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Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter
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A novel LncRNA transcript, RBAT1, accelerates tumorigenesis through interacting with HNRNPL and cis-activating E2F3
Xiaoyu He1,2, Peiwei Chai1,2, Fang Li1,2
1Department of Ophthalmology, Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China.
Molecular Cancer
|July 17, 2020
Summary
Retinoblastoma associated transcript-1 (RBAT1) is overexpressed in retinoblastoma and bladder cancer, promoting tumor growth by activating the E2F3 oncogene. Silencing RBAT1 shows therapeutic potential for these cancers.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Long non-coding RNAs (lncRNAs) are key epigenetic regulators in human cancers.
- The precise roles of lncRNAs in tumorigenesis require further investigation.
- This study focuses on the novel lncRNA, retinoblastoma associated transcript-1 (RBAT1), in tumorigenesis.
Purpose of the Study:
- To investigate the molecular mechanisms of RBAT1 in tumorigenesis.
- To explore the potential clinical applications of RBAT1 in cancer.
- To identify RBAT1 as a potential therapeutic target for retinoblastoma and bladder cancer.
Main Methods:
- RBAT1 expression was quantified using real-time PCR in cancer cell lines and tissues.
- Chromatin isolation by RNA purification (ChIRP) identified RBAT1-interacting proteins.
- Therapeutic efficacy of RBAT1-targeting GapmeRs was assessed in patient-derived retinoblastoma xenograft models.
Main Results:
- RBAT1 expression was significantly elevated in retinoblastoma (Rb) and bladder cancer (BCa) tissues.
- RBAT1 promoted tumor growth in vitro and in vivo.
- RBAT1 recruits HNRNPL to the E2F3 promoter, enhancing E2F3 transcription.
Conclusions:
- RBAT1 overexpression activates the oncogene E2F3 by recruiting HNRNPL to its promoter.
- This study reveals a novel lncRNA mechanism with potential diagnostic and therapeutic implications for Rb and BCa.
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