The Role of Long Non-Coding RNA NNT-AS1 in Neoplastic Disease

Simple Summary Nicotinamide nucleotide transhydrogenase-antisense 1 (NNT-AS1), which is a newly-discovered long non-coding RNA (lncRNA), has been found to be dysregulated in a variety of neoplastic diseases. With the accumulation of studies on NNT-AS1 in recent years, the mechanism of NNT-AS1 and its significance for tumor occurrence and progression are constantly being updated and improved. Thus, this paper aims to summarize the abnormal expression of NNT-AS1 and its prognostic values in different neoplastic diseases. In addition, the detailed competing endogenous RNA networks and subsequent biology behaviors, as well as the role of NNT-AS1 in mediating cisplatin resistance are revealed in this paper. This review not only summarizes the past research of NNT-AS1, but also provides some ideas for future research in this field. Studies have shown that non-coding RNAs (ncRNAs), especially long non-coding RNAs (lncRNAs), play an important regulatory role in the occurrence and development of human cancer. Nicotinamide nucleotide transhydrogenase-antisense 1 (NNT-AS1) is a newly-discovered cytoplasmic lncRNA. Many studies have shown that it has abnormally-high expression levels in malignant tumors, but there are also a few studies that have reported low expression levels of NNT-AS1 in gastric cancer, breast cancer, and ovarian cancer. At present, the regulatory mechanism of NNT-AS1 as a miRNA sponge, which may be an important reason affecting tumor cell proliferation, invasion, metastasis, and apoptosis is being studied in-depth. In addition, NNT-AS1 has been found to be related to cisplatin resistance. In this review, we summarize the abnormal expression of NNT-AS1 in a variety of neoplastic diseases and its diagnostic and prognostic value, and we explain the mechanism by which NNT-AS1 regulates cancer progression by competing with miRNAs. In addition, we also reveal the correlation between NNT-AS1 and cisplatin resistance and the potential clinical applications of NNT-AS1.