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High Expression MicroRNA-206 Inhibits the Growth of Tumor Cells in Human Malignant Fibrous Histiocytoma.

ABSTRACT: Background: Malignant fibrous histiocytoma (MFH) is a common type of soft tissue sarcoma and a serious threat to human health. MFH often relapses locally after the curettage is related to the residual cancer stem cells (CSCs). Currently, the dysregulation of microRNA (miRNA) has been found to be closely related to the recurrence of CSCs. However, whether dysregulations of miRNAs exist in MFH, CSCs remained unknown. Methods: In this study, miRNAs in MFH CSCs and MFH common cells were examined by gene probe. Then, target genes and their functions involved in the signal pathway were predicted by the relevant database. Finally, the miRNAs' target regulatory network was constructed. Furthermore, the miRNAs and target genes were identified by quantitative polymerase chain reaction, whereas miRNA analogs and antagonists were transfected in tumor cells to investigate cell proliferation ability further. Results: Results showed that a total of 47 miRNAs were found, including 16 that were upregulated and 31 that were downregulated. The screened differential miRNA showed a different expression in the cell resistant strains compared with the control group. Quantitative polymerase chain reaction analysis confirmed that the relative abundance of seven miRNAs and four target genes varied significantly. The encouraging issue is that we found Hsa-miR-206 significantly inhibited MFH proliferative activity. Conclusion: Hsa-miR-206 played a key role in regulating MFH CSC properties that might be a representative marker and target for the diagnosis and treatment of MFH in the future.

SUBMITTER: Li D

PROVIDER: S-EPMC8656228 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Mitochondria play an essential role in cellular energy metabolism and apoptosis. Previous studies have demonstrated that decreased mitochondrial biogenesis is associated with cancer progression. In mitochondrial biogenesis, peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) regulates the activities of multiple nuclear receptors and transcription factors involved in mitochondrial proliferation. Previously, we showed that overexpression of PGC-1α leads to mitochondrial proliferation and induces apoptosis in human malignant fibrous histiocytoma (MFH) cells in vitro. We also demonstrated that transcutaneous application of carbon dioxide (CO(2)) to rat skeletal muscle induces PGC-1α expression and causes an increase in mitochondrial proliferation. In this study, we utilized a murine model of human MFH to determine the effect of transcutaneous CO(2) exposure on PGC-1α expression, mitochondrial proliferation and cellular apoptosis. PGC-1α expression was evaluated by quantitative real-time PCR, while mitochondrial proliferation was assessed by immunofluorescence staining and the relative copy number of mitochondrial DNA (mtDNA) was assessed by real-time PCR. Immunofluorescence staining and DNA fragmentation assays were used to examine mitochondrial apoptosis. We also evaluated the expression of mitochondrial apoptosis related proteins, such as caspases, cytochorome c and Bax, by immunoblot analysis. We show that transcutaneous application of CO(2) induces PGC-1α expression, and increases mitochondrial proliferation and apoptosis of tumor cells, significantly reducing tumor volume. Proteins involved in the mitochondrial apoptotic cascade, including caspase 3 and caspase 9, were elevated in CO(2) treated tumors compared to control. We also observed an enrichment of cytochrome c in the cytoplasmic fraction and Bax protein in the mitochondrial fraction of CO(2) treated tumors, highlighting the involvement of mitochondria in apoptosis. These data indicate that transcutaneous application of CO(2) may represent a novel therapeutic tool in the treatment of human MFH.

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High Expression MicroRNA-206 Inhibits the Growth of Tumor Cells in Human Malignant Fibrous Histiocytoma.

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