Compared to normal cells, cancer cells exhibit specific metabolic characteristics that facilitate the growth and metastasis of cancer. It is now widely appreciated that long noncoding RNAs (lncRNAs) exert extensive regulatory effects on a spectrum of biological processes through diverse mechanisms. In this review, we focus on the rapidly advancing field of lncRNAs and summarize the relationship between the dysregulation of lncRNAs and cancer metabolism, with a particular emphasis on the specific roles of lncRNAs in glycolysis, mitochondrial function, glutamine and lipid metabolism. These investigations reveal that lncRNAs are a key factor in the complexity of malignant cancer metabolism. Only through understanding the relevance between lncRNAs and cancer metabolic reprogramming can we open a new chapter in the history of carcinogenesis, one that promises to alter the methods of cancer diagnosis and treatment.

Pseudogenes were once considered to be genomic fossils without biological function. Interestingly, recent evidence showed that a lot of pseudogenes are transcribed in human cancers, and their alterations contribute to multiple cancer development and progression. It is apparent that many pseudogenes transcribe noncoding RNAs and contribute to the role noncoding genome plays in human cancers. On this basis, some pseudogene transcripts are currently ranked among the classes of long noncoding RNAs. In this study, we identified a new pseudogene-derived long noncoding RNA termed SFTA1P by analyzing the microarray data of non–small cell lung cancer from Gene Expression Omnibus datasets. We found that SFTA1P expression was significantly decreased in non–small cell lung cancer tissues compared with normal tissues in non–small cell lung cancer microarray data. Moreover, decreased SFTA1P expression is only correlated with lung adenocarcinoma patients’ poor survival time but not with lung squamous cell carcinoma patients’ survival. In addition, gain-of-function studies including growth curves, migration, invasion assays, and in vivo studies were performed to verify the tumor suppressor role of SFTA1P in non–small cell lung cancer. Finally, the potential underlying pathways involved in SFTA1P were investigated by analyzing the SFTA1P-correlated genes in The Cancer Genome Atlas lung adenocarcinoma and normal tissues RNA sequencing data. Taken together, these findings demonstrate that pseudogene-derived long noncoding RNA SFTA1P exerts the tumor suppressor functions in human lung adenocarcinoma. Our investigation reveals the novel roles of pseudogene in lung adenocarcinoma, which may serve as a new target for lung adenocarcinoma diagnosis and therapy.