Investigating the correlation between DNA methylation and immune-associated genes of lung adenocarcinoma based on a competing endogenous RNA network

In recent years, there have been major breakthroughs in immunotherapies for the treatment of cancer. However, different patients have different responses to immunotherapy. Numerous studies have shown that the accumulation of epigenetic abnormalities, such as DNA methylation, serve an important role in the immune response of lung adenocarcinoma (LUAD). To investigate the effects of DNA methylation on tumor immunity with survival and prognosis, relevant studies can be performed based on the regulatory mechanisms of RNA molecules. For example, long non-coding RNAs (lncRNAs), which regulate gene expression through epigenetic levels. By constructing an immune-associated competitive endogenous RNA (ceRNA) network, the present study identified the regulatory associations among 3 key immune-associations mRNAs, 2 microRNAs (miRs) and 29 lncRNAs that were closely associated with the prognosis of patients with LUAD. The molecular biology analysis indicated that hypomethylation of the 1101320–1104290 regions of chromosome 1 resulted in the low expression levels of LINC00337 and that LINC00337 may affect the expression levels of CHEK1 by competitively binding with human (has)-miR-373 and hsa-miR-195. Therefore, abnormal DNA methylation in lncRNA-associated regions caused their abnormal expression levels, which further affected the interactions between RNA molecules. The interactions between these RNA molecules may have regulatory effects on tumor immunity and the prognosis of patients with LUAD.