circCTIC1 promotes the self-renewal of colon TICs through BPTF-dependent c-Myc expression.
Animals
Antigens, Nuclear
/ genetics
Apoptosis
Cell Proliferation
Cell Self Renewal
Cell Transformation, Neoplastic
Colonic Neoplasms
/ genetics
Gene Expression Regulation, Neoplastic
Humans
Mice
Mice, Inbred BALB C
Mice, Nude
Neoplastic Stem Cells
/ metabolism
Nerve Tissue Proteins
/ genetics
Promoter Regions, Genetic
Proto-Oncogene Proteins c-myc
/ genetics
RNA, Circular
/ genetics
Signal Transduction
Transcription Factors
/ genetics
Tumor Cells, Cultured
Xenograft Model Antitumor Assays
Journal
Carcinogenesis
ISSN: 1460-2180
Titre abrégé: Carcinogenesis
Pays: England
ID NLM: 8008055
Informations de publication
Date de publication:
10 06 2019
10 06 2019
Historique:
received:
28
08
2018
revised:
10
10
2018
pubmed:
8
11
2018
medline:
26
2
2020
entrez:
8
11
2018
Statut:
ppublish
Résumé
Colon tumor is a conman tumor in the world. There are various kinds of cells in colon tumor bulk, and only a small population can initiate tumor efficiently and termed as tumor-initiating cells (TICs). With self-renewal and differentiation capacities, colon TICs drive colon tumorigenesis, metastasis and relapse. However, the molecular mechanisms of colon TICs self-renewal are elusive. Here, we found that circular RNA (circCTIC1) was highly expressed in colon tumor and colon TICs. circCTIC1 knockdown impaired the self-renewal of colon TICs, and its overexpression played an opposite role. circCTIC1 promoted the expression of c-Myc and drove the self-renewal of colon TIC through c-Myc-dependent manner. circCTIC1 interacted with nuclear remodeling factor (NURF) complex, recruited NURF complex onto c-Myc promoter and finally drove the transcriptional initiation of c-Myc. Altogether, circCTIC1 drove the self-renewal of colon TICs through bromodomain PHD finger transcription factor (BPTF)-mediated c-Myc expression.
Identifiants
pubmed: 30403769
pii: 5156288
doi: 10.1093/carcin/bgy144
doi:
Substances chimiques
Antigens, Nuclear
0
MYC protein, human
0
Nerve Tissue Proteins
0
Proto-Oncogene Proteins c-myc
0
RNA, Circular
0
Transcription Factors
0
fetal Alzheimer antigen
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
560-568Informations de copyright
© The Author(s) 2018. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.