Cantharidin overcomes IL-2Rα signaling-mediated vorinostat resistance in cutaneous T-cell lymphoma through reactive oxygen species.

ABSTRACT:

Background

Vorinostat (SAHA) is a histone deacetylase inhibitor that has shown clinical efficacy against advanced cutaneous T-cell lymphoma (CTCL). However, only a subset of patients with CTCL (30-35%) respond to SAHA and the response is not always sustainable. Thus, understanding the mechanisms underlying evasive resistance in this cancer is an unmet medical need to improve the efficacy of current therapies.

Purpose

This study aims to identify factors contributing to resistance against SAHA in CTCL and ways to mitigate it.

Methods and results

In this study, we demonstrated that attenuated reactive oxygen species (ROS) induces the expression of interleukin (IL)-2Rα, one of the IL-2 receptors, which drives resistance to SAHA in CTCL. We also determined that cantharidin

SUBMITTER: Zhu M 

PROVIDER: S-EPMC11253763 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature