ライフサイエンスコーパス: Warburg effect

1 act GBM model, consistent with the accepted "Warburg effect".

2 condition is known as pseudohypoxia or the "Warburg Effect".

3 profound effect on aerobic glycolysis (the 'Warburg effect').

4 metabolism (a cancer phenomenon termed the 'Warburg effect').

5 even in the presence of abundant oxygen (the Warburg effect).

6 and lactate dehydrogenase A (LDHA) activity (Warburg effect).

7 arity to the glycolytic phenotype in cancer (Warburg effect).

8 ism and is up-regulated in cancer cells (the Warburg Effect).

9 e of ATP to fuel cellular proliferation (the Warburg effect).

10 3 and induction of the glycolytic phenotype (Warburg effect).

11 te despite abundant oxygen availability (the Warburg effect).

12 ion due, in part, to respiration injury (the Warburg effect).

13 olytic enzymes and glucose transporters (the Warburg effect).

14 hen oxygen is available (aerobic glycolysis, Warburg effect).

15 lactate conversion is a hallmark of cancer (Warburg effect).

16 ng to rely mostly on aerobic glycolysis (the Warburg effect).

17 n in the presence of abundant oxygen(4) (the Warburg effect).

18 s the glycolytic adaptation described as the Warburg Effect.

19 similar metabolic alterations, including the Warburg effect.

20 utrients for biomass production known as the Warburg effect.

21 as an increased glycolytic rate known as the Warburg effect.

22 ropensity of AKT to modulate elements of the Warburg effect.

23 se M2 isoform (PKM2), a key regulator of the Warburg effect.

24 ert to regulate PDC activity and promote the Warburg effect.

25 ion, activation of the PI3K pathway, and the Warburg effect.

26 ert to regulate PDC activity and promote the Warburg effect.

27 ess, enabling non-invasive monitoring of the Warburg effect.

28 ase in aerobic glycolysis, also known as the Warburg effect.

29 ll of origin, thereby inhibiting a potential Warburg effect.

30 lar composition of PDC and contribute to the Warburg effect.

31 aerobic glycolysis, a phenomenon termed the Warburg effect.

32 onditions, a hallmark of cancer known as the Warburg effect.

33 it a glycolytic phenotype reminiscent of the Warburg effect.

34 f mitochondrial function and is known as the Warburg effect.

35 energy production, a phenomenon known as the Warburg effect.

36 tp53 GOF and a mechanism for controlling the Warburg effect.

37 tic state of aerobic glycolysis known as the Warburg effect.

38 the pathways classically associated with the Warburg effect.

39 n to generate ATP, a phenomenon known as the Warburg effect.

40 tions and therefore do not fully explain the Warburg effect.

41 gely abolishes mutp53 GOF in stimulating the Warburg effect.

42 imiting glycolytic enzyme known to cause the Warburg effect.

43 s a new molecular player contributing to the Warburg effect.

44 in cancer cells, commonly referred to as the Warburg effect.

45 ential use of glucose, which is known as the Warburg effect.

46 tures of tumor cells: glutaminolysis and the Warburg effect.

47 that p53 status is a key determinant of the Warburg effect.

48 oA in the presence of oxygen is known as the Warburg effect.

49 r role in T-cell activation and induction of Warburg effect.

50 udy of tumor metabolism above and beyond the Warburg effect.

51 iferating cancer cells and contribute to the Warburg effect.

52 ruvate kinase M2 (PKM2) is essential for the Warburg effect.

53 decline of mitochondria thus reinforcing the Warburg effect.

54 tion of cancerous colonocytes undergoing the Warburg effect.

55 ation in the cell, a phenomenon known as the Warburg effect.

56 es mitochondrial respiration, leading to the Warburg effect.

57 se M2 isoform (PKM2), a key regulator of the Warburg effect.

58 CEFs (Ski-CEFs) do not display the classical Warburg effect.

59 is abundant, a phenomenon referred to as the Warburg effect.

60 ing oxygen consumption, thereby inducing the Warburg effect.

61 erobic glycolysis, a phenomenon known as the Warburg effect.

62 abolism to aerobic glycolysis, the so-called Warburg effect.

