Source: insciences.org
Author: staff

In new research from Boston University Henry M. Goldman School of Dental Medicine (GSDM), Dr. Maria Kukuruzinska and her team are the first to show, in vivo, a direct relationship between expression of the gene DPAGT1 and tumor spread in oral cancer.

“When the gene is highly expressed in oral squamous cell carcinoma, it drives cellular discohesion and tumor spread within the oral cavity,” explains Dr. Kukuruzinska, Professor of Molecular and Cell Biology at GSDM.

Researchers found that overexpression of DPAGT1, the gene that determines glycosylation capacity, led to abnormal glycosylation of e-cadherin, causing it to malfunction as a cell-cell adhesion receptor and tumor suppressor.

When researchers suppressed the gene using oral cancer cell lines, cancer spread was interrupted. The findings suggest the potential to stop or reverse oral cancer tumor growth by therapeutically regulating DPAGT1. Researchers plan to find what causes overexpression of DPAGT1 in cancer and hope to find the key repressor molecule to regulate the gene.

Unlike many cancers, which metastasize early, oral cancer forms massive tumors and generally stays in the mouth. One of the deadliest cancer diagnoses, the current survival rate is about five years.

Notes:
1. Dr. Kukuruzinska worked with Dr. Mihai Nita-Lazar, Research Associate in the Department of Molecular and Cell Biology; Dr. Vikki Noonan, formerly of the Department of Oral Pathology; Drs. A. Sue Menko and Janice Walker of the Department of Anatomy, Pathology, and Cell Biology at Thomas Jefferson University; and Dr. Ivan Rebustini of the National Institute for Dental and Craniofacial Research/National Institutes of Health.

2. The paper, “Overexpression of DPAGT1 Leads to Aberrant N-Glycosylation of E-Cadherin and Cellular Discohesion in Oral Cancer”, appears in the July 15 issue of Cancer Research and is available online at cancerres.aacrjournals.org.