ライフサイエンスコーパス: luminal cell

1 ed absorptive villus cells and the prostatic luminal cell.

2 of fully differentiated CK5+ basal and CK8+ luminal cells.

3 higher levels of ANTXR1 compared with mature luminal cells.

4 ficient basal cells was traced to neoplastic luminal cells.

5 ell receptors DP1 and CRTH2 was evaluated on luminal cells.

6 tin marker H3K27me3 than more differentiated luminal cells.

7 differentiate into transformation-competent luminal cells.

8 egative stem/progenitor cells to ER-positive luminal cells.

9 egative stem/progenitor cells to ER-positive luminal cells.

10 maintaining ductal integrity and survival of luminal cells.

11 integrity and the proper differentiation of luminal cells.

12 XO, with XO concentrated on and in vascular luminal cells.

13 m cells and are the candidate progenitors of luminal cells.

14 erplasia, and atrophic glands denuded of the luminal cells.

15 n the cell cycle of primary myoepithelial or luminal cells.

16 wer luminal progenitor cells but more mature luminal cells.

17 elial cells that drove directional change in luminal cells.

18 lar cell type expressing KRT14, hereby named luminal cells.

19 from the reprogramming of androgen-dependent luminal cells.

20 arker genes, before transitioning to Krt8(+) luminal cells.

21 ) and not in the larger population of ERG(+) luminal cells.

22 y deficient expression of features of mature luminal cells.

23 se, JFK, as CREB1 transcriptional targets in luminal cells.

24 ifferentiating and terminally differentiated luminal cells.

25 hift from luminal progenitor cells to mature luminal cells.

26 TF gene for luminal progenitors and alveolar luminal cells.

27 le alpha6beta4E expressed within a subset of luminal cells.

28 lower levels, in oestrogen receptor-positive luminal cells.

29 hymal cells acting in a paracrine fashion on luminal cells.

30 c basal cells into transformation-preferable luminal cells.

31 tional progenitor, and CK8(+) differentiated luminal cells.

32 ynamic throughout pregnancy when compared to luminal cells.

33 basal conversion of the more differentiated luminal cells.

34 of its original size because of the loss of luminal cells.

35 l cells (MECs) except the secretory alveolar luminal cells.

36 elia are composed predominantly of basal and luminal cells.

37 ntified 11 differentiation states for normal luminal cells.

38 nt basal cells into transformation-competent luminal cells.

39 roid reductase 2, comparatively low-activity luminal cell 2B15 undergoes a complex pattern of regulat

40 se the proliferation of normal mouse mammary luminal cells adjacent to tumors.

41 imilar to the expression pattern of prostate luminal cells, also characterize a small series of Gleas

42 In contrast, AR deletion in luminal cells alters cell morphology and induces transie

43 uces the differentiation of basal cells into luminal cells, an alteration that rarely occurs under no

44 ary luminal cell lineage led to a paucity of luminal cells and an excessive expansion of basal cells,

45 of the lung contains ciliated and secretory luminal cells and basal stem/progenitor cells.

46 ) binding to the 11-kb region in both normal luminal cells and CARNs and discovered new androgen resp

47 n the apical plasma membrane of the prostate luminal cells and demonstrated its release into semen as

48 ch3 caused a decrease of Notch activation in luminal cells and diminished luminal progenitors at pube

49 f the basal cell transcription factor p63 in luminal cells and excessive proliferation of basal cells

50 um containing both p63+ basal cells and p63- luminal cells and expressing a variety of prostate-speci

51 terized by gain of acetylation at markers of luminal cells and GATA2 activation and loss of LRP5 and

52 e first step required for basal extrusion of luminal cells and identify aPKCi and vinculin as regulat

53 nt largely dominated by castration-resistant luminal cells and immunosuppressive infiltrates.

54 irculating XO can then bind avidly to vessel luminal cells and impair vascular function by creating a

55 al AR have increased apoptosis in epithelial luminal cells and increased proliferation in epithelial

56 ce new secretory acini composed of secretory luminal cells and myoepithelium.

