Ginsenoside Rh2 Suppresses the Fanconi Anemia Pathway by Inhibiting NF-κB-Mediated FANCL Transcription in Bladder Cancer.

ABSTRACT:

Objectives

Cisplatin, a frontline chemotherapeutic agent for bladder cancer (BC), induces DNA interstrand crosslinks that are primarily repaired through the Fanconi anemia (FA) pathway. Hyperactivation of this repair mechanism contributes to cisplatin resistance, underscoring the need for FA-targeted sensitizers. This study investigated the effect of ginsenoside Rh2 on FA signaling and cisplatin sensitivity in bladder cancer cells.

Methods

Bladder cancer cell lines (T24, 5637, and RT4) were treated with cisplatin, with or without Rh2 pretreatment. FANCI/FANCD2 (ID2) complex monoubiquitination, FANCD2 foci formation, and interactions with downstream repair proteins (FANCP, FANCQ, PCNA) were examined. FANCL expression was analyzed at the transcriptional level, and rescue exper

SUBMITTER: Li C 

PROVIDER: S-EPMC12717414 | biostudies-literature | 2025 Oct-Dec

REPOSITORIES: biostudies-literature