Long noncoding RNA BHLHE40‐AS1 promotes early breast cancer progression through modulating IL‐6/STAT3 signaling

Autor: Cristian Coarfa, Ali S. Ropri, Emilio O. Herrera, William P. Smith, Rebecca Sinnott DeVaux, Jason I. Herschkowitz, Peter A. Hall, Fariba Behbod, Sandra L. Grimm, Sridar V. Chittur
Rok vydání: 2020
Předmět:
STAT3 Transcription Factor
0301 basic medicine
Breast Neoplasms
Biochemistry
Article
03 medical and health sciences
0302 clinical medicine
Breast cancer
Cell Movement
Cell Line
Tumor
Ductal carcinoma in situ (DCIS)
Basic Helix-Loop-Helix Transcription Factors
Tumor Microenvironment
medicine
Humans
Neoplasm Invasiveness
RNA
Antisense
Overdiagnosis
skin and connective tissue diseases
Interleukin 6
STAT3
neoplasms
Molecular Biology
Cell Proliferation
Homeodomain Proteins
biology
Interleukin-6
business.industry
Gene Expression Profiling
Cell Cycle
Interleukin
Cell Biology
Ductal carcinoma
medicine.disease
Long non-coding RNA
Gene Expression Regulation
Neoplastic
body regions
Carcinoma
Intraductal
Noninfiltrating
030104 developmental biology
030220 oncology & carcinogenesis
Disease Progression
Cancer research
biology.protein
Female
RNA
Long Noncoding
business
Signal Transduction
Zdroj: J Cell Biochem
ISSN: 1097-4644
0730-2312
Popis: 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.
Databáze: OpenAIRE
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