Abemaciclib induces G1 arrest and lysosomal dysfunction in canine melanoma cells: synergistic effects with fenbendazole.

ABSTRACT:

Introduction

Abemaciclib, a CDK4/6 inhibitor, is well-established for treating hormone receptor-positive and HER2-negative (HR⁺/HER2^-) human breast cancer by inducing G1 cell cycle arrest. However, its antitumor effects in other cancers, including canine melanoma, remain largely unexplored. Canine melanoma often harbors CDK4/6 copy number gains and cell cycle dysregulation, suggesting it may be a suitable target for abemaciclib.

Methods

Five canine melanoma cell lines (CMeC1, KMeC, LMeC, UCDK9M4, and UCDK9M5) were used to evaluate the antitumor effects of abemaciclib. Cell viability and migration were assessed using Cell Counting Kit-8 and wound healing assays, respectively. Cell cycle distribution was analyzed by flow cytometry, and the expression of c

SUBMITTER: Kim SH 

PROVIDER: S-EPMC12240792 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature