Comprehensive Analysis of KCNJ14 Potassium Channel as a Biomarker for Cancer Progression and Development

Int J Mol Sci. 2023 Jan 20;24(3):2049. doi: 10.3390/ijms24032049.

Abstract

Cancer is a global epidemic that has affected millions of lives. Discovering novel cancer targets is widely viewed as a key step in developing more effective therapies for cancer and other fatal illnesses. More recently, potassium (K+) channels have been studied as a potential biological target for the creation of cancer treatments. Potassium Inwardly Rectifying Channel Subfamily J Member 14 (KCNJ14) is one of the cancer genome's least investigated genes. This study conducted a comprehensive examination of the relationships between KCNJ14 gene expression analysis, survival, RNA modification, immunotherapy participation, and cancer stemness using several databases. KCNJ14 was shown to be dysregulated in a variety of cancers, including lung, intestinal, head and neck, oesophageal, and stomach. Additionally, KCNJ14 was shown to be linked to RNA and DNA stemness in 18 and 15 different tumour types, respectively. Moreover, KCNJ14 was discovered to be positively linked with immunological checkpoints and suppressor cells and to have a negative immunophenoscore (IPS). KCNJ14 was linked to tumour mutation burden (TMB), microsatellite instability (MSI), neoantigen (NEO), and programmed death ligand 1 (PD-L1); all four are potential targets for immunotherapies. In addition, a favourable relationship between genomic-instability markers such as heterozygosity (LOH), homologous recombination deficiency (HRD), and mutant-allele tumour heterogeneity (MATH) was demonstrated with KCNJ14. Based on these novel findings, KCNJ14 may be a useful independent prognostic biomarker for a range of cancers.

Keywords: K+ channel; KCNJ14; RNA modification; cancer therapy; pan-cancer analysis.

MeSH terms

  • Biomarkers, Tumor / analysis
  • Biomarkers, Tumor / genetics
  • DNA
  • Humans
  • Microsatellite Instability
  • Mutation
  • Neoplasms* / genetics
  • Neoplasms* / pathology
  • Potassium Channels* / genetics

Substances

  • Biomarkers, Tumor
  • DNA
  • Kir2.4 channel
  • Potassium Channels

Grants and funding

The author extends his appreciation to the Deanship of Scientific Research at Imam Mohammad Ibn Saud Islamic University for funding this work through Research Group No. RG-21-11-05.