Ability to produce epiregulin may influence cancer development.
A potential biomarker for lung cancer, epiregulin (Ereg), was identified during a recent study published in Molecular Carcinogenesis.
In order to determine if upregulation was happenstance, correlative, or causative to the disease, researchers examined the effects of Ereg deletion in mouse models.
“A couple years ago, we identified epiregulin, or Ereg, as a potential biomarker during transcriptomic studies using 2 separate mouse models of lung cancer,” said researcher Alison Bauer, PhD.
In wildtype mice and mice unable to produce Ereg, researchers initiated the development of lung cancer.
“Basically, we saw that mice without Ereg developed fewer tumors,” Bauer said.
Additionally, mice without Ereg saw a reduction in inflammation, and in cell studies, human and mouse lung epithelial cells treated with Ereg saw a significant increase in wound healing.
“This is in line with what you would expect from a functional growth factor,” Bauer said. “It appears as if Ereg increases cell proliferation, with increased levels of Ereg in cancer cells promoting the growth and proliferation of tumors.”
Although Ereg seems in have an effect on inflammation, the how, why, and consequences of the influences are unknown. This is because Ereg is understudied compared with its cousin EGF and much of the science surrounding it is poorly understood.
“This really is new and while that presents a challenge in the lack of science surrounding Ereg, it also presents an exciting opportunity to push forward with a promising biomarker that hasn't been described in this context,” Bauer said.
Although Ereg as a biomarker is unknown, many cancer therapy targets like EGFR, ALK, and ROS1 started as biomarkers of unknown significance.
“This is the first step -- well, actually the second step -- in the exploration of Ereg as a prognostic marker and potential target in a subset of lung cancers,” Bauer said. “We hope that our future studies continue to prove its promise.”