scispace - formally typeset
Proceedings ArticleDOI

Abstract 2547: Discovery and characterization of late-stage breast cancer estrogen receptor alpha 1 bound long non-coding RNAs

TLDR
This work aimed to identify lncRNAs bound to the estrogen receptor alpha 1 protein (ESR1) that promote late-stage relapse breast cancer and discovered 1192 altered lnc RNAs when comparing the metastatic to the primary samples.
Abstract
Breast cancer (BC) is the second most common newly diagnosed cancer and the second leading cause of cancer death among women in the United States. Despite the proven benefits of adjuvant endocrine therapy in women with hormone receptor positive BC, relapses still occur even after initial treatment with endocrine therapy for 5 years, referred to as late-stage relapse. Long non-coding RNAs (lncRNAs) have been shown to be dysregulated in breast cancer. Recent studies have also shown lncRNAs to function by interfacing with corresponding RNA binding proteins to play critical regulatory roles of diverse cellular processes. Therefore, we hypothesize that lncRNAs may interact with ER to regulate genes promoting late-stage relapse. To address this, we aimed to identify lncRNAs bound to the estrogen receptor alpha 1 protein (ESR1) that promote late-stage relapse breast cancer. We first used transcriptome sequencing to identify altered expression levels of lncRNAs between 72 primary tumors and 24 late-stage relapse breast cancer patients. We detected 1192 altered lncRNAs when comparing the metastatic to the primary samples (FDR Citation Format: Jessica Monique Silva-Fisher, Abdallah M. Eteleeb, Torsten Nielsen, Charles M. Perou, Jorge S. Reis-Filho, Mathew J. Ellis, Elaine R. Mardis, Christopher A. Maher. Discovery and characterization of late-stage breast cancer estrogen receptor alpha 1 bound long non-coding RNAs [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2547. doi:10.1158/1538-7445.AM2017-2547

read more

Citations
More filters
Journal ArticleDOI

MAPK‐mediated upregulation of fibrinogen‐like protein 2 promotes proliferation, migration, and invasion of colorectal cancer cells

TL;DR: MAPK‐mediated upregulation of FGL2 promotes the proliferation, migration, and invasion of CRC cells, and is determined to be downregulated by MAPK signaling inhibitor U0126.
Related Papers (5)