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1 for exercise-dependent suppression of breast cancer cell growth.
2 simulated to predict their ability to reduce cancer cell growth.
3 rone, which might be repositioned to control cancer cell growth.
4 homeostatic mechanism, to increase prostate cancer cell growth.
5 stem cell niche factor, and an inhibitor of cancer cell growth.
6 ed by AR, which in turn facilitates prostate cancer cell growth.
7 ation, binding of colchicine to tubulin, and cancer cell growth.
8 ologically restoring BRM and thereby inhibit cancer cell growth.
9 treated with fatty acid, E2 promoted breast cancer cell growth.
10 ted degradation of DHFR and to inhibition of cancer cell growth.
11 loid cells is sufficient to inhibit prostate cancer cell growth.
12 other tumors and are required for efficient cancer cell growth.
13 n of OGT was sufficient to decrease prostate cancer cell growth.
14 r the deleterious effects of MMP-8 on breast cancer cell growth.
15 main eliminated suppression of PC-3 prostate cancer cell growth.
16 anscriptional activity and promotes prostate cancer cell growth.
17 ase activity and thereby selectively inhibit cancer cell growth.
18 r and has a role in the regulation of breast cancer cell growth.
19 rogression by secreting factors that mediate cancer cell growth.
20 d expression of AR target genes and prostate cancer cell growth.
21 of SOCS3 and SOCS4 and this is essential for cancer cell growth.
22 to identify 3D-specific effectors of breast cancer cell growth.
23 at LIN28A functions as an oncogene promoting cancer cell growth.
24 erases that function in pathways critical to cancer cell growth.
25 ed in most human cancers and is critical for cancer cell growth.
26 d eEF2 phosphorylation with little effect on cancer cell growth.
27 was reported to correlate with inhibition of cancer cell growth.
28 Like siRNA, A-484954 had little effect on cancer cell growth.
29 ogen-dependent gene transcription and breast cancer cell growth.
30 called the Warburg effect, is important for cancer cell growth.
31 olism and support a role for ASAH1 in breast cancer cell growth.
32 ctivation and anchorage-independent prostate cancer cell growth.
33 l mechanism for CYP3A4 involvement in breast cancer cell growth.
34 ng the effects of the Reptin-AGR2 complex in cancer cell growth.
35 oaddition (CuAAC) and afforded inhibitors of cancer cell growth.
36 f the metabolic reprogramming that underlies cancer cell growth.
37 ulation of PI3K activity by RGS16 and breast cancer cell growth.
38 mone, estrogen, is known to stimulate breast cancer cell growth.
39 XIAP and for their activity in inhibition of cancer cell growth.
40 oncogenic factor that has been implicated in cancer cell growth.
41 protein, which negatively regulates prostate cancer cell growth.
42 spases in whole cells, and potently inhibits cancer cell growth.
43 s knockdown of Skp2 significantly suppressed cancer cell growth.
44 and Mel-18 may have overlapping functions in cancer cell growth.
45 ing properties, profoundly inhibits prostate cancer cell growth.
46 ona fide tumor suppressor genes that inhibit cancer cell growth.
47 synergize with DNA-damaging agent to inhibit cancer cell growth.
48 other mitogens to enter the CSF and promote cancer cell growth.
49 can positively or negatively regulate human cancer cell growth.
50 racellular asparagine levels is critical for cancer cell growth.
51 first time that FSTL-1 suppresses pancreatic cancer cell growth.
52 ignaling networks, resulting in reduction of cancer cell growth.
53 ch drugs to inhibit KRAS(G12C) signaling and cancer cell growth.
54 rs, and its inhibition can result in reduced cancer cell growth.
55 ive kinase signaling, which is essential for cancer cell growth.
56 litates lung cancer progression by promoting cancer cell growth.
57 ne and vitamin D to suppress KSHV-associated cancer cell growth.
58 NRG1, in turn, activates YAP and stimulates cancer cell growth.
59 because androgens are essential for prostate cancer cell growth.
60 ion, attenuated Wnt signaling, and repressed cancer cell growth.
61 t MSI2 loss-of-function abrogates colorectal cancer cell growth.
62 es AR-dependent gene expression and prostate cancer cell growth.
63 t protein kinase 4 (CaMKIV) to control liver cancer cell growth.
64 ecific HIF-dependent expression and prostate cancer cell growth.
