LINC00520 is induced by Src, STAT3, and PI3K and plays a functional role in breast cancer

Whitney S Henry1, David G Hendrickson2,3, Francisco Beca1

  • 1Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.

Oncotarget
|September 15, 2016
PubMed

Insights

A novel long non-coding RNA, LINC00520, is upregulated by oncogenes like v-Src and PI3K in breast cancer cells. Its depletion impairs cell migration, suggesting a role in breast cancer development.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) are crucial in cellular functions and diseases, including cancer.
  • Oncogenic signaling pathways play a significant role in breast cancer pathogenesis.

Purpose of the Study:

  • To identify novel lncRNAs involved in breast cancer development.
  • To characterize the role and regulation of LINC00520 in breast cancer.

Main Methods:

  • Global gene expression profiling of mammary epithelial cells.
  • Analysis of LINC00520 expression in response to oncogenic signaling (v-Src, PI3K, STAT3).
  • Functional assays including cell migration and 3D invasion, and RNA sequencing.

Main Results:

  • Identified LINC00520 as a novel lncRNA upregulated by v-Src and PI3K signaling, dependent on STAT3.
  • LINC00520 is elevated in a subset of human breast carcinomas, particularly basal-like subtype.
  • Depletion of LINC00520 reduced cell migration and invasion, and altered gene expression profiles.

Conclusions:

  • LINC00520 is regulated by key oncogenic pathways (Src, PI3K, STAT3) in breast epithelial cells.
  • LINC00520 contributes to breast cancer cell migration and invasion.
  • LINC00520 is a potential therapeutic target and biomarker for breast cancer.

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