Dataset Information

LINC01198 promotes proliferation and temozolomide resistance in a NEDD4-1-dependent manner, repressing PTEN expression in glioma.

ABSTRACT:

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.

SUBMITTER: Chen WL

PROVIDER: S-EPMC6738407 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Publications

LINC01198 promotes proliferation and temozolomide resistance in a NEDD4-1-dependent manner, repressing PTEN expression in glioma.

Chen Wei-Lin WL Chen Hong-Jin HJ Hou Guo-Qiang GQ Zhang Xiao-Hua XH Ge Jian-Wei JW

Aging 20190830 16

<h4>Background</h4>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.<h4>Results</h4>LINC01198 was elevated in glioma, and this predicted a poorer prognosis for patients with glioma. LINC01198 knockdown inhibited, while LINC01198 ...[more]

PMID: 31469661

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Project description:Background The aquaporin (AQP) family of proteins has been implicated in the proliferation and growth of gliomas. Expression of AQP8 is higher in human glioma tissues than in normal brain tissues and is positively correlated with the pathological grade of glioma, suggesting that this protein is also involved in the proliferation and growth of glioma. However, the mechanism by which AQP8 promotes the proliferation and growth of glioma remains unclear. This study aimed to investigate the mechanism and role of abnormal AQP8 expression in glioma development. Methods The dCas9-SAM and CRISPR/Cas9 techniques were used to construct viruses with overexpressed and knocked down AQP8, respectively, and infect A172 and U251 cell lines. The effects of AQP8 on the proliferation and growth of glioma and its mechanism via the intracellular reactive oxygen species (ROS) level were observed using cell clone, transwell, flow cytometry, Hoechst, western blotting, immunofluorescence, and real-time quantitative polymerase chain reaction assays. A nude mouse tumor model was also established. Results Overexpression of AQP8 resulted in an increased number of cell clones and cell proliferation, enhanced cell invasion and migration, decreased apoptosis and phosphatase and tensin homolog (PTEN) expression, and increased phosphorylated serine/threonine protein kinase (p-AKT) expression and ROS level, whereas the AQP8 knockdown groups showed opposite results. In the animal experiments, the AQP8 overexpression group had higher tumor volume and weight, whereas the AQP8 knockdown group had lower tumor volume and weight compared with those parameters measured in the control group. Conclusions Our results preliminary suggest that AQP8 overexpression alters the ROS/PTEN/AKT signaling pathway, promoting the proliferation, migration, and invasion of gliomas. Therefore, AQP8 may be a potential therapeutic target in gliomas. Supplementary Information The online version contains supplementary material available at 10.1186/s12885-023-11025-8.

Dataset Information

LINC01198 promotes proliferation and temozolomide resistance in a NEDD4-1-dependent manner, repressing PTEN expression in glioma.

Background

Results

Conclusions

Methods

Publications

LINC01198 promotes proliferation and temozolomide resistance in a NEDD4-1-dependent manner, repressing PTEN expression in glioma.

Similar Datasets

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