65 inhibit CREB-mediated gene transcription and cancer cell growth.
66 ced AR transcriptional activity and prostate cancer cell growth.
67 al to the tumor microenvironment and promote cancer cell growth.
68 nced genes that encode negative mediators of cancer cell growth.
69 homoserine lactones that selectively inhibit cancer cell growth, a library of phenacylhomoserine lact
70 androgen-dependent AR program, and prostate cancer cell growth, acting, at least in part, by functio
73 Stromal SOD3 had a stimulatory effect on cancer cell growth and an inhibitory effect on cancer ce
76 ppaB/miR-148a/152 feedback loop can regulate cancer cell growth and angiogenesis, and is also associa
78 ansduction pathways for inhibition of breast cancer cell growth and can be used as a dietary suppleme
80 ession of miR-502 inhibited autophagy, colon cancer cell growth and cell-cycle progression of colon c
82 of AR decreases EGF stimulation of prostate cancer cell growth and demonstrate a mechanistic link be
83 models through two mechanisms: inhibition of cancer cell growth and deregulation of angiogenesis.
85 that high DAPK1 expression causes increased cancer cell growth and enhanced signaling through the mT
87 amined for their ability to block pancreatic cancer cell growth and found to be about 10-fold more po
88 of enzymatic activity of PRP4 in regulating cancer cell growth and identified an array of potential
90 XL2 stabilized cyclin D3 levels, accelerated cancer cell growth and increased cell viability after vi
93 adopt a secretory phenotype that facilitates cancer cell growth and invasion when they become senesce
94 o induced apoptosis and decreased pancreatic cancer cell growth and invasion, indicating that downreg
97 at extracellular lumican inhibits pancreatic cancer cell growth and is associated with prolonged surv
98 a histone demethylase that promotes gastric cancer cell growth and is enriched in drug-resistant lun
100 ms through which CXCR4 contributes to breast cancer cell growth and metastases are poorly understood.
105 in multiple anabolic processes that support cancer cell growth and proliferation (reviewed in ref.
108 E235Q) promotes anchorage-independent breast cancer cell growth and resistance to gefitinib, U0126, a
111 logs and mTOR kinase inhibitors in targeting cancer cell growth and survival and provide support for
112 bolic pathway reprogramming is a hallmark of cancer cell growth and survival and supports the anaboli
113 stitutively active CREB is important to lung cancer cell growth and survival and therefore could be a
114 downstream AREG-EGFR signaling in human MEC cancer cell growth and survival in vitro and in vivo usi
117 cited a substantially stronger inhibition of cancer cell growth and survival, protein synthesis, cell
131 broblasts to enhance ERalpha-positive breast cancer cell growth and the level of soluble interleukin-
132 cylate induced apoptosis and decreased colon cancer cell growth and the sodium salt of aspirin also i
133 bility to inhibit hormone-independent breast cancer cell growth and to regulate ERalpha and cyclin D1
134 that arsenic trioxide (ATO) suppresses human cancer cell growth and tumor development in mice by inhi
135 hibited TNFalpha-induced NF-kappaB activity, cancer cell growth and tumor growth in an ovarian cancer
138 lighted miRNAs, substantially repressed lung cancer cell growth and tumorigenicity in a dose-dependen
139 we find that loss of SREBP activity inhibits cancer cell growth and viability by uncoupling fatty aci
142 PSMA4 is a strong candidate mediator of lung cancer cell growth, and may directly affect lung cancer
143 sion has an important role in promoting lung cancer cell growth, and that its oncogenic function is p
145 MKK2 function is sufficient to inhibit liver cancer cell growth, and the growth defect resulting from
146 L curcumin inhibited 253JB-V and KU7 bladder cancer cell growth, and this was accompanied by inductio
147 s many cardinal features of cancer including cancer cell growth, apoptosis resistance, DNA damage res
148 against specific signaling pathways driving cancer cell growth, are needed to pave the way for the d
151 ylation offers much potential for inhibiting cancer cell growth, as does disruption of interactions b
152 -38 at 1 microM, FL118 effectively inhibited cancer cell growth at less than nM levels in a p53 statu
153 6-methoxybenzo[b]furan (3g), which inhibited cancer cell growth at nanomolar concentrations (IC50 val
155 mor-associated macrophages inhibits prostate cancer cell growth, at least in part, by derepressing th
156 , PIM-1 kinase isoforms may promote prostate cancer cell growth, at least in part, through modulating
157 antagonizes estradiol (E2) -dependent breast cancer cell growth, but exerts partial agonist/antagonis
160 s citrate across cell membranes, halts liver cancer cell growth by altering both energy production an
163 AC8 expression strongly inhibited pancreatic cancer cell growth by attenuating cell-cycle progression
165 s support the new notion that INZ suppresses cancer cell growth by dually targeting SIRT1 and IMPDH2.
