Downregulation of RAB17 have a poor prognosis in kidney renal clear cell carcinoma and its expression correlates with DNA methylation and immune infiltration

RAB17 下调在肾透明细胞癌中预后不良,其表达与 DNA 甲基化和免疫浸润相关

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作者:Zhenhao Zeng, Zhicheng Zhang, Xiaofeng Cheng, Heng Yang, Binbin Gong, Xiaochen Zhou, Cheng Zhang, Xinyi Wang, Gongxian Wang

Background

RAB17 is one of the RAB family members. It has been reported to be closely associated with a variety of tumors and has different roles in various tumors. However, the effect of RAB17 in KIRC remains unclear. Materials and

Conclusion

RAB17 can be used as a potential prognostic biomarker for patients with KIRC and for assessing immunotherapy response.

Methods

We analyzed the differential expression of RAB17 in kidney renal clear cell carcinoma (KIRC) tissues and normal tissues using the public databases. The prognostic role of RAB17 in KIRC was analyzed using the Cox regression methods, and a prognostic model was constructed based on the

Results

RAB17 was low-expressed in KIRC. Downregulation of RAB17 expression is correlated with unfavorable clinicopathological characteristics and a worse prognosis in KIRC. The RAB17 gene alteration in KIRC was primarily characterized by copy number alteration. Six CpG sites of RAB17 DNA methylation levels are higher in KIRC tissues than in normal tissues, and are correlated with RAB17 mRNA expression levels, showing a significant negative correlation. cg01157280 site DNA methylation levels are associated with pathological stage and overall survival, and it may be the only CpG site with independent prognostic significance. Functional mechanism analysis revealed that RAB17 is closely associated with immune infiltration. RAB17 expression was found to be negatively correlated with most immune cell infiltration according to two different methods. Furthermore, most immunomodulators were significantly negatively correlated with RAB17 expression, and significantly positively correlated with RAB17 DNA methylation levels. RAB17 was significantly low expression in KIRC cells and KIRC tissues. In vitro, silencing of RAB17 promoted KIRC cell migration.

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