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Thirdhand smoke can damage epithelial cells in the respiratory system by stressing cells and causing them to fight for survival, a research team led by scientists at the University of California, Riverside, has found. The finding could assist physicians treating patients exposed to thirdhand smoke.
"Our data show that cells in humans are affected by thirdhand smoke," said Prue Talbot, a professor in the Department of Molecular, Cell and Systems Biology, who led the research. "The health effects of THS, have been studied in cultured cells and animal models, but this is the first study to show a direct effect of thirdhand smoke on gene expression in humans."
Study results appear in JAMA Network Open.
Thirdhand smoke, or THS, results when exhaled smoke and smoke emanating from the tip of burning cigarettes settles on surfaces such as clothing, hair, furniture, and cars. Not strictly smoke, THS refers to the residues left behind by smoking.
"THS can resurface into the atmosphere and can be inhaled unwillingly by nonsmokers," said Giovanna Pozuelos, the first author of the research paper and a graduate student in Talbot's lab. "It has not been widely studied, which may explain why no regulations are in place to protect nonsmokers from it."
The researchers obtained nasal scrapes from four healthy nonsmokers who had been exposed to THS for three hours in a laboratory setting at UC San Francisco. The UCR researchers then worked to get good quality RNA from the scrapes -- necessary to examine gene expression changes. RNA sequencing identified genes that were over- or under-expressed. They found 382 genes were significantly over-expressed; seven other genes were under-expressed. They then identified pathways affected by these genes.
"THS inhalation for only three hours significantly altered gene expression in the nasal epithelium of healthy nonsmokers," Pozuelos said. "The inhalation altered pathways associated with oxidative stress, which can damage DNA, with cancer being a potential long-term outcome. It's extremely unlikely a three-hour exposure to THS would cause cancer, but if someone lived in an apartment or home with THS or drove a car regularly where THS was present, there could be health consequences."
Because gene expression in the nasal epithelium is similar to the bronchial epithelium, the researchers note that their data is relevant to cells deeper in the respiratory system. In the samples they studied, the researchers also found that brief THS exposure affected mitochondrial activity. Mitochondria are organelles that serve as the cell's powerhouses. If left unchecked, the observed effects would lead to cell death.
Pozuelos explained that the team focused on the nasal epithelium because the nasal passage is one way THS can enter people's lungs. The other common exposure route is through the skin, which the researchers did not study, but plan to in the future.
Already, the researchers are working with groups in San Diego, California, and Cincinnati to study long-term exposure to THS, made possible with access to homes where people are being exposed to THS.
"Many people do not know what THS is," said Talbot, the director of the UCR Stem Cell Center. "We hope our study raises awareness of this potential health hazard. Many smoking adults think, 'I smoke outside, so my family inside the house will not get exposed.' But smokers carry chemicals like nicotine indoors with their clothes. It's important that people understand that THS is real and potentially harmful."
Cancer cells use a bizarre strategy to reproduce in a tumor's low-energy environment; they mutilate their own mitochondria! Researchers at Cold Spring Harbor Laboratory (CSHL) also know how this occurs, offering a promising new target for pancreatic cancer therapies.
Why would a cancer cell want to destroy its own functioning mitochondria? "It may seem pretty counterintuitive," admits M.D.-Ph.D. student Brinda Alagesan, a member of Dr. David Tuveson's lab at CSHL.
According to Alagesan, the easiest way to think about why cancer cells may do this is to think of the mitochondria as a power plant. "The mitochondria is the powerhouse of the cell," she recites, recalling the common grade school lesson. And just like a traditional power plant, the mitochondria create their own pollution.
"These harmful byproducts, or pollutants, are called reactive oxygen species, or ROS," Alagesan adds. "A lot of it can be damaging to cells. We believe that [by eating their own mitochondria] the pancreatic cancer cells are reducing the production of these damaging ROS while still making enough energy to proliferate."
This is still a hypothesis but it could explain why pancreatic cancer cells become prone to mitophagy, a form of autophagy or 'self eating' of their mitochondria.
In the journal Cancer Discovery, Alagesan and co-lead author Dr. Timothy Humpton describe what happens when a protein called KRAS becomes active in the uniquely nutrient-depleted environment of a pancreas tumor. KRAS starts a "signaling cascade" which results in the cell eating its own mitochondria and the diversion of glucose and glutamine away from the remaining mitochondria. These diverted nutrients are used to support cell division.
"Ideally, we would want to inhibit the cancer promoting KRAS protein directly, but unfortunately so far no one has been able to do that in a clinically relevant way," Alagesan explains.
Instead of stopping KRAS directly, the Tuveson team traced the cascade of protein signals that follows KRAS activation. They found one pathway which leads to an increase in the protein NIX. NIX is directly responsible for triggering that mitophagy stage which appears to be so crucial for cancer cell proliferation.
"Results in mice are showing us that, by inhibiting the NIX pathway, we might prevent cancer cells from using energy the way they need to in order to proliferate," Alagesan says.
The Tuveson team is now turning its attention to disrupting this same NIX pathway in human pancreatic cancer cells, and applying this to the design of clinical trials.
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