g receptors P2X7 and A2A signaling on breast cancer cell growth, migration and bone metastasis.

244 ast cancer cells effectively inhibits breast cancer cell growth, migration, and invasion in vitro, an

245 emonstrate that DZIP3 is a crucial driver of cancer cell growth, migration, and invasion.

246 e the loss of ERalpha significantly impaired cancer cell growth, migration, invasion and anchorage-in

247 ls that selective USP7 inhibition suppresses cancer cell growth predominantly through a p53-dependent

248 rations of intracellular metabolites lead to cancer cell growth, proliferation or death.

249 e dynamics and that the embryonal theory for cancer cell growth/proliferation is overly simplistic, a

250 blood vessel formation and contributing to a cancer cell growth-promoting milieu.

251 5 expression levels are well correlated with cancer cell growth rate and that p53 is able to negative

252 coholism drug, could potently inhibit breast cancer cell growth regardless of the PIK3CA status.

253 EDD9's potential biological role in prostate cancer cell growth regulation.

254 Cancer cell growth requires fatty acids to replicate cel

255 ed in CCA and that its up-regulation induces cancer cell growth retardation through multiple targets

256 Metabolic reprogramming facilitates cancer cell growth, so quantitative metabolic flux measu

257 ed the hypothesis that aldosterone regulates cancer cell growth/spread via G protein-coupled estrogen

258 While inflammation plays a critical role in cancer cell growth, studies remain uncharacterized on th

259 o promote epithelial-mesenchymal transition, cancer cell growth, survival in circulation, and angioge

260 Platelets also promote cancer cell growth, survival in circulation, and angioge

261 se/AKT signaling pathway plays a key role in cancer cell growth, survival, and angiogenesis.

262 , and AR, important for controlling prostate cancer cell growth, survival, and progression.

263 IL-8 promotes cancer cell growth, survival, angiogenesis, and metastas

264 ol 3-kinase (PI3K) signaling axis impacts on cancer cell growth, survival, motility, and metabolism.

265 nique source of signalling cues that affects cancer cell growth, survival, movement and metastasis.

266 2A and MAT2beta genes are required for liver cancer cell growth that is induced by the profibrogenic

267 nificant inhibitory effects on human bladder cancer cell growth that was accompanied by marked apopto

268 er, they display modest ability to attenuate cancer cell growth; their physicochemical properties, an

269 MiR-190a contributes the human prostate cancer cell growth through AR-dependent signaling.

270 s oncogenic stress, whereas it promoted lung cancer cell growth through inducing the cell proliferati

271 suggests that metformin directly antagonizes cancer cell growth through its actions on complex I of t

272 ctional role for macropinocytosis in fueling cancer cell growth through the internalization of extrac

273 trate that YHL-14 inhibits bladder and colon cancer cell growth through up-regulation of p21 expressi

274 l problems, ranging from circadian rhythm to cancer cell growth to longevity, have begun to give evid

275 to RT and investigated changes in colorectal cancer cell growth, transcriptome, metabolome, and kinom

276 Siah2 is required for prostate cancer cell growth under androgen-deprivation conditions

277 Of note, YAP1 activation was critical for cancer cell growth under hypoxia.

278 , both PIM-1 isoforms could promote prostate cancer cell growth under low-androgen conditions.

279 etyl-CoA synthetase 2 (ACSS2) contributes to cancer cell growth under low-oxygen and lipid-depleted c

280 results indicated that PL could inhibit lung cancer cell growth via inhibition of NF-kappaB signaling

281 erexpressed in prostate cancer and regulates cancer cell growth via its unexpected role as a hormone-

282 a novel mechanism whereby LKB1 may restrict cancer cell growth via the inhibition of Yap.

283 a novel mechanism whereby LKB1 may restrict cancer cell growth via the inhibition of Yap.Oncogene ad

284 re we demonstrate that AR regulates prostate cancer cell growth via the metabolic sensor 5'-AMP-activ

285 3p and miR-642-5p in the control of prostate cancer cell growth via the regulation of DOHH expression

286 Inhibition of cancer cell growth was demonstrated at micromolar concen

287 inhibitor of PTP4A3 and human A2780 ovarian cancer cell growth was reduced.

288 In TK(-/-) hosts, prostate cancer cell growth was significantly reduced as compared

289 The best results for inhibition of cancer cell growth were obtained with the p-Me, m,p-diMe

290 and CAP for synergistic inhibition of breast cancer cell growth when compared to each treatment separ

291 o identify gene pairs that inhibited ovarian cancer cell growth when they were targeted.

292 ate-specific antigen expression and prostate cancer cell growth, which is associated with decreased S

293 Warburg effect and the inhibition of breast cancer cell growth, which may serve as a useful approach

294 umour suppressor-oncogene cascade to control cancer cell growth with FBXW2 acting as a tumour suppres

295 teins with K(i) values of <1 nM and inhibits cancer cell growth with IC50 values of 1-2 nM in four sm

296 and screening identified 29 which inhibited cancer cell growth with low-muM potency.

297 ally inhibits glioma, breast, and pancreatic cancer cell growth, with IC50 values of 6-19 muM.

298 cellular matrix, stromal hormone output, and cancer cell growth within the same microenvironment.

299 of allosteric inhibitors of GAC that inhibit cancer cell growth without affecting their normal cellul

300 666-15 also potently inhibited cancer cell growth without harming normal cells.