166 igen-specific IgEs were reported to restrict cancer cell growth by engaging high-affinity Fc receptor
167 t PRMT5 may function as an oncogene to drive cancer cell growth by epigenetic inactivation of several
168 rovide evidence that PRMT5 promotes prostate cancer cell growth by epigenetically activating transcri
169 re examples of RNAa-based drugs that inhibit cancer cell growth by inducing expression of tumor suppr
170 6]-gingerol suppresses anchorage-independent cancer cell growth by inhibiting LTA(4)H activity in HCT
171 ent ubiquinone coenzyme Q(10.) Inhibition of cancer cell growth by MitoQ was associated with G(1)/S c
173 d anchorage-dependent and -independent colon cancer cell growth by reducing ERK-RSK phosphorylation a
174 We also provide evidence that SNHG1 promotes cancer cell growth by regulating gene expression both in
175 findings indicate that HIF-2alpha increases cancer cell growth by up-regulating YAP1 activity, sugge
176 er intrinsic properties of metastatic breast cancer cell growth can be regulated through an extrinsic
177 Depletion of hSETD1A inhibits colorectal cancer cell growth, colony formation, and tumor engraftm
178 requent point mutation (A127T) enhanced lung cancer cell growth, colony formation, focal adhesion for
180 at Toll-like receptor 4 (TLR4) drives breast cancer cell growth differentially based on the presence
182 Schweinfurthins are potent inhibitors of cancer cell growth, especially against human central ner
183 p/Dcaf1 did not significantly affect ovarian cancer cell growth, even though it was expressed by ovar
185 ing, metabolic homeostasis, inflammation and cancer cell growth highlighting its potential as a thera
186 -Me was a potent inhibitor of LNCaP prostate cancer cell growth (IC(50) approximately 1 muM) and acti
188 expression led to abrogated in vivo ovarian cancer cell growth in a tumor xenograft system and resul
189 onstrate a novel mechanism of YHL-14 against cancer cell growth in bladder and colon cancer cell line
190 required for ERbeta-dependent inhibition of cancer cell growth in culture and in murine xenografts.
191 eported to have a pivotal role in epithelial cancer cell growth in culture and in xenograft tumors, p
192 glutathione conjugates, prevents human colon cancer cell growth in culture as well as in nude mouse x
193 lso potently inhibits triple-negative breast cancer cell growth in human cells and in animal models b
194 d ATF mRNA resulted in inhibition of ovarian cancer cell growth in nude mice accompanied with Maspin
195 xygenase that promotes Stat3-mediated breast cancer cell growth in part through (+/-)-14,15-EET biosy
197 vity increases castration-recurrent prostate cancer cell growth in response to EGF by site-specific s
198 ere found to be very effective inhibitors of cancer cell growth in the HupT3 (IC(50) = 50 nM) and Mia
199 on of Bcl-xL expression, followed by reduced cancer cell growth in the presence of Met-targeting drug
200 target distinct pathways to inhibit prostate cancer cell growth in this system and that the unique pr
201 ate production and synergistically inhibited cancer cell growth in vitro (HepG2) and in vivo (H22).