57 tates acquisition of MaSC-like properties by luminal cells and predisposes them to development of mam

58 epithelium, LEFTY1 expression in a subset of luminal cells and rare basal cells opposes BMP7 to promo

59 epithelium made up of ciliated and secretory luminal cells and undifferentiated basal progenitor cell

60 ytokeratin 14 (basal cells), cytokeratin 18 (luminal cells), and dorsolateral protein over time in th

61 rvival factor of prostatic cancer epithelial luminal cells, and as a suppressor for prostate cancer b

62 AR variants), terminal differentiation into luminal cells, and cell death.

63 of cell proliferation, increased survival of luminal cells, and loss of cell polarity, resulting in t

64 s sandwiched between the basal cells and the luminal cells, and this layer was consistently p27Kip1 n

65 ntly decreased, and epithelial sloughing and luminal cell apoptosis increased from 6 to 32 weeks of a

66 autophagy in PI3K-H1047R structures triggers luminal cell apoptosis, resulting in lumen clearance.

67 Disrupting luminal cell AR signaling in mouse models promotes cytok

68 We show that both types of the luminal cell are susceptible to oncogenic transformation

69 ence has shown that both prostatic basal and luminal cells are able to initiate oncogenic transformat

70 Luminal cells are believed to be the cells of origin for

71 -vivo lineage-tracing work demonstrates that luminal cells are capable of producing basal cells on ac

72 asive form of breast cancer where neoplastic luminal cells are confined to the ductal tree.

73 cing, demonstrates that castration-resistant luminal cells are distinct from the pre-existent urethra

74 we show that adult rodent prostate basal and luminal cells are independently self-sustained in vivo.

75 rganoid cells derived from the TACSTD2(high) luminal cells are more predisposed to neuroendocrine dif

76 Prostate luminal cells are more responsive to Pten null-induced m

77 more, we show that mouse distal and proximal luminal cells are most similar to human acinar and ducta

78 Prevailing theories suggest that luminal cells are the origin of prostate cancer because

79 The CD57+ luminal cells are the terminally differentiated secretor

80 The prostate gland consists of basal and luminal cells arranged as pseudostratified epithelium.

81 opment and regulating ESR1/ERalpha and other luminal cell-associated genes in breast cancer.

82 on in vitro and in vivo, but does not affect luminal cell biology.

83 common in malignant tumors, are enriched in luminal cells but absent in basal myoepithelial cells.

84 t LXN is highly expressed in normal prostate luminal cells but downregulated in high Gleason grade ca

85 h a phenotype that resembles normal prostate luminal cells, but at their intermediate state of differ

86 -/-) UGS grafts contained neuroendocrine and luminal cells, but basal cells were absent.

87 CREB1 is active in luminal cells, but not basal cells.

88 mouse tracheal epithelium after ablation of luminal cells by inhaled SO2.

89 t loss of TRIM29 expression in normal breast luminal cells can contribute to malignant transformation

90 Here we demonstrate that luminal cells can develop independently of basal cells,

91 models have demonstrated that both basal and luminal cells can serve as cells of origin for prostate

92 G1P3 enhanced the survival of MCF10A acinar luminal cells causing hyperplasia by suppressing detachm

93 a failure in the apoptosis and clearance of luminal cells (cavitation).

94 nitor/differentiated cell balance within the luminal cell compartment towards the progenitors.

95 cells have been identified in both basal and luminal cell compartments.

96 to physically deform the innermost layer of luminal cells, compelling them to discharge the fluid th

97 The prostate gland mainly contains basal and luminal cells constructed as a pseudostratified epitheli

98 The adult mouse prostate luminal cells contain both castration-resistant Sox2-exp

99 basal type, a comparison of normal basal and luminal cells could yield insight into the tissue and ce

100 minal cell formation, but ultimately induced luminal cell death.

101 ING4 expression, suppressed JFK, and led to luminal cell death.

102 lure to properly down-regulate ING4 leads to luminal cell death.

103 cently, a subpopulation of multipotent human luminal cells defined by CD26 expression that retains pr

104 ative activity of basal cells in response to luminal cell-derived CXCL12.

105 and basal cells give rise to organoids, yet luminal-cell-derived organoids more closely resemble pro

106 Mutant luminal cells did not exhibit their distinctive transcri

107 tudy elucidates a role for TET2 in governing luminal cell differentiation and endocrine response that

108 tor that regulates genes involved in mammary luminal cell differentiation and tumor suppression.

