N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) reader IGF2BP1 facilitates clear-cell renal cell carcinoma aerobic glycolysis
Bao Yuan, Jin Zhou
Abstract
Emerging articles have reported that N 6 -methyladenosine (m 6 A) modification is mainly involved in clear-cell renal cell carcinoma (ccRCC) tumorigenesis. However, the regulatory mechanisms of m 6 A reader IGF2BP1 involved in ccRCC tumor energy metabolism are currently unknown. Results showed that the m 6 A reader IGF2BP1 exhibited significantly higher expression in ccRCC cells. Functionally, results by gain/loss functional assays indicated that IGF2BP1 promoted the glycolytic characteristics, including glucose uptake, lactate production and extracellular acidification rate (ECAR). Mechanistically, IGF2BP1 recognized the m 6 A modified sites on LDHA mRNA and enhanced its mRNA stability, thereby accelerating tumor energy metabolism. Thus, our work reveals a novel facet of the m 6 A that promoted mRNA stability and highlighted the functional importance of IGF2BP1 as m 6 A readers in post-transcriptional gene regulation.