![]() |
New research shows how lung cancer cells can survive better and exhibit less cell damage when exposed to cigarette smoke in cell culture experiments compared to non-cancerous lung cells. Image shows non-cancerous lung cells (left) and lung cancer cells (right), subjected to the same concentration of cigarette smoke condensate. Non-cancerous cells have more pronounced protein aggregation granules (shown with an arrow), stained by Proteostat, a type of cell damage that can eventually lead to cell death. Image Credit: Krasilnikova Lab / Penn State (CC BY-NC-ND 4.0 DEED) |
Lung cancer cells survive better and exhibit less cell damage when exposed to cigarette smoke in cell culture experiments compared to non-cancerous lung cells. New research by a team of undergraduate students led by a Penn State molecular biologist may have revealed how lung cancer cells can persist in smoke. The mechanism could be related to how cancer cells develop resistance to pharmaceutical treatments as well.
The team found that a protein, which is expressed at high levels in some lung cancer cells and acts as a pump to transport molecules across the cell membrane, could potentially be clearing the damaging molecules coming from cigarette smoke. These molecules, if left uncleared inside the cells, can lead to protein aggregation that can damage and eventually kill lung cells.
“Cigarette smoke contains carcinogenic compounds, such as hydrocarbons and reactive oxygen and nitrogen species, that can damage cells in various ways,” said Maria Krasilnikova, associate research professor of biochemistry and molecular biology in the Eberly College of Science at Penn State and the lead author of the paper. “One way these compounds can damage cells is by causing proteins to misfold, which can lead to the formation of protein aggregates.”