63 increase in aerobic glycolysis known as the Warburg effect.

64 ten develop an acidic environment due to the Warburg effect.

65 s glucose uptake and aerobic glycolysis; the Warburg effect.

66 terns of expression were consistent with the Warburg effect.

67 mmHg, ATP levels rapidly decrease due to the Warburg effect.

68 oxia can explain some characteristics of the Warburg effect.

69 ysis, a phenomenon known historically as the Warburg effect.

70 phenomenon that is historically known as the Warburg effect.

71 r 70 years ago and known historically as the Warburg effect.

72 to generate energy, a phenomenon termed the Warburg effect.

73 r lactate production, indicating an enhanced Warburg effect.

74 deprivation (hypoxia), is a hallmark of the Warburg effect.

75 nd instead promotes a metabolic shift to the Warburg effect.

76 and/or hypoxia (Hyp), known inducers of the Warburg effect.

77 r conditions of high glycolysis, such as the Warburg effect.

78 de and water-a phenomenon referred to as the Warburg Effect.

79 ma enabled quantitative visualization of the Warburg effect.

80 e quiescent state, a phenomenon known as the Warburg effect.

81 inflammatory sites undergoing hypoxia or the Warburg effect.

82 intellectual disability, apoptosis, and the Warburg effect.

83 er-enhancers in several genes related to the Warburg effect.

84 der aerobic conditions characteristic of the Warburg effect.

85 lysis for ATP production, referred to as the Warburg effect.

86 eir energy supply, a phenomenon known as the Warburg effect.

87 toward aerobic glycolysis, also known as the Warburg effect.

88 the lactate produced by cancer cells in the Warburg effect.

89 ize the potential benefit from targeting the Warburg effect.

90 rosine phosphorylation and gives rise to the Warburg effect.

91 metabolic requirement, a phenomenon known as Warburg effect.

92 on to aerobic glycolysis, referred to as the Warburg effect.

93 vide new insights into the regulation of the Warburg effect.

94 presented by a glycolytic shift known as the Warburg effect.

95 gulate non-cell-cycle functions, such as the Warburg effect.

96 respiration, as observed in the Crabtree and Warburg effects.

97 s while decreasing glycolysis, i.e. an 'anti-Warburg' effect.

98 n tumours compared with healthy tissues (the Warburg effect(2,3)), but this increase is insufficient

99 olic status of cancer cells experiencing the Warburg effect(2,3).

100 ryos transiently exhibit aerobic glycolysis (Warburg effect), a metabolic adaptation also observed in

101 The Warburg effect, a common metabolic alteration of most tu

102 The Warburg effect adapts cells to tumor environments and is

103 We propose that KSHV induction of the Warburg effect adapts infected cells to tumor microenvir

104 ealing how CD44 could be a gatekeeper of the Warburg effect (aerobic glycolysis) in cancer cells and

105 h HIF-1alpha and N-Myc are essential for the Warburg effect (aerobic glycolysis) in neuroblastomas by

106 aerobic glycolysis, a phenomenon termed "the Warburg effect." Aerobic glycolysis is an inefficient wa

107 er normoxic conditions, commonly called the "Warburg effect." Aerobic glycolysis often directly corre

108 gramming, known as aerobic glycolysis or the Warburg effect, allows tumor cells to sustain their fast

109 IF1, revealing a potential mechanism for the Warburg effect, an elevation in aerobic glycolytic metab

110 eir mitochondria, a phenomenon known as the 'Warburg effect.' An abundance of evidence shows not only

111 mor growth by suppressing the HIF-1-mediated Warburg effect and angiogenesis.

112 h cancer-specific splicing that promotes the Warburg effect and breast cancer progression.

113 ies document a therapeutical approach to the Warburg effect and demonstrate that oxidative stress and

114 In this Essay, we re-examine the Warburg effect and establish a framework for understandi

115 provide a novel mechanistic insight into the Warburg effect and explain how metabolic alteration in c

116 ese results support an interpretation of the Warburg effect and glutamine addiction as features of a

117 n altered metabolism, including an increased Warburg effect and glutamine dependence, making the glut

118 Because the Warburg effect and hypoxia are frequently seen in human

119 lic and epigenetic therapy for reversing the Warburg effect and inducing differentiation in neuroblas

120 e in hepatocellular carcinoma, reversing the Warburg effect and inhibiting tumorigenesis.

