FAM83H-AS1 was upregulated in glioma tissues and cell lines and high level of FAM83H-AS1 was associated with poor prognosis of glioma. Loss-of-function assays demonstrated that silenced FAM83H-AS1 obviously suppressed cell proliferation via regulating the cell-cycle distribution and cell apoptosis rate, and mechanistic experiments revealed that FAM83H-AS1 could epidemically silence CDKN1A expression through recruiting EZH2 to the promoter of CDKN1A, thereby influencing the cell cycle and proliferation. Moreover, the the Kaplanâ??Meier method (log-rank test) was used to analyze the correlation between FAM83HAS1 expression and overall survival of all patients and we found that high level of FAM83Hâ??AS1 was associated with poor prognosis ( p < 0.001, log-rank test).