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Selective expression of long non‐coding RNAs in a breast cancer cell progression model
Author(s) -
Tracy Kirsten M.,
Tye Coralee E.,
Page Natalie A.,
Fritz Andrew J.,
Stein Janet L.,
Lian Jane B.,
Stein Gary S.
Publication year - 2018
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25997
Subject(s) - breast cancer , transcriptome , biology , hras , long non coding rna , tumor progression , cancer , cancer research , computational biology , rna , bioinformatics , gene , gene expression , genetics , kras , colorectal cancer
Long non‐coding RNAs (lncRNAs) are acknowledged as regulators of cancer biology and pathology. Our goal was to perform a stringent profiling of breast cancer cell lines that represent disease progression. We used the MCF‐10 series, which includes the normal‐like MCF‐10A, HRAS‐transformed MCF‐10AT1 (pre‐malignant), and MCF‐10CA1a (malignant) cells, to perform transcriptome wide sequencing. From these data, we have identified 346 lncRNAs with dysregulated expression across the progression series. By comparing lncRNAs from these datasets to those from an additional set of cell lines that represent different disease stages and subtypes, MCF‐7 (early stage, luminal), and MDA‐MB‐231 (late stage, basal), 61 lncRNAs that are associated with breast cancer progression were identified. Querying breast cancer patient data from The Cancer Genome Atlas, we selected a lncRNA, IGF‐like family member 2 antisense RNA 1 (IGFL2‐AS1), of potential clinical relevance for functional characterization. Among the 61 lncRNAs, IGFL2‐AS1 was the most significantly decreased. Our results indicate that this lncRNA plays a role in downregulating its nearest neighbor, IGFL1, and affects migration of breast cancer cells. Furthermore, the lncRNAs we identified provide a valuable resource to mechanistically and clinically understand the contribution of lncRNAs in breast cancer progression.