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MicroRNA expression profiling reveals the potential function of microRNA-31 in chordomas
Omer Faruk Bayrak1, Sukru Gulluoglu, Esra Aydemir
1Department of Medical Genetics, Yeditepe University Medical School and Yeditepe University Hospital, Istanbul, Turkey.
Abstract:
Chordomas are rare bone tumors arising from remnants of the notochord. Molecular studies to determine the pathways involved in their pathogenesis and develop better treatments are limited. Alterations in microRNAs (miRNAs) play important roles in cancer. miRNAs are small RNA sequences that affect transcriptional and post-transcriptional regulation of gene expression in most eukaryotic organisms. Studies show that miRNA dysregulation is important for tumor initiation and progression. We compared the expression profile of miRNAs in chordomas to that of healthy nucleus pulposus samples to gain insight into the molecular pathogenesis of chordomas. Results of functional studies on one of the altered miRNAs, miR-31, are presented. The comparison between the miRNA profile of chordoma samples and the profile of normal nucleus pulposus samples suggests dysregulation of 53 miRNAs. Thirty miRNAs were upregulated in our tumor samples, while 23 were downregulated. Notably, hsa-miR-140-3p and hsa-miR-148a were upregulated in most chordomas relative to levels in nucleus pulposus cells. Two other miRNAs, hsa-miR-31 and hsa-miR-222, were downregulated in chordomas compared with the control group. Quantification with real-time polymerase chain reaction confirmed up or downregulation of these miRNAs among all samples. Functional analyses showed that hsa-miR-31 has an apoptotic effect on chordoma cells and downregulates the expression of c-MET and radixin. miRNA profiling showed that hsa-miR-31, hsa-miR-222, hsa-miR-140-3p and hsa-miR-148a are differentially expressed in chordomas compared with healthy nucleus pulposus. Our profiling may be the first step toward delineating the differential regulation of cancer-related genes in chordomas, helping to reveal the mechanisms of initiation and progression.
Insights
MicroRNA (miRNA) expression is altered in chordoma, a rare bone tumor. This study identified specific miRNAs, like miR-31, that may drive chordoma development and progression, offering new therapeutic targets.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Chordomas are rare bone tumors originating from notochordal remnants, with limited molecular insights into their pathogenesis and treatment.
- MicroRNAs (miRNAs) are crucial regulators of gene expression, and their dysregulation is implicated in various cancers, including tumor initiation and progression.
Purpose of the Study:
- To investigate the differential expression profile of miRNAs in chordoma samples compared to healthy nucleus pulposus.
- To identify specific miRNAs involved in the molecular pathogenesis of chordomas.
- To explore the functional role of dysregulated miRNAs, such as miR-31, in chordoma cells.
Main Methods:
- MicroRNA expression profiling was performed on chordoma and healthy nucleus pulposus samples.
- Differential miRNA expression was analyzed, with 53 miRNAs found to be dysregulated.
- Real-time polymerase chain reaction (PCR) was used to validate the expression levels of key miRNAs.
- Functional studies were conducted to assess the impact of miR-31 on chordoma cell apoptosis and target gene expression (c-MET, radixin).
Main Results:
- A total of 53 miRNAs were found to be differentially expressed between chordoma and normal samples, with 30 upregulated and 23 downregulated.
- Specific miRNAs, including hsa-miR-140-3p and hsa-miR-148a, were upregulated, while hsa-miR-31 and hsa-miR-222 were downregulated in chordomas.
- Functional analysis demonstrated that hsa-miR-31 induces apoptosis in chordoma cells and downregulates c-MET and radixin expression.
Conclusions:
- MicroRNA profiling reveals significant alterations in miRNA expression in chordomas compared to healthy tissues.
- The identified differentially expressed miRNAs, particularly hsa-miR-31, hsa-miR-222, hsa-miR-140-3p, and hsa-miR-148a, are potentially involved in chordoma pathogenesis.
- These findings represent a crucial step towards understanding the molecular mechanisms underlying chordoma initiation and progression, potentially paving the way for novel therapeutic strategies.
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