ChIP Analysis Shows Aspirin May Inhibit Lung Cancer Via TAZ/PD-L1 Axis
According to the CDC, lung cancer is the second most common cancer in both men and women in the United States. Due to
the rapid development of society, new cases of lung cancer continue to increase each year due to smoking, high
levels of pollution, exposure to asbestos, radiation and other environmental causes. While aspirin is a drug most
commonly used for pain-relief and anti-inflammation, in recent years, research data has shown that aspirin may
reduce the risk of lung cancer.
In a study out of the First Affiliated Hospital of Dalian Medical University in China, Yixiang Zhang and his team
evaluated the inhibitory effect of aspirin on the lung cancer cell line including A549 and H1299 via targeting the
TAZ / Programmed cell
death-ligand 1 (PD-L1) axis. The research team provided the conclusion that aspirin can inhibit the proliferation of
lung cancer cells, due to its suppressing effect on cell cycle distribution and apoptosis.
Figure 1. Aspirin controls PD-L1 transcription via TAZ transcriptional coactivator.
(a,b ) Luciferase reporter gene analysis was used to examine the role of aspirin
(ASA) in the regulation of PD-L1 transcription in A549 and H1299 cell lines
(a,b) (white) ASA 0 mM,(black) ASA 2.5 mM, (grey) ASA 5.0 mM;
(c) ChIP & PCR were used to analyze the interaction of TAZ with PD-L1 promoter in
lung cancer cells with aspirin treatment.
First, the researchers used an MTT cell viability assay, and treated the lung cancer cell lines with saline/elevated
concentrations of aspirin (2.5 mM and 5.0 mM). Their data suggested that the growth of lung cancer cells was inhibited
when aspirin was present.
Diving deeper into their study, the team used Western blot and RT-PCR assays to examine the expression of PD-L1 at the
mRNA and protein levels in cells treated with different doses of aspirin. The results showed that there was a
significant decrease of oncogenic PD-L1 in aspirin-treated lung cancer cells, thus confirming the team’s
inference.
In order to better understand the blockade role of aspirin on lung cancer cell proliferation, the team sought to analyze
whether TAZ was involved in aspirin-controlled PD-L1 transcription. To complete this step, they turned to the EpiQuik Chromatin
Immunoprecipitation (ChIP) kit to further explore a finding from a previous study that revealed the role of
transcription cofactor TAZ in PD-L1 transcription.
This was a key step as it explained the molecular mechanism by which aspirin regulates PD-L1 transcription in lung
cancer. Using the ChIP assay kit, Yixiang Zhang and team found that the interaction of TAZ with PD-L1 promoter was
interrupted/blocked by aspirin. Thus, the researchers were able to find that aspirin has the potential to inhibit the
proliferation of lung cancer cell by targeting the TAZ/PD-L1 axis.
Lastly, the team observed the function of aspirin-treated PD-L1 in growth inhibition of lung cancer cells in vitro. The
addition of 5.0 mM aspirin was added in A549 cell and they found that cell growth was visibly suppressed. In this
observation, Yixiang Zhang and his team subsequently concluded that aspirin blocked the growth of lung cancer cells via
targeting PD-L1.
According to CDC statistics, lung cancer is the leading cause of cancer death in the US for both men and women. Every
year, about 200,000 people are diagnosed and 150,000 people die. These findings mark an influential discovery that
aspirin may help inhibit the effects of lung cancer, and could yield further findings in the future. Though the
anticarcinogenic effects of aspirin could serve as a potential medication to treat lung cancer, further research is
needed on its implications on human health.
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