Volume 62, Issue 340, January - April 2026

Potential role of boron-containing compounds as a therapeutic adjuvant in the treatment or management of certain chronic diseases: The role Polo-like kinase 1 (PLK1) modulation

Batari M. Latayo¹, Ibrahim Abdulwaliyu^1♦, Shirley O. Yakubu², Shefiat O. Arekemase³, Razaq A. Mustapha⁴, Ayuba M. Haruna⁵, Evelyn H. Odeke¹, Amina I. Baba⁶, Owolabi S. Olusina⁷, Elizabeth A. Musa⁸, Rebecca T. Dah⁹, Usman Bello¹⁰

¹Scientific and Industrial Research Department, National Research Institute for Chemical Technology, Zaria, Nigeria
²Department of Science Laboratory Technology, Federal Polytechnic, Kaltungo, Nigeria
³Petrochemical and Allied Department, National Research Institute for Chemical Technology, Zaria, Nigeria
⁴Department of Nutrition and Dietetics, Rufus Giwa Polytechnic, Owo, Nigeria
⁵Ministry of Agriculture and Rural Development, Jos, Nigeria
⁶Department of Food Science and Technology Federal University of Technology, Minna, Nigeria
⁷Food Technology Department, Federal Institute of Industrial Research, Oshodi, Nigeria
⁸Department of Pharmaceutical Services, Jos University Teaching Hospital, Nigeria
⁹Medical Centre, National Research Institute for Chemical Technology, Zaria, Nigeria
¹⁰Demonstration School, Ahmadu Bello University, Zaria, Nigeria

^♦Corresponding Author
Ibrahim Abdulwaliyu, Scientific and Industrial Research Department, National Research Institute for Chemical Technology, Zaria, Nigeria

ABSTRACT

Polo-like kinase-1 (PLK1) is a crucial serine/threonine kinase that co-ordinates cell division. It also ensures genome stability by controlling centrosome maturation, spindle assembly, chromosome segregation, and cytokinesis. Therefore, overexpression of PLK1 can disrupts numerous essential biological functions, leading to the development or exacerbation of certain chronic diseases, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. The overexpression of PLK1 has a multifaceted mechanism in the pathogenesis of chronic diseases. Its overexpression induces dysregulation of NF-kB, leading to inflammation. It can also instigate NLRP3 inflammasome dysregulation, possibly through multiple pathways. This study suggests that PLK1 overexpression activates Never in Mitosis Gene A (NIMA)-related kinase 9 (NEK9), and subsequently NEK7, causing NLRP3 inflammasome dysregulation. Given that PLK1 contains a nucleophile amino acid residue in its ATP-binding pocket within the kinase domain, we suggest that a substance with electrophilic properties, such as boron, could be utilized as a targeted drug. Therefore, it is mechanistically plausible for a boroncontaining compound to inhibit the activity of PLK1 by forming covalent bonds or through substrate binding mechanisms with a nucleophile amino acid residue. This could potentially slow down the progression of certain chronic diseases.

Keywords: Polo-like kinase 1, Boron, Inflammation, Chronic diseases

Discovery, 2026, 62, e11d3243

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DOI: https://doi.org/10.54905/disssi.v62i340.e11d3243

Published: 24 April 2026