Breast cancer metastasis to bone: a study of the effect of bone cell conditioned media on triple negative breast cancer cells in bone microenvironment

Date
2013
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University of Delaware
Abstract
Breast cancer is the second leading cause of death in women- behind lung cancer. Statistics have shown that 1 in 36 women in the United States die from the pandemic. Triple negative breast cancer, TNBC, which accounts for 10-20% of all breast cancer subtypes, is classified as aggressive in growth and invasiveness and is associated with poorer short-term prognosis. Due to their independence from hormone receptors, these cancer cells lack effective therapeutics and treatment of patients is limited to chemotherapy. Death occurrence from breast cancer is prevalent in patients with metastatic breast cancer. In the United States, approximately 200,000 cases of metastatic breast cancer and 50,000 cases of non-invasive breast cancer are estimated to be diagnosed annually. Breast cancer is frequently associated with skeletal metastases. Over 70% of breast cancer metastasis occurs in bone. Bone metastasis causes bone pain, fracture, hypercalcemia, and paralysis. This is because tumor-bone interaction in the bone microenvironment creates a vicious cycle that upsurges bone resorption. While the effect of triple negative breast cancer tumor cells on bone are widely known, the effect of bone cells on metastatic triple negative breast cancer cells is not fully understood. The present study was designed to investigate the effect of bone-conditioned medium on TNBC using conditioned medium from different lineages of cells within the bone marrow. Conditioned media harvested from new born mice Calvaria, mouse myoblast cell line C2C12, preosteoblast cell line MC3T3, 8-weeks old mice BMSC, 6-months old mice BMSC and osteoclast were all used as treatment to determine the effects on migration of TNBC. Breast cancer cells, MDA-MB-231, extracted from older Caucasian patients, MDA-MB435, extracted from younger Caucasian patients and MDA-MB468, extracted from older African American patients were used as triple negative breast cancer cells. Here, we report that in comparison to the above conditioned medium, myoblast-conditioned medium greatly inhibited these breast cancer cells. However, the degree of inhibition depended on the type of TNBC. Further investigations were conducted to determine the effect of myoblastconditioned medium on proliferation and invasion activities of TNBC and it was found that myoblast-conditioned medium greatly inhibited triple negative breast cancer proliferation and invasion of MDA-MB-435. Additionally, results indicated that invasion of MDA-MB-231 and MDA-MB-468 to bone was inhibited under the influence of myoblast-conditioned medium. However, it was observed that minimal myoblast-conditioned medium inhibited triple negative breast cancer proliferation of MDA-MB-231 while it promoted triple negative breast cancer proliferation of MDAMB- 468.
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