Bin1: A Novel Tumor Suppressor Protein
Bin1 is a novel gene product which offers utility as a diagnostic marker for malignant prostate cells. Bin1 (also known as amphiphysin II; amphiphysin-like protein, AMLP; and ALP) was identified through its ability to interact with and inhibit the oncogenic properties of the Myc oncoprotein and has features of a tumor suppressor protein. In preliminary clinical studies, monoclonal antibodies to Bin1 have been useful in the identification of malignant prostate cancer cells.
Bin1 structure suggests that it functions in a signal transduction pathway. This protein has features of a tumor suppressor that is widely lost in breast, prostate, and liver carcinoma. Detecting or manipulating Bin1 function in cells has potential applications for carcinoma and possibly other cancers involving Myc. Preliminary evidence suggests that Bin1 acts independently of p53. The Bin1 gene is located at a hotspot for deletion in metastatic prostate carcinoma and may be mutated in these and other tumor types, including cancers of breast, liver, and cervix.
Recent investigation of Bin1 indicates that it promotes cell differentiation (in the absence of activated Myc) and apoptosis (in its presence). Bin1 has several features of a tumor suppressor: it suppresses the oncogene activity of Myc, inhibits the growth of tumor cell lines, and has been implicated in cell differentiation and apoptosis. Thus, Bin1 is a molecule that is functionally deleted in cancer and that may have important roles in normal cell regulation.
Antibodies That Detect a Novel Tumor Supressor (BIN1) Implicated in Human Carcinomas and Apoptosis
Wistar researchers have developed polyclonal and monoclonal antibodies (PAb 99Pst and MAbs 99D through 99I) that bind to BIN1, a novel tumor suppressor protein that interacts with and inhibits the oncogenic activity of the MYC oncoprotein. BIN1 is functionally deleted in carcinomas of the breast, colon, lung, liver and cervix and has been implicated in programmed cell death (apoptosis). Apoptosis is an active process of physiological cell suicide that is critical to normal tissue homeostasis but that does not function properly in tumor cells. Work aimed at defining the genetic control of apoptosis and understanding its dysfunction in cancer has centered on the MYC oncoprotein, because it can promote either cell proliferation or apoptosis. Wistar scientists theorize that BIN1 may activate or facilitate apoptosis, thereby overcoming MYC's malignant growth activity. The antibodies generated by Wistar scientists are useful for research aimed at understanding the role of the BIN1 protein in the genetic events associated with apoptosis.