N-methyladenosine (mA) reader HNRNPA2B1 accelerates the cervical cancer cells aerobic glycolysis.

N-methyladenosine (mA) modification is, a more common epigenetic modification, mainly found in mRNA. More and more researches have shown the important functions of mA on human cancers. This study seeks to explore the role of hnRNPA2B1 and mA-dependent mechanism in cervical cancer. Elevated hnRNPA2B1 indicated the poor prognosis of cervical cancer patients. Enforced hnRNPA2B1 reduced the apoptosis, and accelerated the proliferation and migration of cervical cancer cells in vitro. Besides, hnRNPA2B1 promoted the aerobic glycolysis of cervical cancer cells, including the lactate secretion, glucose uptake, ATP production, extracellular acidification rate (ECAR) and oxygen consumption rate (OCR). LDHA was found as the downstream target of hnRNPA2B1 by mA site. Moreover, hnRNPA2B1 enhanced the mRNA stability of LDHA through mA-dependent manner. LDHA inhibitor (FX-11) could reverse the effect of hnRNPA2B1. Taken together, the data revealed that hnRNPA2B1 promoted the proliferation, migration and aerobic glycolysis of cervical cancer cells by mA/LDHA-dependent manner. These findings might bring a new idea for cervical cancer treatment.