Protein tyrosine phosphatase, nonreceptor type 13 (PTPN13), has emerged as a critical cancer-related gene that is implicated in a wide range of cancer types. However, the role of PTPN13 in clear cell renal cell carcinoma (ccRCC) is poorly understood. In the present study, we aimed to evaluate whether PTPN13 participates in the progression of ccRCC. Decreased expression of PTPN13 was found in ccRCC tissues, which predicted a shorter survival rate in ccRCC patients. PTPN13 expression was also lower in ccRCC cell lines, and the upregulation of PTPN13 repressed the proliferation, colony formation and invasion, but enhanced the apoptosis of ccRCC cells. In contrast, the silencing of PTPN13 produced the opposite effects. Further data showed that PTPN13 overexpression decreased the phosphorylation of Akt, while PTPN13 silencing increased the phosphorylation of Akt. Treatment with Akt inhibitor markedly abrogated the PTPN13 silencing-evoked oncogenic effect in ccRCC cells. Xenograft tumor experiments revealed that overexpression of PTPN13 remarkably restricted the tumor formation and growth of ccRCC cells in vivo associated with inactivation of Akt. In conclusion, our data demonstrated that overexpression of PTPN13 restricts the proliferation and invasion of ccRCC cells through inactivation of Akt. Our study suggests a tumor suppressive function of PTPN13 in ccRCC and highlights the potential role of PTPN13 in the progression of ccRCC.

蛋白酪氨酸磷酸酶，非受体类型13（PTPN13），已经成为与癌症相关的关键基因，与多种癌症类型有关。但是，对PTPN13在透明细胞肾细胞癌（ccRCC）中的作用了解甚少。在本研究中，我们旨在评估PTPN13是否参与ccRCC的进展。在ccRCC组织中发现PTPN13的表达降低，这预示着ccRCC患者的生存期较短。PTPN13在ccRCC细胞系中的表达也较低，并且PTPN13的上调抑制了ccRCC细胞的增殖，集落形成和侵袭，但增强了其凋亡。相反，PTPN13的沉默产生相反的效果。进一步的数据显示PTPN13过表达降低了Akt的磷酸化，而PTPN13沉默增加Akt的磷酸化。用Akt抑制剂治疗显着消除了ccRCC细胞中PTPN13沉默诱发的致癌作用。异种移植肿瘤实验表明PTPN13的过度表达显着限制了ccRCC细胞的肿瘤形成和生长体内与Akt失活有关。总之，我们的数据表明PTPN13的过表达通过Akt的失活限制了ccRCC细胞的增殖和侵袭。我们的研究表明PTPN13在ccRCC中具有肿瘤抑制功能，并强调了PTPN13在ccRCC进展中的潜在作用。