RESUMEN
Objective: To investigate the effects of different concentrations of follicle-stimulating hormone (FSH) on the proliferation and apoptosis of human hemangioma stem cells, it will provide a basis for studying the mechanism of FSH in treating hemangioma. Methods: Hemangioma specimens were collected from the Longgang District Maternity & Child Healthcare Hospital of Shenzhen City. Hemangioma stem cells were treated with different concentrations of FSH. Cell viability was detected by CCK8 method and cell apoptosis was analyzed by flow cytometry. Results: Hemangioma stem cells (HemSCs) were extracted from fresh tissue of infantile hemangioma by the CD133 immunomagnetic bead method. Under the influence of FSH at different concentrations (0, 100, 1000 IU/L), the cell viability of hemangioma stem cells increased significantly in a concentration-dependent manner (P < 0.05). At the same time, the apoptosis of hemangioma stem cells decreased with increasing concentrations of follicle-stimulating hormone (P < 0.05). Specifically, 1000 IU/L FSH significantly promoted the proliferation of hemangioma stem cells and inhibited their apoptosis. Conclusion: High concentration of follicle-stimulating hormone can maintain the growth of hemangioma by promoting the proliferation and inhibiting the apoptosis of hemangioma stem cells.
RESUMEN
It is difficult for traditional therapies to further improve the prognosis of hepatocellular carcinoma (LIHC), and immunotherapy is considered to be a promising approach to overcome this dilemma. However, only a minority of patients benefit from immunotherapy, which greatly limits its application. Therefore, it is particularly urgent to elucidate the specific regulatory mechanism of tumor immunity so as to provide a new direction for immunotherapy. NOP2/Sun RNA methyltransferase 3 (NSUN3) is a protein with RNA binding and methyltransferase activity, which has been shown to be involved in the occurrence and development of a variety of tumors. At present, the relationship between NSUN3 and immune implication in LIHC has not been reported. In this study, we first revealed that NSUN3 expression is upregulated in LIHC and that patients with high NSUN3 expression have a poor prognosis through multiple databases. Pathway enrichment analysis demonstrated that NSUN3 may be participated in cell adhesion and cell matrix remodeling. Next, we obtained a set of genes coexpressed with NSUN3 (NCGs). Further LASSO regression was performed based on NCGs, and a risk score model was constructed, which proved to have good predictive power. In addition, Cox regression analysis revealed that the risk score of NCGs model was an independent risk factor for LIHC patients. Moreover, we established a nomogram based on the NCGs-related model, which was verified to have a good predictive ability for the prognosis of LIHC. Furthermore, we investigated the relationship between NCGs-related model and immune implication. The results implied that our model was closely related to immune score, immune cell infiltration, immunotherapy response, and multiple immune checkpoints. Finally, the pathway enrichment analysis of NCGs-related model showed that the model may be involved in the regulation of various immune pathways. In conclusion, our study revealed a novel role of NSUN3 in LIHC. The NSUN3-based prognostic model may be a promising biomarker for inspecting the prognosis and immunotherapy response of LIHC.