121 This phenomenon is known as the Warburg effect and is considered as one of the most fund

122 Mannan-tolDCs shift glucose metabolism from Warburg effect and lactate production to mitochondrial o

123 er cells, SR9243 significantly inhibited the Warburg effect and lipogenesis by reducing glycolytic an

124 as sustaining tumor metabolism including the Warburg effect and mitochondria respiration.

125 duced kinase 1 (PINK1) is a regulator of the Warburg effect and negative regulator of glioblastoma gr

126 tion provides a possible explanation for the Warburg effect and offers new clues as to how p53 might

127 asis, immune escape, tumor angiogenesis, the Warburg effect and oncogene addiction and has been valid

128 s miR-199a maturation to link hypoxia to the Warburg effect and suggest a promising therapeutic strat

129 This results in the reversal of the Warburg effect and the inhibition of breast cancer cell

130 nhances LDH-A enzyme activity to promote the Warburg effect and tumor growth by regulating the NADH/N

131 osphorylation activates PDHK1 to promote the Warburg effect and tumor growth.

132 Today this phenomenon is known as the "Warburg effect" and recognized as a hallmark of cancer.

133 lytic pathway from the TCA cycle (i.e., the "Warburg effect") and as a result, often become dependent

134 cer cells-part of a phenomenon known as the "Warburg effect"- and is mediated by monocarboxylate tran

135 ignant cells exhibit aerobic glycolysis (the Warburg effect) and become dependent on de novo lipogene

136 t glycolysis even in the presence of oxygen (Warburg effect) and use of glutamine for increased biosy

137 ated androgen signaling, aerobic glycolysis (Warburg effect), and aberrant activation of transcriptio

138 regulating energy metabolism, especially the Warburg effect, and antioxidant defense, and thus the fu

139 ing defective oxidative phosphorylation, the Warburg effect, and autophagy/mitophagy addiction.

140 t mechanistically connects aberrant ROS, the Warburg effect, and carcinogenesis.

141 suppressor in PCa that prevents EMT and the Warburg effect, and indicates that ABHD5 is a potential

142 y a preference for aerobic glycolysis or the Warburg effect, and the cells resist matrix detachment-i

143 , development of multi-drug resistance, the 'Warburg effect', angiogenesis and cell growth (i.e. dist

144 umption and lactate production, known as the Warburg effect, are almost universal hallmarks of solid

145 that regulate the PI3K pathway, and thus the Warburg effect, are elusive.

146 Drastic metabolic alterations, such as the Warburg effect, are found in most if not all types of ma

147 tivation of either Akt or c-Myc leads to the Warburg effect as indicated by increased cellular glucos

148 M1 (adult) isoform leads to reversal of the Warburg effect, as judged by reduced lactate production

149 ng in Akt activation and aerobic glycolysis (Warburg effect), associated with ulceration.

150 eased oxygen consumption, and attenuated the Warburg effect at the cellular level.

151 As such, the Warburg effect becomes a signature of excess glucose bei

152 ic metabolism in an aerobic environment, the Warburg effect, but the explanation for this preference

153 wild-type p53 prevents manifestation of the Warburg effect by controlling Pdk2.

154 Finally, miR-644a expression suppresses the Warburg effect by direct targeting of c-Myc, Akt, IGF1R,

155 llular metabolism, frequently exploiting the Warburg effect by increasing aerobic glycolysis and gluc

156 is an anticancer agent that can reverse the Warburg effect by inhibiting a key enzyme in cancer cell

157 ndicated that CO transiently induces an anti-Warburg effect by rapidly fueling cancer cell bioenerget

158 ain a growth advantage through the so-called Warburg effect by shifting glucose metabolism from oxida

159 Here I show that the Warburg effect can be explained as a form of cooperation

160 cose to lactate conversion indicative of the Warburg effect can be imaged without hyper-polarization

