NEAT1 and neoplasm: Similarly, adenovirus infection of glioma cells promotesGSC formation via the TLR9/NEAT1/STAT3 pathway [127].STAT3 also contributes to tumor cell invasion and cell cycle regulation through mechanismssuch as TGFBI secretion by tumor-associated macrophages (TAMs) and ARPC1B activation,which supports mesenchymal phenotype maintenance and radiotherapy resistance in GSCs [ 128– 130].