Our lab has previously shown that ECM1 overexpression may have potential utility as a diagnostic marker for thyroid cancers. We have also demonstrated that ECM1 overexpression is an independent marker of poor prognosis is primary breast cancers.

ECM1 is an important part of the scaffolding or extracellular matrix surrounding cells. It is overexpressed in a number of epithelial malignancies including invasive ductal breast carcinomas, esophageal squamous cell carcinomas, gastric cancers, colorectal, lung, laryngeal, hepatocellular, biliary and thyroid cancers. In small studies, ECM1 overexpression has also been correlated with metastasis and poor prognosis in lung, breast, laryngeal and hepatocellular cancers, in addition to cholangiocarcinomas.

Although ECM1 expression may have prognostic significance, not much is known about the regulation of its expression or the mechanisms via which it affects tumor prognosis. Using a melanoma cell line model, our lab has recently identified the ECM1 promoter and noted that it is regulated, at least in part, by the transcription factor TFAP2C. With respect to the mechanisms affecting prognosis, ECM1 has been reported to play a role in promoting angiogenesis and its expression appears to correlate with rapid cell division. Despite ECM1 over-expression in a number of carcinomas, ECM1 transgenic mice do not appear to have a cancer predisposition, suggesting that ECM1 may be important in cancer progression, rather than initiation. In this regard, our lab has also shown that ECM1 downregulation led to reduced adhesion of melanoma cells in culture.

Ongoing projects in the laboratory include:

  • Examining the effects of altering ECM1 expression¬†in vivo¬†in a mouse model of metastatic melanoma
  • Evaluating the expression of ECM1 in primary melanoma tumors and its correlation with clinico-pathologic variables and
  • Expanding our understanding of the mechanisms underlying the effects of ECM1 expression on tumor prognosis using both melanoma and breast cancer cell lines