161 Notwithstanding the renewed interest in the Warburg effect, cancer cells also depend on continued mi

162 Due to the Warburg effect, cancerous colonocytes rely on glucose as

163 mediated PKM2 dephosphorylation promotes the Warburg effect, cell proliferation and brain tumorigenes

164 may be an approach for altering the classic Warburg effect characteristic of aberrant metabolism in

165 The Warburg effect contributes to cancer progression and is

166 Aerobic glycolysis-the Warburg effect-converts glucose to lactate via the enzym

167 respiration makes this behaviour, namely the Warburg effect, counter-intuitive, although it has now b

168 The Warburg effect defines a pro-oncogenic metabolism switch

169 The classic Warburg effect described in macrophages infected by Myco

170 The Warburg effect describes an increase in aerobic glycolys

171 The "Warburg effect" describes a peculiar metabolic feature o

172 increased glycolysis for ATP generation (the Warburg effect) due in part to mitochondrial respiration

173 ve recently emerged as key regulators of the Warburg effect during tumorigenesis and normal cellular

174 llectively, these findings indicate that key Warburg effect enzymes play a central role in mediating

175 mented that methylene blue (MB) reverses the Warburg effect evidenced by the increasing of oxygen con

176 aerobic production of lactate from glucose (Warburg effect), extensive glutamine utilization and imp

177 metabolic genes associated with glycolysis (Warburg effect), fatty acid metabolism (lipogenesis, oxi

178 se findings imply that efforts to target the Warburg effect for cancer prevention are mechanistically

179 However, targeting oncogenic regulators of Warburg effect has always been challenging owing to the

180 A metabolic phenomenon known as the Warburg effect has been characterized in certain cancero

181 oxygen-rich environment, referred to as the Warburg effect, has been noted as a nearly universal bio

182 n increase in the generation of lactate (the Warburg effect) have been frequently detected in those t

183 lls benefit from this phenomenon, termed the Warburg effect, have renewed discussions about its exact

184 lysis-driven metabolic program, known as the Warburg effect; however, few have been identified.

185 its Fc and F(ab')(2) fragments regulate the Warburg effect in activated PBMCs depending on the gluco

186 ed glycolysis and visibly reduced markers of Warburg effect in ADPGK knock-out cells, finally leading

187 the ERK and JNK pathways in controlling the Warburg effect in cancer and discuss their implication i

188 cogenic signaling pathways that regulate the Warburg effect in cancer cells has therefore become an a

189 the glycolytic pathway and contribute to the Warburg effect in cancer cells.

190 ase (PKM2), a key enzyme contributing to the Warburg effect in cancer, is significantly induced in DM

191 thod has proven highly useful to monitor the Warburg effect in cancer, through MR detection of increa

192 mitochondrial function, contributing to the Warburg effect in cancer.

193 erized by a glycolytic switch similar to the Warburg effect in cancer.

194 a lack of a quantitative explanation for the Warburg effect in cancer.

195 estoration of Parkin expression reverses the Warburg effect in cells.

196 43B osteosarcoma (OS) cell lines showing the Warburg effect in comparison with actively respiring Sao

197 that tumour-associated mutp53 stimulates the Warburg effect in cultured cells and mutp53 knockin mice

198 How ACAT1 is "hijacked" to contribute to the Warburg effect in human cancer remains unclear.

199 itochondrial membrane potential-promotes the Warburg effect in leukemia cells, and may contribute to

200 remutation, we evaluated the presence of the Warburg effect in peripheral blood mononuclear cells (PB

201 However, evidence for the occurrence of the Warburg effect in physiological processes has also been

202 conserved mammalian UCPs may facilitate the Warburg effect in the absence of permanent respiratory i

203 Known as the Warburg effect in the context of cancer growth, this phe

204 by DERL3 epigenetic loss contributes to the Warburg effect in the studied cells and pinpoints a subs

205 tory axis is an important determinant of the Warburg effect in tumor cells, and provide a mechanistic

206 rkin deficiency is a novel mechanism for the Warburg effect in tumors.

