PKIB, a Novel Target for Cancer Therapy

Int J Mol Sci. 2024 Apr 25;25(9):4664. doi: 10.3390/ijms25094664.

Abstract

The serine-threonine kinase protein kinase A (PKA) is a cyclic AMP (cAMP)-dependent intracellular protein with multiple roles in cellular biology including metabolic and transcription regulation functions. The cAMP-dependent protein kinase inhibitor β (PKIB) is one of three known endogenous protein kinase inhibitors of PKA. The role of PKIB is not yet fully understood. Hormonal signaling is correlated with increased PKIB expression through genetic regulation, and increasing PKIB expression is associated with decreased cancer patient prognosis. Additionally, PKIB impacts cancer cell behavior through two mechanisms; the first is the nuclear modulation of transcriptional activation and the second is the regulation of oncogenic AKT signaling. The limited research into PKIB indicates the oncogenic potential of PKIB in various cancers. However, some studies suggest a role of PKIB in non-cancerous disease states. This review aims to summarize the current literature and background of PKIB regarding cancer and related issues. In particular, we will focus on cancer development and therapeutic possibilities, which are of paramount interest in PKIB oncology research.

Keywords: PKA; PKIB; cancer; cyclic AMP and AKT.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Molecular Targeted Therapy / methods
  • Neoplasms* / drug therapy
  • Neoplasms* / genetics
  • Neoplasms* / metabolism
  • Protein Kinase Inhibitors / metabolism
  • Signal Transduction / drug effects

Substances

  • Antineoplastic Agents
  • Cyclic AMP-Dependent Protein Kinases
  • Protein Kinase Inhibitors
  • PKIB protein, human
  • Intracellular Signaling Peptides and Proteins

Grants and funding

This research received no external funding.