109 The molecular mechanisms of luminal cell differentiation are not understood well eno

110 In contrast, Smo expression altered luminal cell differentiation in a cell-autonomous manner

111 trongly indicative of a progressive basal to luminal cell differentiation program based on human expr

112 C ablation, BSCs activate a hybrid basal and luminal cell differentiation program before giving rise

113 methylation patterns observed in the normal luminal cell differentiation program were significant ta

114 del that upon androgen exposure commits to a luminal cell differentiation trajectory from that of a b

115 on patterns associated with androgen induced luminal cell differentiation were found to have signific

116 In summary, Foxc1 regulates sweat duct luminal cell differentiation, and mutant mice mimic mili

117 ster regulator of mammary alveologenesis and luminal cell differentiation, is markedly reduced in mam

118 at regulate luminal progenitor cell renewal, luminal cell differentiation, mammary tumorigenesis, tam

119 During luminal cell differentiation, transient induction of ING

120 resses ING4 expression causing disruption of luminal cell differentiation.

121 ogenitors, which express both basal cell and luminal cell-enriched genes.

122 these cultured cells, we show that basal and luminal cells exhibit distinct responses to ionizing rad

123 a2(mut/WT) mammary glands, Brca2(mut/WT) HR- luminal cells exhibit greater organoid formation and pre

124 The Pb-Csf1 prostate luminal cells exhibit increased stem cell features and u

125 cer, because the disease is characterized by luminal cell expansion and the absence of basal cells.

126 loss, adult mice exhibited undifferentiated luminal cell expansion with basement-membrane detachment

127 Lower-level expression of ETV4 caused mild luminal cell expansion without histologic abnormalities,

128 lly defined by basal cell loss and malignant luminal cell expansion.

129 f Tspan8 or Thrsp prevents Brca2(mut/WT) HR- luminal cell expansion.

130 r, with loss of basal cells and expansion of luminal cells expressing prostate-specific antigen and a

131 gation in/on the gallbladder epithelium with luminal cell extrusion, for Salmonella maintenance in th

132 Even though luminal cells fail to respond, basal/stem cells demonstr

133 lls could no longer fully differentiate into luminal cells, failed to express ING4, and displayed a u

134 development during pregnancy by maintaining luminal cell fate and preventing uncontrolled basal cell

135 criptional corepressor TLE3 is a guardian of luminal cell fate in breast cancer and operates independ

136 Increased differentiation correlated with a luminal cell fate that could be reversed by inhibition o

137 urrounding many genes that are important for luminal cell fate, and supported the transcription of th

138 ssor DEAR1/TRIM62 is a critical regulator of luminal cell fate.

139 k consisting of GATA3, FOXA1, and PPAR drive luminal cell fate.

140 or synthesize testosterone for transport to luminal cells for reduction to DHT by 5alpha-steroid red

141 t the resistance is due to lower affinity of luminal cells for virus attachment, which can be overcom

142 vivo, rescued ING4 expression, and restored luminal cell formation, but ultimately induced luminal c

143 and efficient method for isolating basal and luminal cells from normal human breast tissue.

144 murine lineage-tracing experiments show that luminal cells generate basal cells.

145 yoepithelial cell types, with the genomes of luminal cells harbouring more than twice the number of h

146 Luminal cells have long been considered the cellular ori

147 sults in a decrease in basal cell number and luminal cell hyperproliferation.

148 er a critical role for ARID1A in maintaining luminal cell identity and endocrine therapeutic response

149 ressed genes, the LATS1-NCOR1 axis maintains luminal cell identity and restricts breast cancer progre

150 s associated with increased transcription of luminal cell identity genes and enhanced tamoxifen sensi

151 Induced loss of LSD1 in luminal cells in a mouse model of luminal breast cancer,

152 ntified populations of murine basal/stem and luminal cells in an in vivo prostate regeneration assay.

153 ation of both Foxa1 and Pten in intermediate/luminal cells in mice results in development of bladder

154 r cognate receptors expressed in a subset of luminal cells in the mammary epithelium.

155 tubule structures containing both basal and luminal cells in vivo.

156 ch mouse basal cells self-renew and generate luminal cells, including differentiated ciliated cells,

157 creased nuclear cyclin D3 protein in D1(-/-) luminal cells, indicating one compensatory mechanism.

158 Downregulation of JARID1B in luminal cells induces basal genes expression and growth

159 whether attenuating AR activity in prostate luminal cells induces inflammation.

