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TROP2 methylation and expression in tamoxifen-resistant breast cancer

Stephanie M Zimmers1, Eva P Browne1, Kristin E Williams1

  • 11Department of Veterinary & Animal Sciences, University of Massachusetts, Amherst, Life Sciences Laboratories, Room 540D, 240 Thatcher Road, Amherst, MA 01003 USA.

Cancer Cell International
|July 14, 2018
PubMed
Abstract

Insights

5-Aza-2'deoxycytidine (5-Aza-dC) shows differential effects on breast cancer cells, impacting hormone-resistant and estrogen receptor-negative tumors more significantly. TACSTD2 re-expression alone did not fully explain decreased proliferation, highlighting complex signaling networks.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • 5-Aza-2'-deoxycytidine (5-Aza-dC) is a DNA methyltransferase 1 inhibitor explored for breast cancer treatment.
  • Response to 5-Aza-dC varies among breast tumors, particularly in hormone-resistant types.

Purpose of the Study:

  • To investigate the differential effects of 5-Aza-dC on estrogen receptor-positive and -negative breast cancer cells.
  • To identify genes regulated by DNA methylation and 5-Aza-dC treatment in breast cancer.

Main Methods:

  • Comparative analysis of 5-Aza-dC treatment on MCF7 (ER-positive) and TMX2-28 (ER-negative) cell lines.
  • Utilized HM450 Methylation Bead Chip, pyrosequencing, and RT-qPCR to identify and validate gene expression changes.
  • Assessed DNA methylation and protein expression of TACSTD2/TROP2 in primary and recurrent breast tumors.

Main Results:

  • 5-Aza-dC exhibited a stronger effect on the ER-negative TMX2-28 cell line compared to the ER-positive MCF7 cell line.
  • Identified TACSTD2 as a gene silenced by methylation in TMX2-28, re-expressed upon 5-Aza-dC treatment.
  • No significant correlation found between TROP2 protein levels and TACSTD2 methylation in primary or recurrent tumors; TACSTD2 knockdown increased MCF7 proliferation, but re-expression in TMX2-28 did not inhibit proliferation.

Conclusions:

  • The re-expression of TACSTD2 alone does not fully account for the anti-proliferative effects of 5-Aza-dC in TMX2-28 cells.
  • The TROP2 signaling network is complex, suggesting TROP2 may be a therapeutic target in specific cancer contexts.
  • Further research is required to identify biomarkers for TROP2's role in tumor growth and its therapeutic potential.
Keywords:
5-aza-2′-deoxycytidine (or decitabine or 5-Aza-dC)DNA methylationHuman Methylation 450 BeadChipTACSTD2TROP2Tamoxifen-resistant breast cancer (or Tamoxifen resistance breast cancer)

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