Long noncoding RNA FAM83H-AS1 exerts an oncogenic role in glioma through epigenetically silencing CDKN1A (p21)
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Updated: Feb 9, 2026

In Vitro Selection of Engineered Transcriptional Repressors for Targeted Epigenetic Silencing
Published on: May 5, 2023
Yong-Yan Bi1, Gang Shen1, Yong Quan1
1Department of Neurosurgery, Minhang Hospital, Fudan University, Shanghai, China.
Abstract:
Gliomas are the commonest and most aggressive primary malignant tumor in the central nervous system. Long noncoding RNAs (lncRNAs) have been identified to act as crucial regulators in multiple biological processes, including tumorigenesis. FAM83H antisense RNA1 (FAM83H-AS1) has been uncovered to be dysregulated in several cancers. However, the biological role of FAM83H-AS1 in glioma still needs to be investigated. Currently, our findings indicated that 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. Collectively, our findings suggested that FAM83H-AS1 participated in the progression of glioma and might act as a potential therapeutic target and prognosis biomarker for human glioma.
Insights
FAM83H-AS1, a long noncoding RNA, is upregulated in glioma, promoting tumor growth by silencing CDKN1A. Silencing FAM83H-AS1 suppresses glioma progression, suggesting it as a therapeutic target.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cancer Genetics
Background:
- Gliomas are aggressive primary central nervous system tumors.
- Long noncoding RNAs (lncRNAs) play roles in tumorigenesis.
- FAM83H-AS1 is dysregulated in various cancers, but its role in glioma is unclear.
Purpose of the Study:
- Investigate the biological role of FAM83H-AS1 in glioma.
- Determine if FAM83H-AS1 can serve as a prognostic biomarker or therapeutic target for glioma.
Main Methods:
- Analysis of FAM83H-AS1 expression in glioma tissues and cell lines.
- Loss-of-function assays to assess the impact of FAM83H-AS1 silencing on cell proliferation and apoptosis.
- Mechanistic studies to elucidate the molecular pathways involving FAM83H-AS1, EZH2, and CDKN1A.
Main Results:
- FAM83H-AS1 expression is upregulated in glioma tissues and cell lines.
- High FAM83H-AS1 levels correlate with poor glioma prognosis.
- Silencing FAM83H-AS1 suppresses glioma cell proliferation by regulating cell cycle and apoptosis.
- FAM83H-AS1 recruits EZH2 to silence CDKN1A expression, impacting cell cycle and proliferation.
Conclusions:
- FAM83H-AS1 promotes glioma progression.
- FAM83H-AS1 acts as a potential therapeutic target and prognostic biomarker for human glioma.
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