Abstract
The Receptor for HA Mediated Motility (RHAMM) was initially described in 1982 as a soluble hyaluronan binding protein released by sub-confluent migrating cells.1 In 1992, RHAMM, was cloned and initially was demonstrated to play a pivotal role in locomotion. By 1995 RHAMM has already been proposed as a novel oncogene.2 Since then, many studies implicated RHAMM in several cellular processes such as motility, adhesion, wound healing, angiogenesis, migration, metastasis, invasion and growth. Furthermore, RHAMM is highly expressed in a variety of human tumors such as B-cell chronic lymphocytic leukemia, multiple myeloma, squamous cell lung carcinoma, pancreatic cancer, breast cancer, colon cancer, stomach cancer, mammary carcinoma, gastro carcinoma, endometrial carcinoma and oral squamous cell carcinoma. RHAMM is regulated by several growth-promoting factors, among them are: H-Ras, TGF-β1, FGF, β1 integrins and PKC. Although the oncogenic capabilities of RHAMM are well documented, the molecular mechanisms unde...
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