Let-7: a regulator of the ERα signaling pathway in human breast tumors and breast cancer stem cells

Oncol Rep. 2013 May;29(5):2079-87. doi: 10.3892/or.2013.2330. Epub 2013 Mar 6.

Abstract

The oncogenic role of estrogen receptor (ER)α and its correlation with let-7 microRNAs (miRNAs) have been studied and confirmed in breast tumors; however, this correlation has not been investigated in breast cancer stem cells (BCSCs). In the present study, we detected the expression of let-7 and ERα in ER-positive breast tumor tissues. Furthermore, we used a FACSAria cell sorter to separate side population (SP) cells from the MCF-7 and T47-D cell lines by Hoechst 33342 staining. The expression of let-7 miRNAs, ERα and its downstream genes in SP and non-SP (NSP) cells were analyzed. In additional experiments, we transfected a plasmid expressing let-7a into SP cells isolated from the MCF-7 and T47-D cell lines in order to observe changes in the expression of downstream genes (cyclin D1 and pS2). The correlation among let-7, ERα and ERα downstream genes suggested that let-7 acts as a tumor suppressor by inhibiting ERα-mediated cellular malignant growth in ER-positive breast cancer stem cells. The suppression of ERα by the upregulation of let-7 expression may be a promising strategy for the inhibition of the ER signaling pathway and for the elimination of cancer stem cells, thus aiding in the treatment of breast cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / genetics
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism*
  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cyclin D1 / genetics
  • Cyclin D1 / metabolism
  • Estrogen Receptor alpha / genetics
  • Estrogen Receptor alpha / metabolism*
  • Female
  • Humans
  • MCF-7 Cells
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Middle Aged
  • Neoplastic Stem Cells / metabolism*
  • Presenilin-2 / genetics
  • Presenilin-2 / metabolism
  • Side-Population Cells / metabolism
  • Signal Transduction
  • Up-Regulation

Substances

  • Estrogen Receptor alpha
  • MicroRNAs
  • PSEN2 protein, human
  • Presenilin-2
  • mirnlet7 microRNA, human
  • Cyclin D1