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SGK2 promotes renal cancer progression via enhancing ERK 1/2 and AKT phosphorylation

Y Liu1, J-B Chen, M Zhang

  • 1Department of Urology, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China. liang_chaozhao@ahmu.edu.cn.

European Review for Medical and Pharmacological Sciences
|April 20, 2019
PubMed
Abstract

Insights

Serum- and glucocorticoid-inducible kinase 2 (SGK2) promotes renal cell cancer (RCC) progression. Silencing SGK2 inhibits RCC cell growth and metastasis, suggesting SGK2 as a potential therapeutic target for kidney cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Serum- and glucocorticoid-inducible kinases (SGKs) are implicated in various cancers.
  • The specific role of SGK2 in renal cell cancer (RCC) requires further investigation.

Purpose of the Study:

  • To explore the function of SGK2 in the tumorigenesis of renal cell cancer (RCC).
  • To determine if SGK2 can serve as a prognostic marker or therapeutic target for RCC.

Main Methods:

  • Quantified SGK2 expression in RCC cell lines using Western blot (WB).
  • Performed in vitro SGK2 knockdown and overexpression experiments.
  • Analyzed SGK2's association with RCC patient prognosis using The Cancer Genome Atlas (TCGA) database.

Main Results:

  • SGK2 was upregulated in RCC tissues and cell lines, correlating with poorer patient survival.
  • SGK2 knockdown inhibited RCC cell proliferation, migration, colony formation, and invasion.
  • SGK2 overexpression enhanced these malignant behaviors and promoted ERK1/2 and AKT phosphorylation.

Conclusions:

  • SGK2 promotes RCC progression by mediating ERK1/2 and AKT phosphorylation.
  • SGK2 represents a potential prognostic marker and therapeutic target for renal cancer.

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