207 ory axis is an important determinant for the Warburg effect in tumour cells and provide a mechanistic

208 oupled with elevated aerobic glycolysis (the Warburg effect) in cancer cells and is closely correlate

209 of increased aerobic glycolysis, known as a Warburg effect, including cytosolic PKM2 (pyruvate kinas

210 factor-1alpha's downstream processes and the Warburg effect; induction of autophagy; augmentation of

211 The Warburg effect is a chronic increase in glycolytic index

212 Warburg effect is a hallmark of cancer manifested by con

213 ese findings support the hypothesis that the Warburg effect is a precisely regulated developmental me

214 The Warburg effect is a tumor-related phenomenon that could

215 The Warburg effect is a tumorigenic metabolic adaptation pro

216 g to Warburg himself, the consequence of the Warburg effect is cell dedifferentiation.

217 Although Warburg effect is considered a peculiarity critical for

218 Therefore, similar to cancer cells, the Warburg effect is necessary for maintaining KSHV latentl

219 The Warburg effect is one of the metabolic hallmarks of canc

220 This study reveals a mechanism that the Warburg effect is regulated by CHIP through its function

221 It remains a matter of debate as to how the Warburg effect is regulated during tumor progression.

222 izing higher-grade tumors, we found that the Warburg effect is relatively more prominent at the expen

223 ormulated hypothesis that the benefit of the Warburg Effect is to increase ATP production rate by swi

224 We demonstrated that "Warburg effect" is not modulated in the initial stage of

225 gulation of glycolysis in cancer cells (the "Warburg effect") is common and has implications for prog

226 Aerobic glycolysis (the Warburg effect) is a metabolic hallmark of activated T c

227 both animal models and patients, glycolysis (Warburg effect) is also an early manifestation of CRPC t

228 olism of enhanced aerobic glycolysis (or the Warburg effect) is known as a hallmark of cancer.

229 e data indicate that aerobic glycolysis (the Warburg effect) is not an intrinsic component of the tra

230 olism to a highly glycolytic phenotype, i.e. Warburg effect, is a common phenotype of cancer and acti

231 etabolism of most solid tumors, known as the Warburg effect, is associated with resistance to apoptos

232 ilability of oxygen, a phenomenon called the Warburg effect, is important for cancer cell growth.

233 te kinase M2 (PKM2), a glycolytic enzyme for Warburg effect, is strongly upregulated in BC.

234 g cells-with the latter process known as the Warburg effect-is historically considered a mere waste p

235 he degree of aerobic glycolysis-known as the Warburg effect-is thus predicted to represent an adaptat

236 ed role of PKM2 in aerobic glycolysis or the Warburg effect, its non-metabolic functions remain elusi

237 Warburg effect linked to cognitive-executive deficits in

238 Aerobic glycolysis or the Warburg effect links the high rate of glucose fermentati

239 ated aerobic glycolysis in cancer cells (the Warburg effect) may be attributed to respiration injury

240 Reversing this phenomenon, known as the Warburg effect, may offer a generalized anticancer strat

241 ion and underlying mechanism of UQCRH in the Warburg effect metabolism of ccRCC have not been charact

242 t in vitro proof of concept that reversal of Warburg effect might be a novel therapy for GBM.

243 Here we explore how the Warburg effect might be linked to inflammation and infla

244 These results suggest that the Warburg effect, more specifically, diminished glucose ox

245 ation analysis revealed a uniform pattern of Warburg effect mutations influencing prognosis across al

246 e for the pyruvate kinase M2 (PKM2)-mediated Warburg effect, namely aerobic glycolysis, in the regula

247 We suggest that, similar to the Warburg effect observed in tumor cells, starving yeast a

248 Described decades ago, the Warburg effect of aerobic glycolysis is a key metabolic

249 tion in aerobic glycolysis counteracting the Warburg effect of cancer cells.

250 to the altered metabolic state known as the Warburg effect; one metabolic pathway, highly dependent

251 Warburg effect or aerobic glycolysis provides selective

252 etabolic phenotype of cancer is known as the Warburg effect or aerobic glycolysis that consists of in

253 n oxidative phosphorylation capacity i.e the Warburg effect (P = 3.62E-03) and urea cycle (P = 7.95E-

254 xhibited disruption of the TCA cycle and the Warburg effect pathway.

