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Effects of estrogen receptor expression on growth and transformation of cells overexpressing neu

K Russell1, E Lee, N Kiyokawa

  • 1UNIV TEXAS,MD ANDERSON CANC CTR,DEPT TUMOR BIOL,HOUSTON,TX 77030. UNIV TEXAS,MD ANDERSON CANC CTR,BREAST CANC RES PROGRAM,HOUSTON,TX 77030. KUMAMOTO UNIV,SCH MED,DEPT ONCOL,KUMAMOTO 860,JAPAN.

Oncology Reports
|May 20, 2011
PubMed

Insights

Estrogen receptor (ER) and E2 signaling can repress breast cancer cell transformation and promote proliferation. This suggests a key role for ER and neu in regulating breast cancer progression and hormone independence.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Breast cancer progression to hormone independence can occur without loss of estrogen receptor (ER) function.
  • Altered cellular pathways disrupting estrogen-regulated growth contribute to hormone independence.
  • An inverse relationship exists between estrogen stimulation and neu expression in ER(+) breast cancer cells.
  • Neu amplification/overexpression enhances cellular transformation and metastasis, correlating with aggressive phenotypes.

Purpose of the Study:

  • To investigate the role of estrogen (E2) and ER in modulating neu-mediated transformation.
  • To examine the effects of E2/ER on the growth and transformation of ER(+), neu-overexpressing breast cancer cells.

Main Methods:

  • NIH/3T3 cells were analyzed for transformation by the neu oncogene in the presence of E2/ER.
  • ER(+), neu-overexpressing breast cancer cell lines were treated with E2/ER.
  • Anchorage-independent growth was measured to assess transformation.
  • Cellular proliferation in monolayer culture was evaluated.

Main Results:

  • E2/ER repressed the transformation of NIH/3T3 cells induced by the neu oncogene.
  • In ER(+), neu-overexpressing breast cancer cells, E2/ER repressed the transformed phenotype (anchorage-independent growth).
  • E2/ER stimulated cellular proliferation in monolayer culture.

Conclusions:

  • The presence of E2/ER can repress oncogenic transformation mediated by neu.
  • E2/ER signaling plays a dual role in breast cancer cells: repressing transformation while stimulating proliferation.
  • A model is proposed where neu acts as a key regulator in the progression to hormone independence, influenced by E2/ER status.

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