Emerging articles have reported that N-methyladenosine (mA) modification is mainly involved in clear-cell renal cell carcinoma (ccRCC) tumorigenesis. However, the regulatory mechanisms of mA reader IGF2BP1 involved in ccRCC tumor energy metabolism are currently unknown. Results showed that the mA 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 mA modified sites on LDHA mRNA and enhanced its mRNA stability, thereby accelerating tumor energy metabolism. Thus, our work reveals a novel facet of the mA that promoted mRNA stability and highlighted the functional importance of IGF2BP1 as mA readers in post-transcriptional gene regulation.