Overexpression of KMT9α Is Associated with Aggressive Basal-like Muscle-Invasive Bladder Cancer

Cells. 2023 Feb 11;12(4):589. doi: 10.3390/cells12040589.

Abstract

Muscle-invasive bladder cancer (MIBC) is associated with limited response rates to systemic therapy leading to a significant risk of recurrence and death. A recently discovered histone methyltransferase KMT9, acts as an epigenetic regulator of carcinogenesis in different tumor entities. In this study, we investigated the presence and association of histological and molecular subtypes and their impact on the survival of KMT9α in MIBC. We performed an immunohistochemical (IHC) analysis of KMT9α in 135 MIBC patients undergoing radical cystectomy. KMT9α was significantly overexpressed in the nucleus in MIBC compared to normal urothelium and low-grade urothelial cancer. Using the HTG transcriptome panel, we assessed mRNA expression profiles to determine molecular subtypes and identify differentially expressed genes. Patients with higher nuclear and nucleolar KMT9α expression showed basal/squamous urothelial cancer characteristics confirmed by IHC and differentially upregulated KRT14 expression. We identified a subset of patients with nucleolar expression of KMT9α, which was associated with an increased risk of death in uni- and multivariate analyses (HR 2.28, 95%CI 1.28-4.03, p = 0.005). In conclusion, basal-like MIBC and the squamous histological subtype are associated with high nuclear KMT9α expression. The association with poor survival makes it a potential target for the treatment of bladder cancer.

Keywords: MIBC; chemotherapy; histone methyltransferase; molecular subtypes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers, Tumor / metabolism
  • Carcinoma, Squamous Cell* / pathology
  • Carcinoma, Transitional Cell* / genetics
  • Carcinoma, Transitional Cell* / metabolism
  • Carcinoma, Transitional Cell* / pathology
  • Humans
  • Muscles / metabolism
  • Urinary Bladder Neoplasms* / pathology

Substances

  • Biomarkers, Tumor

Grants and funding

Florestan Koll was funded by the Mildred Scheel Career Center Frankfurt (Deutsche Krebshilfe). This work was supported by grants of the Deutsche Forschungsgemeinschaft—Project ID 192904750–SFB 992 Medical Epigenetics, Project-ID 89986987–SFB 850, and Schu688/15-1 to R. S.