GSTO1 regards as a meritorious regulator in cutaneous malignant melanoma cells
| Autor: | Hai-Long Yue, Shu-Juan Zhang, Xiao-Jing Peng, Li-Kun Wang |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Epithelial-Mesenchymal Transition
Skin Neoplasms Regulator Apoptosis Biology Flow cytometry Cell Line 03 medical and health sciences Western blot Cell Line Tumor Proliferating Cell Nuclear Antigen medicine Humans Molecular Biology Melanoma 030304 developmental biology Cell Proliferation Glutathione Transferase 0303 health sciences medicine.diagnostic_test 030306 microbiology Cell Cycle Cell Biology Cell cycle medicine.disease Prognosis In vitro Proliferating cell nuclear antigen Up-Regulation Cancer research biology.protein Tumor Suppressor Protein p53 |
| Zdroj: | Molecular and cellular probes. 48 |
| ISSN: | 1096-1194 |
| Popis: | Background Glutathione S-transferase omega 1 (GSTO1), as a member of the glutathione S-transferase (GST) family genes, has been discovered to be up-regulated in several cancer cell lines which exhibited strong aggressiveness. However, the function of GSTO1 on cutaneous malignant melanoma (CMM) has not been illuminated. Methods Outcome of expression level and prognosis of GSTO1 were obtained from Oncomine and TCGA database. The specific effects of GSTO1 on the characteristics and regulatory mechanism of CMM cells were demonstrated by cell counting kit-8, colony formation, flow cytometry, and transwell assays in vitro. Western blot was employed to analyze the expression of proliferating cell nuclear antigen (PCNA), p53 and epithelial-to-mesenchymal (EMT) related proteins. Results We observed that GSTO1 was up-regulated in CMM samples when compared with the corresponding controls. Moreover, patients in CMM with high expression of GSTO1 were more likely to have a poor prognosis. Through in vitro experiments, silenced GSTO1 resulted in inhibition of CMM cells growth and aggressiveness, increased cell apoptosis, and blocked cell cycle. Finally, the expression of PCNA, p53 and EMT-related proteins were changed due to reduction of GSTO1. Conclusions To sum up, our outcomes exhibited that weakening GSTO1 reduced the proliferation and mobility of CMM cells, increased the apoptosis ability of CMM cells, and arrested cell cycle at G1 phase, which can be achieved by affecting the expression of PCNA, p53 and the EMT process. This discovery provided a new perspective for elucidating the mechanism of CMM, and offered theoretical support for searching clinical therapeutic targets in the future. |
| Databáze: | OpenAIRE |
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