160 Transient expression of ING4 is required for luminal cell induction; however, failure to properly dow

161 l plasticity by reprogramming differentiated luminal cells into a progenitor-like state through activ

162 and Sox9 suffices to convert differentiated luminal cells into MaSCs with long-term mammary gland-re

163 on, angiogenesis, and local and disseminated luminal cell invasion in vivo.

164 In basal progenitor-derived luminal cells, Klf5 deacetylation increases their prolif

165 ponse that selectively expands Brca2(mut/WT) luminal cells lacking hormone receptor expression (HR-).

166 lands, are composed of basal cells (BCs) and luminal cells (LCs)(1,2).

167 ort that induced p53 loss in Krt8(+) mammary luminal cells leads to their clonal expansion without di

168 of PKCzeta directs the resistant CSCs to the luminal cell-like state and sensitization to tamoxifen,

169 rate that germline mutations in Brca1 impair luminal cell lineage and mammary development, with its d

170 Establishment of the mammary luminal cell lineage is controlled primarily by hormones

171 Deletion of Kdm6a in the mammary luminal cell lineage led to a paucity of luminal cells a

172 mammary epithelial cells in a differentiated luminal cell lineage.

173 tricted to the oestrogen receptor-expressing luminal cell lineage.

174 ting tubular structures containing basal and luminal cell lineages in a dissociated cell prostate reg

175 g is detected in both the prostate basal and luminal cell lineages.

176 this is a significant barrier to generating luminal cell lines and experimental tumours in vivo and

177 positive and ER-negative (MDA-MB-453, SKBR3) luminal cell lines in the presence or absence of transie

178 Luminal cell lines repressed a large number of cell cycl

179 Starting from ER(+)PR(+) luminal cell lines, we generated lines with varying lumi

180 more dependent on glycolysis for growth than luminal cell lines.

181 ed a unique luminal cell type (termed type C luminal cell (Luminal-C)) marked by Tacstd2, Ck4 and Psc

182 orally ablating Pten in keratin 8-expressing luminal cells, luminal-derived Pten-deficient prostate t

183 es from flow dependence of Na+ uptake across luminal cell membranes; however, the underlying physical

184 land explants, epithelial reorganization and luminal cell morphological changes were induced by the a

185 prostate duct combined with weakly directed luminal cell movement toward the proximal region of the

186 eneration is driven by nearly all persisting luminal cells, not just by rare stem cells.

187 Nkx3.1 is ubiquitously expressed in luminal cells of hormonally intact prostate but, upon an

188 expression of the androgen receptor (AR) in luminal cells of human BPH specimens correlates with a h

189 GATA-3 was found in the luminal cells of mammary ducts and the body cells of ter

190 expressed heterogeneously in both basal and luminal cells of normal alveoli.

191 Further, as luminal cells of normal breast epithelial cells are enri

192 IL-1alpha is expressed predominantly by luminal cells of the genital tract in response to infect

193 CK14 mRNA was absent in the luminal cells of the most of the PIN lesions but was see

194 s approach, we discovered that the basal and luminal cells of the prostate exhibit distinct metabolom

195 ere persistently expressed in both basal and luminal cells of the tubular portion of normal glands as

196 ter and cellular proliferation, and detached luminal cells only in proximal tubules.

197 in the establishment and maintenance of the luminal cell phenotype during carcinogenesis and mammary

198 n human breast cancer and in influencing the luminal cell phenotype during normal mammary development

199 1 marks a specific subpopulation of proximal luminal cells (PLCs), enriched in the periurethral regio

200 o- and functional differentiation, a role in luminal cell polarity and lumenization of the ducts was

201 ng to a reduction in the CD24(hi)/CD49f(mid) luminal cell population and concomitant gain of the CD24

202 tin signaling also led to amplification of a luminal cell population that was positive for stem cell

203 significant diversification of intermediate luminal cell populations characterized by a range of and

204 t claudin-low breast cancer can develop from luminal cells, possibly via a basal-like intermediate st

205 uring pregnancy leads to dramatic defects in luminal cell proliferation and differentiation, resultin

206 impaired Akt and MAPK signaling and reduced luminal cell proliferation and survival.

207 paB activity independent of Hes1, stimulates luminal cell proliferation by potentiating PI3K-AKT sign

208 These data identify luminal cell rearrangements necessary for mammary develo

209 ncy contributes to breast tumorigenesis from luminal cells remains elusive.

210 noids are established from isolated basal or luminal cells, retaining their characteristics.

