The protein transforming growth factor beta (TGF-beta) can act as either a tumor suppressor or a tumor promoter depending on the stage of cancer. Loss of TGF-beta’s tumor suppressor activity may play an important role in lung cancer progression.
Pran Datta, Ph.D., and colleagues previously showed that this loss of responsiveness to TGF-beta occurs mainly through loss of expression of the TGF-beta type II receptor (TbRII). However little is known about the mechanisms underlying this loss of expression – or how it might be restored.
In a recent study published in Neoplasia, Datta and colleagues identify several proteins/pathways involved in regulating TbRII expression in lung cancer cell lines, and that histone deacetylation – an “epigenetic” change that modulates gene expression – is involved in the loss of TbRII expression in lung cancer cells. Additionally, drugs called histone deacetylase inhibitors (HDIs) were shown to restore expression of TbRII, suggesting that these compounds – either alone or in combination with other agents – may hold potential in treating or slowing the progression of lung cancer.
The research was supported by grants from the National Cancer Institute and the Department of Veterans Affairs.
