Metabolism is a complex network of regulatory system. Cells often alter their metabolism in response to the changes in their environment. These adaptive changes are particularly pronounced in tumor cells, known as metabolic reprogramming. Metabolic reprogramming is considered to be one of the top 10 characteristics of tumor cells. Glucose and lipid metabolism are important components of metabolic reprogramming. A large number of experimental studies have shown that long non-coding RNAs (lncRNAs) play an important role in glucose and lipid metabolism. The current review briefly introduces the regulatory effect of lncRNAs on glucose and lipid metabolism of tumor cells, and the significance of lncRNA-mediated metabolism in tumor therapy, hoping to provide new strategies for clinical targeting tumor therapy.

Bacterial noncoding RNAs are essential in many cellular processes, including response to environmental stress, and virulence. Deep sequencing analysis of the Salmonella enterica serovar Typhi (S. Typhi) transcriptome revealed a novel antisense RNA transcribed in cis on the strand complementary to rseC, an activator gene of sigma factor RpoE. In this study, expression of this antisense RNA was confirmed in S. Typhi by Northern hybridization. Rapid amplification of cDNA ends and sequence analysis identified an 893 bp sequence from the antisense RNA coding region that covered all of the rseC coding region in the reverse direction of transcription. This sequence of RNA was named as AsrC. After overexpression of AsrC with recombinantant plasmid in S. Typhi, the bacterial motility was increased obviously. To explore the mechanism of AsrC function, regulation of rseC and rpoE expression by AsrC was investigated. We found that AsrC increased the levels of rseC mRNA and protein. The expression of rpoE was also increased in S. Typhi after overexpression of AsrC, which was dependent on rseC. Thus, we propose that AsrC increased RseC level and indirectly activating RpoE which can initiate fliA expression and promote the motility of S. Typhi.

Long non-coding RNAs (lncRNAs) are a class of transcripts exceeding 200 nucleotides (nt) in length, which are broadly implicated in a broad spectrum of physiological and pathological processes, including allelic imprinting, genome packaging, chromatin remodeling, transcriptional activation and disruption, as well as the occurrence and progression of oncogenesis. N6-methyladenosine (m6 A) methylation stands as the most prevalent RNA modification, affecting multiple facets of RNA biology such as stability, splicing, transport, translation, degradation, and tertiary structure. Aberrant m6 A modifications are intimately implicated in cancer progression. In recent years, there has been a growing number of studies illuminating the dynamic interplay between lncRNAs and m6 A modifications, revealing that lncRNAs can modulate the activity of m6 A regulators, while m6 A not only affects the structural integrity but also the translational efficiency and stability of lncRNAs. Together, the interactions between lncRNAs and m6 A modifications significantly impact downstream oncogenes, cancer suppressor genes, cellular metabolism, epithelial-mesenchymal transition, angiogenesis, drug transport, DNA homology repair, and epigenetics, subsequently influencing tumorigenesis, metastasis, and drug resistance. This article endeavors to clarify the functions and mechanisms of lncRNAs and m6 A modifications interaction in cancer to provide promising insights for cancer diagnosis and therapeutic strategies.