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.

中文翻译：

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GSTO1被认为是皮肤恶性黑色素瘤细胞中的一种功绩调节剂。

背景技术已经发现谷胱甘肽S-转移酶ω1（GSTO1）是谷胱甘肽S-转移酶（GST）家族基因的成员，在表现出强侵袭性的几种癌细胞系中被上调。但是，GSTO1对皮肤恶性黑色素瘤（CMM）的功能尚未阐明。方法通过Oncomine和TCGA数据库获得GSTO1的表达水平和预后。通过细胞计数试剂盒8，集落形成，流式细胞术和体外穿孔测定法证明了GSTO1对CMM细胞特征和调控机制的特异性作用。Western blot用于分析增殖细胞核抗原（PCNA），p53和上皮间质（EMT）相关蛋白的表达。结果我们观察到，与相应的对照相比，CMM样品中的GSTO1上调。此外，高表达GSTO1的CMM患者更有可能预后不良。通过体外实验，沉默的GSTO1抑制了CMM细胞的生长和侵袭性，增加了细胞凋亡，并阻断了细胞周期。最后，由于GSTO1的减少，改变了PCNA，p53和EMT相关蛋白的表达。结论综上所述，我们的结果表明，减弱GSTO1会降低CMM细胞的增殖和迁移率，增加CMM细胞的凋亡能力，并使细胞周期停滞在G1期，这可以通过影响PCNA，p53和PCNA的表达来实现。 EMT流程。这一发现为阐明CMM的机理提供了新的视角，