Asset Details
Do you wish to reserve the book?
Largazole targets Musashi protein expression via miR-125b-5p and sensitizes triple-negative breast cancer cells to radiation
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Largazole targets Musashi protein expression via miR-125b-5p and sensitizes triple-negative breast cancer cells to radiation
Do you wish to request the book?
Largazole targets Musashi protein expression via miR-125b-5p and sensitizes triple-negative breast cancer cells to radiation
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Largazole targets Musashi protein expression via miR-125b-5p and sensitizes triple-negative breast cancer cells to radiation
2026
Overview
Recent findings implicate the histone deacetylase (HDAC) inhibitor largazole as an inhibitor of Musashi RNA-binding protein function. Here, we assess this interplay and evaluate the relevance of largazole for triple-negative breast cancer (TNBC) progression and resistance to radiotherapy.
Primary patient-derived TNBC cells and cell lines were treated with largazole and cell vitality, proliferation, motility, cell cycle, DNA synthesis as well as repair, and stemness were analyzed via MTT assay, digital holographic microscopy, and flow cytometry. To unravel the connection between largazole treatment and Musashi expression, miR-125b-5p was assessed after largazole treatment, and overexpressed as well as downregulated in TNBC wildtype cells to determine influence on Musashi levels. Targeted mRNA and protein expression analyses were complemented with RNA sequencing data after largazole treatment. Finally, DNA double strand breaks and post-radiogenic survival were quantified using γ-H2AX, 53BP1, and clonogenic assays.
Largazole showed reduced metabolic activity in TNBC, but not in non-malignant cultures. Largazole treatment strongly abrogated proliferation, DNA synthesis, cell motility, and induced a cell cycle arrest. Levels of the Musashi proteins were downregulated after largazole treatment via upregulation of the miR-125b-5p. Protein expression and RNA sequencing analysis indicated a loss of cancer stemness-, cell cycle progression-, and DNA repair-associated signaling. Consequently, radiotherapy-induced DNA double strand breaks were increased while post-radiogenic cell survival was decreased in largazole-treated samples.
The HDAC inhibitor largazole compromises tumor growth and motility and downregulates the Musashi proteins via the miR-125b-5p in TNBC. Additionally, largazole acts as a radiosensitizer by attenuating DNA repair, therefore supporting therapeutic efficacy.
