Long noncoding RNA BHLHE40-AS1 promotes early breast cancer progression through modulating IL-6/STAT3 signaling.
Basic Helix-Loop-Helix Transcription Factors
/ genetics
Breast Neoplasms
/ genetics
Carcinoma, Intraductal, Noninfiltrating
/ genetics
Cell Cycle
Cell Line, Tumor
Cell Movement
Cell Proliferation
Disease Progression
Female
Gene Expression Profiling
Gene Expression Regulation, Neoplastic
Homeodomain Proteins
/ genetics
Humans
Interleukin-6
/ genetics
Neoplasm Invasiveness
RNA, Antisense
/ genetics
RNA, Long Noncoding
/ genetics
STAT3 Transcription Factor
/ metabolism
Signal Transduction
Tumor Microenvironment
BHLHE40-AS1
IL-6
ILF3
STAT3
breast cancer progression
ductal carcinoma in situ (DCIS)
long noncoding RNA
Journal
Journal of cellular biochemistry
ISSN: 1097-4644
Titre abrégé: J Cell Biochem
Pays: United States
ID NLM: 8205768
Informations de publication
Date de publication:
07 2020
07 2020
Historique:
received:
26
08
2019
accepted:
19
12
2019
pubmed:
8
1
2020
medline:
3
8
2021
entrez:
8
1
2020
Statut:
ppublish
Résumé
Ductal carcinoma in situ (DCIS) is a nonobligate precursor to invasive breast cancer. Only a small percentage of DCIS cases are predicted to progress; however, there is no method to determine which DCIS lesions will remain innocuous from those that will become invasive disease. Therefore, DCIS is treated aggressively creating a current state of overdiagnosis and overtreatment. There is a critical need to identify functional determinants of progression of DCIS to invasive ductal carcinoma (IDC). Interrogating biopsies from five patients with contiguous DCIS and IDC lesions, we have shown that expression of the long noncoding RNA BHLHE40-AS1 increases with disease progression. BHLHE40-AS1 expression supports DCIS cell proliferation, motility, and invasive potential. Mechanistically, BHLHE40-AS1 modulates interleukin (IL)-6/signal transducer and activator of transcription 3 (STAT3) activity and a proinflammatory cytokine signature, in part through interaction with interleukin enhancer-binding factor 3. These data suggest that BHLHE40-AS1 supports early breast cancer progression by engaging STAT3 signaling, creating an immune-permissive microenvironment.
Identifiants
pubmed: 31907974
doi: 10.1002/jcb.29621
pmc: PMC7263938
mid: NIHMS1065812
doi:
Substances chimiques
BHLHE40 protein, human
0
Basic Helix-Loop-Helix Transcription Factors
0
Homeodomain Proteins
0
IL6 protein, human
0
Interleukin-6
0
RNA, Antisense
0
RNA, Long Noncoding
0
STAT3 Transcription Factor
0
STAT3 protein, human
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
3465-3478Subventions
Organisme : NCI NIH HHS
ID : R01 CA207445
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA168524
Pays : United States
Organisme : NCI NIH HHS
ID : R21 CA185460
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES030285
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA125123
Pays : United States
Informations de copyright
© 2020 The Authors. Journal of Cellular Biochemistry published by Wiley Periodicals, Inc.
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