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重要调节因子。


背景谷胱甘肽S-转移酶omega 1 (GSTO1)作为谷胱甘肽S-转移酶(GST)家族基因的成员，已被发现在多种表现出强烈侵袭性的癌细胞系中上调。然而，GSTO1 在皮肤恶性黑色素瘤 (CMM) 中的功能尚未阐明。方法从Oncomine和TCGA数据库获得GSTO1的表达水平和预后结果。通过细胞计数kit-8、集落形成、流式细胞术和体外transwell实验证明了GSTO1对CMM细胞特性和调控机制的具体影响。采用Western blot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 GSTO1 表达上调。此外，GSTO1高表达的CMM患者预后更可能较差。通过体外实验，沉默的 GSTO1 会抑制 CMM 细胞的生长和攻击性，增加细胞凋亡，并阻断细胞周期。最后，由于 GSTO1 的减少，PCNA、p53 和 EMT 相关蛋白的表达发生变化。结论 综上所述，我们的结果表明，削弱 GSTO1 会降低 CMM 细胞的增殖和迁移能力，增加 CMM 细胞的凋亡能力，并将细胞周期阻滞在 G1 期，这可以通过影响 PCNA、p53 和EMT 流程。这一发现为阐明中药作用机制提供了新的视角，为今后寻找临床治疗靶点提供了理论支持。