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LINC01198 promotes proliferation and temozolomide resistance in a NEDD4-1-dependent manner, repressing PTEN
Wei-Lin Chen1, Hong-Jin Chen1, Guo-Qiang Hou1
1Department of Neurosurgery, RenJi Hospital, Shanghai JiaoTong University School of Medicine, Shanghai 200127, China.
Background:
Dysregulation of numerous lncRNAs has been recently confirmed in glioma; however, the majority of their roles and mechanisms involved in this notorious disease remain largely unclear. This study aims to explore the roles and molecular mechanisms of LINC01198 implicated in the proliferation and chemoresistance in glioma.
Results:
LINC01198 was elevated in glioma, and this predicted a poorer prognosis for patients with glioma. LINC01198 knockdown inhibited, while LINC01198 overexpression promoted, glioma cell proliferation and resistance to temozolomide. Mechanistically, NEDD4-1 (neural precursor cell expressed, developmentally downregulated 4, E3 ubiquitin protein ligase) and phosphatase and tensin homolog (PTEN) were recruited by LINC01198, which functioned as a scaffold. Moreover, we showed that LINC01198 exerted its oncogenic activities by enhancing the NEDD4-1-dependent repression of PTEN.
Conclusions:
Our study elucidated the role of oncogenic LINC01198 in glioma proliferation and temozolomide resistance, and this role may serve as a promising target for glioma therapy.
Methods:
LINC01198 expression in glioma tissues and that in paired normal tissues were measured by qRT-PCR. The functional roles of LINC01198 in glioma were demonstrated by a series of in vitro experiments. CCK-8 assay, RNA pulldown, RNA immunoprecipitation and western blotting were used to demonstrate the potential mechanisms of LINC01198.
Insights
Long non-coding RNA LINC01198 promotes glioma cell growth and temozolomide resistance by interacting with NEDD4-1 and PTEN. This suggests LINC01198 is a potential therapeutic target for glioma.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Dysregulation of long non-coding RNAs (lncRNAs) is implicated in glioma pathogenesis.
- The specific roles and mechanisms of most lncRNAs in glioma remain unclear.
Purpose of the Study:
- To investigate the role and molecular mechanisms of LINC01198 in glioma proliferation and chemoresistance.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to measure LINC01198 expression.
- In vitro experiments to assess functional roles.
- CCK-8 assay, RNA pulldown, RNA immunoprecipitation, and western blotting to elucidate mechanisms.
Main Results:
- LINC01198 expression is elevated in glioma, correlating with poorer prognosis.
- LINC01198 knockdown inhibits glioma cell proliferation and temozolomide resistance; overexpression promotes them.
- LINC01198 acts as a scaffold for NEDD4-1 (neural precursor cell expressed, developmentally downregulated 4, E3 ubiquitin protein ligase) and PTEN (phosphatase and tensin homolog), enhancing NEDD4-1-dependent repression of PTEN.
Conclusions:
- Oncogenic LINC01198 plays a significant role in glioma proliferation and temozolomide resistance.
- LINC01198 represents a promising therapeutic target for glioma treatment.
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