Related Experiment Video
Updated: Feb 22, 2026
Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
Published on: June 15, 2016
LncRNA PLAC2 down-regulates RPL36 expression and blocks cell cycle progression in glioma through a mechanism
Yan-Wei Hu1, Chun-Min Kang1, Jing-Jing Zhao1
1Laboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Abstract:
Current glioma therapies allow in situ delivery of cytotoxic drugs to the tumour; however, gliomas show early recurrence due to their highly proliferative character. Long non-coding (lnc)RNAs play critical roles in tumorigenesis by controlling cell proliferation and cycling. However, the mechanism of action of lncRNAs in glioma development remains unclear. Here, we report that the lncRNA PLAC2 induces cell cycle arrest by targeting ribosomal protein (RP)L36 in glioma. RPL36 promoted cell proliferation and G1/S cell cycle progression. Mass spectrometry analysis revealed that signal transducer and activator of transcription (STAT)1 interacted with both lncRNA PLAC2 and the RPL36 promoter. We also found that the nucleus PLAC2 bind with STAT1 and interact with RPL36 promoters but the cytoplasmic lncRNA PLAC2 inhibited STAT1 nuclear transfer, thereby decreasing RP36 expression, inhibiting cell proliferation and inducing cell cycle arrest. These results provide evidence for a novel cell cycle regulatory network in glioma comprising the lncRNA PLAC2 along with STAT1 and RPL36 that can serve as a therapeutic target for glioma treatment.
Insights
The long non-coding RNA PLAC2 targets ribosomal protein RPL36 to induce cell cycle arrest in glioma. This discovery reveals a new therapeutic target for treating recurrent gliomas by controlling cell proliferation.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Gliomas are highly proliferative and prone to early recurrence despite current therapies.
- Long non-coding RNAs (lncRNAs) are implicated in tumorigenesis, but their specific roles in glioma remain largely unknown.
- Understanding lncRNA mechanisms is crucial for developing novel glioma treatments.
Purpose of the Study:
- To elucidate the mechanism of action of lncRNA PLAC2 in glioma development.
- To identify novel therapeutic targets for glioma treatment.
- To investigate the regulatory network involving PLAC2, STAT1, and RPL36 in glioma.
Main Methods:
- Mass spectrometry was used to identify interactions between lncRNA PLAC2, signal transducer and activator of transcription (STAT)1, and the ribosomal protein (RP)L36 promoter.
- Cellular localization studies investigated the role of nuclear versus cytoplasmic PLAC2.
- Functional assays assessed the impact of PLAC2 on cell proliferation and cell cycle progression.
Main Results:
- The lncRNA PLAC2 was found to induce cell cycle arrest by targeting RPL36 in glioma cells.
- RPL36 was identified as a promoter of cell proliferation and G1/S cell cycle progression.
- Nuclear PLAC2 interacts with STAT1 and the RPL36 promoter, while cytoplasmic PLAC2 inhibits STAT1 nuclear transfer, decreasing RPL36 expression and inducing cell cycle arrest.
Conclusions:
- A novel cell cycle regulatory network involving lncRNA PLAC2, STAT1, and RPL36 in glioma has been identified.
- PLAC2 acts as a critical regulator of cell proliferation and cell cycle progression in glioma.
- This regulatory network presents a promising therapeutic target for glioma treatment, potentially overcoming early recurrence.
Related Concept Videos
01:23Negative Regulator Molecules
02:39lncRNA - Long Non-coding RNAs
02:39lncRNA - Long Non-coding RNAs
01:20The Retinoblastoma Gene
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
02:23Abnormal Proliferation
01:22MicroRNAs