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Functions of long non-coding RNA ROR in patient-derived glioblastoma cells
Tatyana F Kovalenko1, Bhupender Yadav2, Ksenia S Anufrieva3
1Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Moscow, Russia.
Abstract:
Glioblastoma (GBM) is the most frequent and aggressive primary brain cancer in adult patients. A variety of long non-coding RNAs play an important role in the pathogenesis of GBM, however the molecular functions of most of them still remain elusive. Here, we investigated linc-RoR (long intergenic non-protein coding RNA, regulator of reprogramming) using GBM neurospheres obtained from 12 different patients. We demonstrated that the highest level of this transcript is detected in cells with increased EGFR expression. According to our data, linc-RoR knockdown decreases cell proliferation, increases sensitivity to DNA damage, and downregulates the level of cancer stem cell (CSC) markers. On the other hand, linc-RoR overexpression promote cell growth and increases the proportion of CSCs. Analysis of RNA sequencing data revealed that linc-RoR affects expression of genes involved in the regulation of mitosis. In agreement with this observation, we have showen that the highest level of linc-RoR is detected in the G2/M phase of the cell cycle, when linc-RoR is localized on the chromosomes of dividing cells. Based on our results, we can propose that linc-RoR performs pro-oncogenic functions in human gliobalstoma cells, which may be associated with the regulation of mitotic progression and GBM stemness.
Insights
Long non-coding RNA regulator of reprogramming (linc-RoR) promotes glioblastoma growth and stemness by regulating cell division. Its knockdown reduces cancer stem cell markers and increases DNA damage sensitivity in glioblastoma.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Glioblastoma (GBM) is an aggressive brain cancer.
- Long non-coding RNAs (lncRNAs) are implicated in GBM pathogenesis, but their functions are often unclear.
- linc-RoR is a lncRNA investigated for its role in GBM.
Purpose of the Study:
- To investigate the function of linc-RoR in human glioblastoma.
- To determine the relationship between linc-RoR expression and GBM characteristics.
- To elucidate the molecular mechanisms underlying linc-RoR's role in GBM.
Main Methods:
- Utilized patient-derived GBM neurospheres.
- Performed linc-RoR knockdown and overexpression experiments.
- Conducted RNA sequencing and cell cycle analysis.
- Assessed cell proliferation, DNA damage sensitivity, and cancer stem cell (CSC) marker levels.
Main Results:
- linc-RoR expression correlates with EGFR expression in GBM cells.
- linc-RoR knockdown reduces proliferation, increases DNA damage sensitivity, and decreases CSC markers.
- linc-RoR overexpression enhances cell growth and increases CSC proportion.
- linc-RoR influences genes involved in mitosis and is detected in the G2/M phase on chromosomes during cell division.
Conclusions:
- linc-RoR exhibits pro-oncogenic functions in glioblastoma.
- linc-RoR may promote GBM by regulating mitotic progression and cancer stemness.
- Targeting linc-RoR could be a potential therapeutic strategy for glioblastoma.
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