have previously reported molecular and physiologic evidence for an
endothelin-1 autocrine loop in lung cancer. The endothelin-B receptor
(ETBR), which is believed to counter-regulate endothelin-1, is not
expressed in the majority of lung cancer cell lines.
We hypothesized that the inactivation of the ETBR is due to epigenetic
silencing, specifically the hypermethylation of cytosine nucleotides of
the 5CpG “island” surrounding the transcriptional start region of
the ETBR gene. This process has been associated with the silencing of a
number of tumor-suppressor genes.