IGFBP4 and neoplasm: For instance, lncRNA PTV1 contributed to osteosarcoma cell glucose metabolism, cell proliferation and motility through the miR-497/HK2 pathway.33 LncRNA IGFBP4 promoted lung cancer cell proliferation and metastasis through possible mechanism of reprogramming tumor cell energy metabolism.34 Moreover, lncRNA CASC8 suppressed bladder cancer cell proliferation via regulating glycolysis.35 In our study, we demonstrated that UCA1 knockdown significantly inhibited and forced expression of UCA1 promoted NSCLC cell viability.