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.

Aspirin controls PD‐L1 transcription via TAZ coavtivator

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.

Source: Zhang Y et. al. (2020). Aspirin-targeted PD-L1 in lung cancer growth inhibition. Thoracic Cancer. 11(6):1587-1593

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