202 tate resulted in a synergistic inhibition of cancer cell growth in vitro and an enhanced reduction of
203 which we found is able to potently suppress cancer cell growth in vitro and in vivo by binding beta-
211 hown that loss of SALL4 inhibits endometrial cancer cell growth in vitro and tumorigenicity in vivo,
212 tently, overexpression of ZMYND11 suppresses cancer cell growth in vitro and tumour formation in mice
214 xhibited greater inhibition of BT-474 breast cancer cell growth in vitro to a level that could not be
215 -yl)phenyl]amide (4a), suppresses pancreatic cancer cell growth in vitro with the lowest IC(50) value
216 4(nrb) and SREBP-1a were required for breast cancer cell growth in vitro, and p54(nrb) binding to nuc
217 I have been found to synergistically inhibit cancer cell growth in vitro, yet clinical studies of the
222 (PI3K) beta signaling is required to sustain cancer cell growth in which the tumor suppressor phospha
223 ed grapes has been shown to inhibit prostate cancer cell growth, in part, through its antioxidant act
224 h the role of lipids as an energy source for cancer cell growth, in vivo time-course studies revealed
225 otently inhibited tubulin polymerization and cancer cell growth, including stimulation of natural kil
226 ns are generally more active in human breast cancer cell growth inhibition and human leukemia cell di
227 am effects on client protein degradation and cancer cell growth inhibition has not been thoroughly in
228 SAR analyses relating the polar termini with cancer cell growth inhibition revealed that length and v
235 internalization and stability of the ovarian cancer cell growth inhibitor peptide, LSCQLYQR (LR), is
237 e synthesis of (S)-(+)-tylophorine, a potent cancer cell growth inhibitor, has been accomplished in e
238 w potent class of tubulin polymerization and cancer cell growth inhibitors with the potential to inhi
241 iple signal transduction pathways regulating cancer cell growth, invasion, metastasis, survival, and
242 molecular markers and pathways implicated in cancer cell growth is a promising avenue for developing
244 or overexpressed oncogenic proteins driving cancer cell growth, leading to the acceptance of Hsp90 a
245 ntify signaling pathways regulating prostate cancer cell growth led to our discovery that checkpoint
247 lasia found in Pten(+/-) mice but suppressed cancer cell growth, proliferation, and invasion through
248 e dynamics and that the embryonal theory for cancer cell growth/proliferation is overly simplistic, a
250 5 expression levels are well correlated with cancer cell growth rate and that p53 is able to negative
251 tissue-specific fibroblasts directly affect cancer cell growth rates and survival remains largely un
252 coholism drug, could potently inhibit breast cancer cell growth regardless of the PIK3CA status.
255 ed in CCA and that its up-regulation induces cancer cell growth retardation through multiple targets
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
262 ol 3-kinase (PI3K) signaling axis impacts on cancer cell growth, survival, motility, and metabolism.
263 nique source of signalling cues that affects cancer cell growth, survival, movement and metastasis.
264 2A and MAT2beta genes are required for liver cancer cell growth that is induced by the profibrogenic
265 nificant inhibitory effects on human bladder cancer cell growth that was accompanied by marked apopto
266 er, they display modest ability to attenuate cancer cell growth; their physicochemical properties, an
268 s oncogenic stress, whereas it promoted lung cancer cell growth through inducing the cell proliferati
269 suggests that metformin directly antagonizes cancer cell growth through its actions on complex I of t
270 ctional role for macropinocytosis in fueling cancer cell growth through the internalization of extrac
271 trate that YHL-14 inhibits bladder and colon cancer cell growth through up-regulation of p21 expressi
272 l problems, ranging from circadian rhythm to cancer cell growth to longevity, have begun to give evid
273 to RT and investigated changes in colorectal cancer cell growth, transcriptome, metabolome, and kinom
277 etyl-CoA synthetase 2 (ACSS2) contributes to cancer cell growth under low-oxygen and lipid-depleted c
278 results indicated that PL could inhibit lung cancer cell growth via inhibition of NF-kappaB signaling
279 erexpressed in prostate cancer and regulates cancer cell growth via its unexpected role as a hormone-
281 a novel mechanism whereby LKB1 may restrict cancer cell growth via the inhibition of Yap.Oncogene ad
282 re we demonstrate that AR regulates prostate cancer cell growth via the metabolic sensor 5'-AMP-activ
283 3p and miR-642-5p in the control of prostate cancer cell growth via the regulation of DOHH expression
286 increasing alkyl chain length in inhibiting cancer cell growth were evaluated on melanoma, prostate,
288 and CAP for synergistic inhibition of breast cancer cell growth when compared to each treatment separ
290 ate-specific antigen expression and prostate cancer cell growth, which is associated with decreased S
291 Warburg effect and the inhibition of breast cancer cell growth, which may serve as a useful approach
292 + T or G + C nucleotides) strongly inhibited cancer cell growth while sparing non-malignant cells.
293 umour suppressor-oncogene cascade to control cancer cell growth with FBXW2 acting as a tumour suppres
294 teins with K(i) values of <1 nM and inhibits cancer cell growth with IC50 values of 1-2 nM in four sm
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
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