AI Article Synopsis
- LINC00467 plays a significant role in glioma cell regulation, influencing both cell proliferation and migration.
- Knockdown of LINC00467 leads to reduced glioma cell viability and increased apoptosis, highlighting its potential as a therapeutic target.
- The study reveals that LINC00467 negatively regulates miR-200a while promoting E2F3 expression, indicating a complex interaction that drives glioma progression.
Article Abstract
Studies have found that LINC00467 is an important regulator of cancer. However, the function of LINC00467 in glioma cell is unclear. Therefore, this experimental design based on LINC00467 to explore its mechanism of action in glioma cell. RT-qPCR was used to detect the expression of LINC0046 and miR-200a in glioma cell lines. MTT assay, Edru assay and Transwell assay and flow cytometry were used to detect the effects of LINC0046 and miR-200a on PC cell proliferation, migration and apoptosis. Target gene prediction and screening, luciferase reporter assays were used to validate downstream target genes for LINC0046 and miR-200a. Western blotting was used to detect the protein expression of E2F3. The tumor changes in mice were detected by in vivo experiments in nude mice. LINC00467 was up-regulated in glioma cells. Knockdown of LINC00467 inhibited the viability, migration and invasion of glioma cells. In glioma cells, miR-200a was significantly reduced, while E2F3 was significantly rised. LINC00467 negatively regulated the expression of miR-200a in gliomas, while miR-200a negatively regulated the expression of E2F3 in gliomas. INC00467 promoted the development of glioma by inhibiting miR-200a and promoting E2F3 expression. LINC00467 may be a potential therapeutic target for gliomas.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7469466 | PMC |
| http://dx.doi.org/10.1080/15384101.2020.1792127 | DOI Listing |
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