About: TGF-βI Regulates Cell Migration through Pluripotent Transcription Factor OCT4 in Endometriosis

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About: TGF-βI Regulates Cell Migration through Pluripotent Transcription Factor OCT4 in Endometriosis Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	TGF-βI Regulates Cell Migration through Pluripotent Transcription Factor OCT4 in Endometriosis
Creator	Huang, Yen-Hua Au, Heng-Kien Chang, Jui-Hung Chang, Te-Sheng Chen, Yu-Hsi Kuo, Hung-Chih Kuo, Yung-Che Lan, Pei-Chi Lee, Kha-Liang Lee, Mei-Tsu Lee, Wei-Chin Tzeng, Chii-Ruey Wu, Yu-Chih Au, H-K Chang, J-H
Source	PMC
abstract	Transforming growth factor (TGF-β)/TGF-β receptor signal is known to promote cell migration. Up-regulation of TGF-β in serum/peritoneal fluid and increased levels of pluripotent transcription factor OCT4 in endometriotic tissues are frequently observed in patients with endometriosis. However, the mechanisms underlying how TGF-β/TGF-β receptor and OCT4 affect endometriotic cell migration still remain largely unknown. Therefore, endometriotic tissue with high cell migratory capacity were collected from patients with adenomyotic myometrium (n = 23) and chocolate cyst (n = 24); and endometrial tissue with low cell migratory capacity in normal endometrium or hyperplastic endometrium (n = 8) were collected as the controls. We found the mRNA levels of TGF-β receptor I (TGF-β RI) and OCT4 were significantly higher in the high-migratory ectopic endometriotic tissues than those of the low-migratory normal or hyperplastic endometrium. Positive correlations between TGF-β RI and OCT4, and either TGF-β RI or OCT4 with migration-related genes (SNAIL, SLUG and TWIST) regarding the mRNA levels were observed in human endometriotic tissues. TGF-βI dose-dependently increased the gene and protein levels of OCT4, SNAIL and N-Cadherin (N-CAD) and silencing of endogenous OCT4 significantly suppressed the TGF-βI-induced expressions of N-CAD and SNAIL in primary human endometriotic stromal cells and human endometrial carcinoma cell lines RL95-2 and HEC1A. Furthermore, TGF-βI significantly increased the migration ability of endometriotic cells and silencing of OCT4 dramatically suppressed the TGF-βI-induced cell migration activity evidenced by wound-closure assay, transwell assay, and confocal image of F-actin cellular distribution. In conclusion, the present findings demonstrate that the niche TGF-β plays a critical role in initiating expressions of pluripotent transcription factor OCT4 which may contribute to the ectopic endometrial growth by stimulating endometrial cell migration. These findings would be useful for developing therapeutic strategies targeting TGF-β-OCT4 signaling to prevent endometriosis in the future.
has issue date	2015-12-16(xsd:dateTime)
bibo:doi	10.1371/journal.pone.0145256
bibo:pmid	26675296
has license	cc-by
sha1sum (hex)	73962bb05d0fa45657756857801fbb3f9e139b04
schema:url	https://doi.org/10.1371/journal.pone.0145256
resource representing a document's title	TGF-βI Regulates Cell Migration through Pluripotent Transcription Factor OCT4 in Endometriosis
has PubMed Central identifier	PMC4682958
has PubMed identifier	26675296
schema:publication	PLoS One
resource representing a document's body	covid:73962bb05d0fa45657756857801fbb3f9e139b04#body_text
is schema:about of	named entity 'endometrial tissue' named entity 'Up-regulation' named entity 'mechanisms' named entity 'normal' named entity 'OCT4' named entity 'TGF-β' named entity 'endometrium' named entity 'OCT4' named entity 'ECTOPIC' named entity 'INCREASED' named entity 'TWIST' named entity 'NICHE' named entity 'PROTEIN LEVELS' named entity 'CELL MIGRATION' named entity 'SNAIL' named entity 'GENES' named entity 'ENDOMETRIAL' named entity 'LARGELY' named entity 'ASSAY' named entity 'POSITIVE' named entity 'HYPERPLASTIC ENDOMETRIUM' covid:arg/73962bb05d0fa45657756857801fbb3f9e139b04 named entity 'TISSUE' named entity 'IMAGE' named entity 'HUMAN' named entity 'CELL LINES' named entity 'TRANSFORMING GROWTH FACTOR' named entity 'UNKNOWN' named entity 'N-CADHERIN' named entity 'DOSE' named entity 'B2 RECEPTOR' named entity 'UP-REGULATION' named entity 'FOUND' named entity 'EITHER' named entity 'COLLECTED' named entity 'ABILITY' named entity 'PRESENT' named entity 'MYOMETRIUM' named entity 'TGF' named entity 'OCT4' named entity 'ENDOMETRIOSIS' named entity 'TRANSCRIPTION FACTOR' named entity 'PLURIPOTENT' named entity 'HIGH' named entity 'ENDOMETRIOSIS' named entity 'LOW' named entity 'MIGRATION' named entity 'PLURIPOTENT' named entity 'MRNA' named entity 'CHOCOLATE CYST' named entity 'CRITICAL' named entity 'HEC1A' named entity 'SIGNAL' named entity 'INITIATING' named entity 'PATIENTS' named entity 'MIGRATORY' named entity 'SLUG' named entity 'CELLULAR DISTRIBUTION' named entity 'RELATED' named entity 'CONCLUSION' named entity 'ACTIVITY' named entity 'UNDERLYING' named entity 'CAD' named entity 'MECHANISMS' named entity 'FLUID' named entity 'FINDINGS' named entity 'LEVELS'

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