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Phosphorylated MAPK11 promotes the progression of clear cell renal cell carcinoma by maintaining RUNX2 protein

Xiandong Song1, Changming Dong1, Xiaojun Man1

  • 1Department of Urology, The First Hospital of China Medical University, Shenyang, Liaoning, China.

Journal of Cellular and Molecular Medicine
|August 1, 2023
PubMed

Insights

Mitogen-activated protein kinase 11 (MAPK11) and Runt-associated transcription factor 2 (RUNX2) are overexpressed in clear cell renal cell carcinoma (ccRCC). This P-MAPK11/RUNX2 axis promotes ccRCC progression and may be a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Mitogen-activated protein kinase 11 (MAPK11) is crucial in cell signaling pathways, influencing cell viability, differentiation, proliferation, and apoptosis.
  • While MAPK11 is implicated in various cancers, its specific role in clear cell renal cell carcinoma (ccRCC) remains largely unelucidated.
  • Runt-associated transcription factor 2 (RUNX2) is a key transcription factor in osteoblast and chondrocyte development, with known overexpression in several tumor types.

Purpose of the Study:

  • To investigate the expression and molecular mechanisms of MAPK11 and RUNX2 in clear cell renal cell carcinoma (ccRCC).
  • To determine the functional roles of MAPK11 and RUNX2 in ccRCC cell proliferation and migration.
  • To explore the interaction between MAPK11 and RUNX2 and its impact on ccRCC progression.

Main Methods:

  • Analysis of mRNA and protein levels in ccRCC tissues versus adjacent tissues using The Cancer Genome Atlas (TCGA) database and western blotting.
  • Assessment of ccRCC cell proliferation via colony formation and EdU assays, and cell migration using Transwell assays.
  • Detection of protein interactions via immunoprecipitation and measurement of RUNX2 protein stability using cycloheximide chase assays.

Main Results:

  • Overexpression of both MAPK11 and RUNX2 was observed in ccRCC tissues and cell lines.
  • MAPK11 and RUNX2 significantly promoted ccRCC cell proliferation and migration.
  • A physical interaction between RUNX2 and phosphorylated MAPK11 (P-MAPK11) was identified, stabilizing RUNX2 protein and potentially counteracting MAPK11 degradation.

Conclusions:

  • The P-MAPK11/RUNX2 axis is upregulated in ccRCC and drives tumor progression.
  • The interaction between P-MAPK11 and RUNX2 enhances RUNX2 stability, contributing to ccRCC development.
  • Targeting the P-MAPK11/RUNX2 axis presents a potential therapeutic strategy for ccRCC.
Keywords:
MAPK11P-MAPK11RUNX2clear cell renal cell carcinoma (ccRCC)ubiquitination

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