211 directs the final maturation of the adjacent luminal cell sheet during pregnancy.

212 rapid but labile cell cycle arrest, whereas luminal cells show a much more durable arrest, primarily

213 s such as p21(waf1), but the response in the luminal cells showed higher fold changes and included mo

214 partial secretory cell differentiation, the luminal cells showed weak to moderate staining for andro

215 anching, producing stunted ducts filled with luminal cells showing altered ovarian hormone receptor e

216 Thus, paracrine basal-to-luminal cell signaling, controlled by p63 via NRG1, orch

217 iles closely resembling mature human mammary luminal cell signatures.

218 ofiles suggest a key function for JARID1B in luminal cell-specific expression programs.

219 1-dependent R-loop mitigation contributes to luminal cell-specific transcription and differentiation,

220 Notch3 promotes mammary luminal cell specification and forced Notch3 activation

221 lls exhibit partial molecular resemblance to luminal cells, such as elevated Notch signaling and redu

222 impairs secretory function of mouse prostate luminal cells, suppresses anoikis of luminal epithelial

223 The luminal cell surface of the endothelium, which is direct

224 calize Vangl-Celsr polarity complexes at the luminal cell surface where opposite sides of the foregut

225 ble for the suppression of ING4 required for luminal cell survival and maintenance.

226 REB1 plays a central role in maintaining new luminal cell survival and that oncogenesis dramatically

227 eration, without affecting androgen-mediated luminal cell survival or regeneration.

228 ed proportion of multiciliated and secretory luminal cells that are maintained and regenerated by a p

229 rostate epithelium consists of predominantly luminal cells that express androgen receptor and require

230 on of myoepithelial cells and an increase in luminal cells that express keratin 14 and integrin-alpha

231 netic lineage-marking demonstrates that rare luminal cells that express Nkx3-1 in the absence of test

232 tuating a population of surviving autophagic luminal cells that resist anoikis.

233 that preferentially favours outgrowth of HR- luminal cells through the expression of interferon-respo

234 ermline mutation of Brca1 shifts the fate of luminal cells to cause luminal-to-basal mammary tumor tr

235 s by facilitating a switch from ER-dependent luminal cells to ER-independent basal-like cells.

236 Inflammation increased Basal-B-to-luminal cell transdifferentiation, but JAK/STAT inhibiti

237 Both TACSTD2(high) and TACSTD2(low) luminal cells transduced by constitutively activated AKT

238 We also provide evidence that luminal cell translocation may drive clonal selection by

239 rom mouse prostates, and identified a unique luminal cell type (termed type C luminal cell (Luminal-C

240 rmore, Tcfap2c influences development of the luminal cell type during mammary development.

241 er levels in the basal cell type than in the luminal cell type in mouse mammary tumors and human brea

242 nsion of a castration-resistant intermediate luminal cell type that correlates with treatment resista

243 e cells uniformly coexpressed both basal and luminal cell-type cytokeratins and the basal cell marker

244 iate in culture to generate mature basal and luminal cell types, including ER+ cells that have been c

245 erentiation of prostate cells to both NE and luminal cell types.

246 f the basal lineage disappeared, whereas the luminal cells underwent carcinogenesis.

247 cells, which appeared to differentiate from luminal cells via activation of Src.

248 The ability of IFN-gamma to repress FOXA1 in luminal cells was abrogated by ruxolitinib inhibition of

249 A transient enrichment of K6-positive luminal cells was observed upon hormonal treatment sugge

250 Different movement behaviors for TA/ICs and luminal cells were assessed by their ability to recreate

251 in subclasses and isoforms characteristic of luminal cells were detected in this cell type.

252 amplifying/intermediate cells (TA/ICs), and luminal cells were individually modeled within a three-d

253 ion revealed that myosin IIC is expressed in luminal cells, whereas myosin IIB expression is up-regul

254 be bipotent and can generate either basal or luminal cells, whereas the luminal epithelium has not be

255 q analysis corroborates the expansion of HR- luminal cells which express elevated transcript levels o

256 terminal differentiation markers in the duct luminal cells, which most likely contribute to keratotic

257 fferentiation of basal epithelial cells into luminal cells, while sustained ING4 expression induces a

258 transduced primary human prostate basal and luminal cells with lentiviruses expressing c-Myc and act

259 ostates, Klf5 is expressed in both basal and luminal cells, with basal cells preferentially expressin