255 were related to energy production as well as Warburg effect pathways, which may shed light on how ene

256 wever, this treatment demonstrated a Reverse Warburg effect phenotype observed in cancer-associated s

257 ion, agents that scavenge ROS or reverse the Warburg effect prevent the transformation and malignant

258 umarate and succinate may play a role in the Warburg effect providing that appropriate relative conce

259 amming in concert with disruption of several Warburg effect-related super-enhancers.

260 Tumor cells exhibiting the Warburg effect rely on aerobic glycolysis for ATP produc

261 des mechanistic insights into how a specific Warburg effect subtype contributes to glycine accumulati

262 r cells rely more on aerobic glycolysis (the Warburg effect) than mitochondrial oxidative phosphoryla

263 c alterations in cancer cells, including the Warburg effect that describes an increased glycolysis in

264 It is unclear how the Warburg effect that exemplifies enhanced glycolysis in t

265 nce of a synaptic activity-mediated neuronal Warburg effect that may promote mitochondrial homeostasi

266 A new parameter measuring the Warburg effect (the ratio of lactate production flux to

267 abolism, notably of aerobic glycolysis (the "Warburg effect"), the potential involvement of hypoxia-i

268 Despite being known for decades (Warburg effect), the molecular mechanisms regulating thi

269 ons in chRCC tumors, including the classical Warburg effect, the downregulation of gluconeogenesis an

270 This bioenergetic shift is similar to the Warburg effect, the metabolic signature of cancer cells.

271 The discovery of the Warburg effect, the preference of cancer cells to genera

272 Historically known as the Warburg effect, this altered metabolic phenotype has lon

273 Mechanistically, PGC1a suppressed the Warburg effect through down-regulation of pyruvate dehyd

274 Mutp53 stimulates the Warburg effect through promoting GLUT1 translocation to

275 report that loss of PINK1 contributes to the Warburg effect through ROS-dependent stabilization of hy

276 ignaling pathway may be a way to inhibit the Warburg Effect to disrupt tumor growth.

277 ost tumour cells use aerobic glycolysis (the Warburg effect) to support anabolic growth and evade apo

278 Most tumor cells use aerobic glycolysis (the Warburg effect) to support anabolic growth and promote t

279 induced cancer cells, displaying the typical Warburg effect, to death or survival upon progressive gl

280 overns the balance between autophagy and the Warburg effect via BNIP3 alternative splicing, thereby e

281 is study reveals that miR-31-5p promotes the Warburg effect via direct targeting of FIH.

282 MicroRNA-31-5p enhances the Warburg effect via targeting FIH.

283 lonocytes and cancerous colonocytes when the Warburg effect was prevented from occurring, whereas it

284 2, a fetal anabolic enzyme implicated in the Warburg effect, was activated by insulin in vivo and in

285 This metabolic change, the Warburg effect, was one of the first alterations in canc

286 Aerobic glycolysis or the Warburg effect (WE) is characterized by increased glucos

287 Aerobic glycolysis or the Warburg Effect (WE) is characterized by the increased me

288 estigate molecular mechanisms underlying the Warburg effect, we first compared oxygen consumption amo

289 rofound metabolic alterations, including the Warburg effect wherein cancer cells oxidize a decreased

290 nas is dominated by aerobic glycolysis (the "Warburg Effect"), which allows only a small fraction of

291 insights into the regulation of VEGF and the Warburg effect, which describes the propensity for cance

292 ose metabolism in cancer cells is termed the Warburg effect, which describes the propensity of most c

293 eference of aerobic glycolysis, known as the Warburg effect, which facilitates cell proliferation.

294 tochondria (OXPHOS), a phenomenon termed the Warburg effect, which is a general feature of oncogenesi

295 Imaging of the Warburg effect, which is the principal but not the sole

296 The Warburg effect, which originally described increased pro

297 This is the Warburg effect, which provides substrates for cell growt

298 ossible to directly and indirectly image the Warburg effect with hyperpolarized (13)C-pyruvate and (1

299 ngly, the molecular mechanisms that link the Warburg effect with the suppression of apoptosis are not

300 GT1A_i2 proteins in HT115 cells enforced the Warburg effect, with a higher glycolytic rate at the exp