Characterization of a novel breast cancer cell line derived from a metastatic bone lesion of a breast cancer patient.

Purpose: We aimed to generate and characterize a novel cell line from a breast cancer bone metastasis to better study the progression of the disease.

Methods: The cell line, P7731, was derived from a metastatic bone lesion of a breast cancer patient and assessed for marker expression. P7731 was analyzed for DNA copy number variation, somatic mutations, and gene expression and was compared with the primary tumor.

Using the MCF10A/MCF10CA1a Breast Cancer Progression Cell Line Model to Investigate the Effect of Active, Mutant Forms of EGFR in Breast Cancer Development and Treatment Using Gefitinib.

Background: Basal-like and triple negative breast cancer (TNBC) share common molecular features, poor prognosis and a propensity for metastasis to the brain. Amplification of epidermal growth factor receptor (EGFR) occurs in ~50% of basal-like breast cancer, and mutations in the epidermal growth factor receptor (EGFR) have been reported in up to ~ 10% of Asian TNBC patients. In non-small cell lung cancer several different mutations in the EGFR tyrosine kinase domain confer sensitivity to receptor tyrosine kinase inhibitors, but the tumourigenic potential of EGFR mutations in breast cells and their potential for targeted therapy is unknown.

Protein tyrosine phosphatase-alpha complexes with the IGF-I receptor and undergoes IGF-I-stimulated tyrosine phosphorylation that mediates cell migration.

Protein tyrosine phosphatase-alpha (PTPalpha) is a widely expressed receptor-type phosphatase that functions in multiple signaling systems. The actions of PTPalpha can be regulated by its phosphorylation on serine and tyrosine residues, although little is known about the conditions that promote PTPalpha phosphorylation. In this study, we tested the ability of several extracellular factors to stimulate PTPalpha tyrosine phosphorylation.

PRL PTPs: mediators and markers of cancer progression.

Aberrant protein tyrosine phosphorylation resulting from the altered activity of protein tyrosine phosphatases (PTPs) is increasingly being implicated in the genesis and progression of human cancer. Accumulating evidence indicates that the dysregulated expression of members of the phosphatase of regenerating liver (PRL) subgroup of PTPs is linked to these processes. Enhanced expression of the PRLs, notably PRL-1 and PRL-3, promotes the acquisition of cellular properties that confer tumorigenic and metastatic abilities.

PRL-3: a metastasis-associated phosphatase in search of a function.

The molecular and cellular events involved in cancer progression and metastasis remain much less well-defined than those involved in oncogenesis, despite the fact that cell metastasis is the major factor in cancer mortality. Thus, the discovery that the expression of a protein tyrosine phosphatase, protein of regenerating liver-3 (PRL-3), is upregulated in colon cancer metastases provided an exciting indication that the altered regulation of specific protein tyrosine phosphorylation events and signaling pathways might characterize these metastatic cells and/or be key in promoting the tumor-to-metastasis transition in this, and perhaps other, cancers of epithelial origin. However, the cellular substrate(s) of PRL-3 has not been identified, and little is known of PRL-3-mediated cellular signaling pathways.