Proteomics

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Abemaciclib differentially reshapes the immunopeptidome of breast cancer subtypes

ABSTRACT: The cyclin-dependent kinase 4/6 inhibitor (CDK4/6i) Abemaciclib has demonstrated transformative potential in the treatment of hormone receptor-positive (HR+) breast cancer. Beyond its established role in cell cycle arrest, we reveal its capacity to enhance tumor immunogenicity by remodeling the immunopeptidome. Using a proteogenomic approach, we analyzed the antigenic repertoire of HR+ and triple-negative breast cancer (TNBC) models following Abemaciclib treatment. Our findings highlight a substantial increase in MHC-I presentation and antigen diversity, particularly in HR+ cells. This effect is mediated through Rb-dependent transcriptional and epigenetic reprogramming involving bromodomain and extraterminal (BET) proteins. Furthermore, we identified novel abemaciclib-induced neoantigens derived from allegedly non-coding genomic regions with therapeutic potential for CDK4/6i-combinational immunotherapies. Our data provide a molecular rationale for the superior efficacy of Abemaciclib in HR+ breast cancers. They also suggest that treatment with Abemaciclib could synergize with immunotherapies targeting CDK4/6i-induced tumor antigens.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Eric Bonneil  

LAB HEAD: Pierre Thibault

PROVIDER: PXD060684 | Pride | 2026-02-25

REPOSITORIES: Pride

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CAMA1_MAPS_041023_ABEMA_1.mgf Mgf
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Publications

CDK4/6 inhibition reprograms the breast cancer immunopeptidome via Rb-dependent chromatin and transcriptomic remodeling.

Minati Robin R   Cahuzac Maxime M   Perrault Julie J   Lullier Véronique V   Apavaloaei Anca A   Bonneil Eric E   Courcelles Mathieu M   Lanoix Joel J   Kina Eralda E   Perreault Claude C   Thibault Pierre P  

Cell reports 20251213 12

The cyclin-dependent kinase 4/6 inhibitors (CDK4/6is) are standard-of-care therapies for metastatic hormone receptor-positive (HR+) breast cancer, yet their immunomodulatory effects remain underexplored. Here, we demonstrate that CDK4/6 inhibition with Abemaciclib reprograms the tumor antigen landscape by increasing major histocompatibility class I (MHC class I) presentation and reshaping the immunopeptidome in HR+ and triple-negative breast cancer cells. Through multiomics integration, we revea  ...[more]

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