Accession Number:

ADA415463

Title:

Promotion of Breast Cancer Growth Within Bone by the C-terminal Hexapeptide Enzymatically Derived From Osteocalcin, a Bone Matrix Protein

Descriptive Note:

Annual rept.

Corporate Author:

TENNESSEE UNIV MEMPHIS

Personal Author(s):

Report Date:

2002-08-01

Pagination or Media Count:

5.0

Abstract:

Plasm in enzymatically produces an Osteocaicin- derived C-terminal Hexapeptide from bone matrix which promotes the growth of human osteosarcoma cells by blocking the action of the hormone oxytocin. We hypothesize that the C-terminal Hexapeptide promotes the growth of breast cancer cells in bone. Breast cancer cells that are growth inhibited by oxytocin may be growth stimulated in bone where abundant C-terminal Hexapeptide is present. Growth stimulation in bone would enhance the likelihood of bone metastasis by breast cancer cells. Our first objective was to determine the affect of C-terminal Hexapeptide on the growth of MDA-MB-231 breast cancer cells inhibited by oxytocin, as published by others. Oxytocin 10 exp -5 Minhibited growth but this is not in agreement with published results. We have obtained a 1-year no cost extension to examine alternate sources and forms of oxytocin and try cAMP and PGE2 assays to see if biological effectiveness of oxytocin is achieved. Once an effective oxytocin and cell assay is established we will characterize the effects of hexapeptide on breast cancer cells. Counteracting the metastasis of breast cancer to bone could enhance patient survival. Understanding the mechanisms that enable breast cancer cells to metastasize, survive, and grow in bone are vital to alter the process. The experiments should provide new information on the growth stimulatory environment of bone, and contribute to the understanding of bone-seeking breast cancers. The knowledge will be useful for developing strategies to counteract the spread of breast cancer to bone.

Subject Categories:

  • Anatomy and Physiology
  • Medicine and Medical Research

Distribution Statement:

APPROVED FOR PUBLIC RELEASE