Investigation of possible interaction between ARID3A, ARID3B, lncRNAs MALAT1 and NORAD in non-small cell lung cancer (NSCLC)

The most common cancer-related death with a poor prognosis is lung cancer. For attempts at survival, early diagnosis and effective treatment methods are crucial. Approximately 85% of lung cancers are non-small cell lung cancers (NSCLC). Long non-coding RNAs, also known as lncRNAs, are crucial to numerous biological processes. Their conflict causes carcinogenesis and may have an effect on the pathways that are considered important therapeutic targets in various cancers. The neoplastic initiation, progression, metastasis, tumor angiogenesis, chemoresistance, and genomic instability in NSCLC are caused by a lack of regulation of long non-coding RNAs, MALAT1 and NORAD, that are involved in metastasis. Both MALAT1 and NORAD are important for cell cycle progression as they directly regulate the expression of the transcription factor E2F1. It has been reported that the expression of p53 target genes is also affected by MALAT1 by repressing p53 promoter activity followed by cell cycle progression, and NORAD is indirectly regulated by p53. The AT-rich interaction domain (ARID) family of DNA-binding proteins, especially ARID3A and ARID3B are involved in various biological processes, including cell proliferation, differentiation, and development. ARID3A and ARID3B play important roles in E2F-dependent transcription and are transcriptional targets of p53. The pivotal function in promoting either cellular proliferation by pRB-E2F or growth arrest by p53 pathways implies a tight and finely tuned regulation. Both ARID3A, ARID3B and lncRNAs MALAT1, NORAD are involved in pRB-E2F and p53 pathways. In this study, we tried to find probable interactive and functional connectivity among ARID3A, ARID3B, lncRNAs MALAT1 and NORAD in NSCLC.