Nanog plays an important role in the regulation of cancer stem cells (CSCs) which participate in tumorgenesis and progression. In renal cancer, tobacco smoke (TS) is considered a major risk factor. However, the molecular mechanism by which TS induces the development of renal CSC properties remains largely unknown. In this study, we showed that the level of Nanog was elevated in renal cell carcinoma (RCC) patients with a smoking history, and that Nanog overexpression promoted the traits of CSCs in renal cancer. We further demonstrated that a 8‐week exposure of TS enhanced the formation of renal tumorspheres, increased the population of CD133‐positive cells, and stimulated the expression of Nanog and CSC markers. In addition, TS was found to play a role in accelerating the cell growth transition from G1 to S phase in renal CSCs. Finally, we demonstrated that the TS‐induced effects in renal CSCs could be reversed through the downregulation of Nanog. Our results suggested that Nanog plays a role in mediating TS‐induced renal CSC properties. This study may provide new insights into the molecular mechanism of TS‐related renal tumorigenesis, which can contribute to the future development of therapeutics for renal cancer.

中文翻译：

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Nanog介导烟草烟雾诱导的肾癌干细胞特性增强

Nanog 在调节参与肿瘤发生和进展的癌症干细胞 (CSC) 中发挥重要作用。在肾癌中，烟草烟雾 (TS) 被认为是主要的危险因素。然而，TS 诱导肾 CSC 特性发展的分子机制在很大程度上仍然未知。在这项研究中，我们发现有吸烟史的肾细胞癌 (RCC) 患者的 Nanog 水平升高，并且 Nanog 过表达促进了肾癌 CSCs 的特征。我们进一步证明，8 周的 TS 暴露增强了肾肿瘤球的形成，增加了 CD133 阳性细胞的数量，并刺激了 Nanog 和 CSC 标志物的表达。此外，发现 TS 在加速肾 CSCs 中从 G1 期到 S 期的细胞生长转变中发挥作用。最后，我们证明了通过下调 Nanog 可以逆转 TS 诱导的肾 CSCs 效应。我们的结果表明 Nanog 在介导 TS 诱导的肾 CSC 特性中起作用。该研究可能为 TS 相关肾脏肿瘤发生的分子机制提供新的见解，这有助于未来肾癌治疗的发展。