Synthetic Beta-Lactam Antibiotics as a Selective Breast Cancer Cell Apoptosis Inducer: Significance in Breast Cancer Prevention and Treatment

Abstract

Activation of the cellular apoptotic program is a current strategy for the prevention and treatment of human cancer including breast cancer. Because of the ease of synthesis and structural manipulation, small molecules with apoptosis-inducing ability have great potential to be developed into chemotherapeutic drugs. The b-lactam antibiotics have for the past 60 years played an essential role in treating bacterial infections without causing toxic side effects in the host. We hypothesized that active N-thiolated b-lactams can target a tumor-specific protein(s) and selectively induce apoptosis in human breast cancer but not normal cells. In this report, we have designed and synthesized a number of beta-lactams with selected C3 and N1 ring substituents, and evaluated their potencies to inhibit proliferation and induce apoptosis in human breast cancer cells. We have also studied the biochemical targets of these b-lactams by performing microarray assay. Our results supported by this IDEA award strongly support our hypothesis that beta-lactams cause tumor DNA damage, which is responsible for their anti-tumor activities. Our studies have provided strong support for proof-of-concept of the potential use of these b-lactams in breast cancer prevention and treatment.

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Document Details

Document Type
Technical Report
Publication Date
Mar 01, 2008
Accession Number
ADA485735

Entities

People

  • Q. P. Dou

Organizations

  • Wayne State University

Tags

DTIC Thesaurus Topics

  • Antineoplastic Agents
  • Breast Cancer
  • Cell Physiological Processes
  • Cells
  • Chemical Synthesis
  • Chemistry
  • Health Services
  • Lymphocytes
  • Medical Personnel
  • Oncology
  • Programmed Cell Death

Fields of Study

  • Biology
  • Chemistry

Readers

  • Molecular Genetics
  • Oncology (Cancer Research).

Technology Areas

  • Fully Networked C3
  • Fully Networked C3 - Command and Control