Work

KIF18B Modulates SKP2 Ubiquitination to Promote Aerobic Glycolysis and Osteosarcoma Progression

Year: 2026

Type: article

Abstract: Osteosarcoma (OS) is an aggressive bone malignancy with poor prognosis, characterized by high metastasis rates. Kinesin family member 18B (KIF18B), a key protein in cell division and mitosis, has emerged as a potential diagnostic and therapeutic target in various cancers, including OS. This study investigates the role of KIF18B in OS progression and its underlying mechanisms. We found that KIF18B expression is significantly upregulated in OS tissues and correlates with lymph node metastasis (N-stage) and clinical stage. Knockdown of KIF18B inhibited OS cell migration, invasion, proliferation, and tumorigenesis. Mechanistically, KIF18B promotes OS survival through the ubiquitin–proteasome system (UPS) by regulating Skp2 protein degradation. KIF18B knockdown accelerated Skp2 ubiquitination, leading to reduced Skp2 levels and inhibited OS cell viability and glycolytic metabolism. Overexpression of KIF18B enhanced OS cell viability and glycolysis in an Skp2-dependent manner. These findings suggest that the KIF18B-Skp2 axis plays a critical role in the metabolic reprogramming of OS cells and serves as a novel prognostic biomarker and therapeutic target in OS.

Source: International Journal of Molecular Sciences

DOI: 10.3390/ijms27073235

Authors: Haonan Liu, Xin Guo, Chaoxiang Lu, Daifeng Lu

Institution: Harbin Medical University

Language: English

Topic: Sarcoma Diagnosis and Treatment

Subfield: Pulmonary and Respiratory Medicine

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $3,499