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Palmitoylation prevents B7-H4 lysosomal degradation sustaining tumor immune evasion

ABSTRACT: To investigate the function of CDK4/6 inhibitor- Abemaciclib on lysosome function.

ORGANISM(S): Homo sapiens

PROVIDER: GSE272492 | GEO | 2025/02/13

REPOSITORIES: GEO

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Palmitoylation prevents B7-H4 lysosomal degradation sustaining tumor immune evasion

Project description:Palmitoylation prevents B7-H4 lysosomal degradation sustaining tumor immune evasion

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B7-H4 post-translational modifications

Project description:B7-H4 functions as an immune checkpoint in the tumor microenvironment (TME). However, the post-translational modification (PTM) of B7-H4 and its translational potential in cancer remains incompletely understood. We found that ZDHHC3, a zinc finger DHHC-type palmitoyltransferase, palmitoylates B7-H4 at Cys130 in breast cancer cells, preventing its lysosomal degradation and sustaining B7-H4-mediated immunosuppression. Knockdown of ZDHHC3 in tumors resulted in robust anti-tumor immunity and reduced tumor progression in murine models. Moreover, abemaciclib, a CDK4/6 inhibitor, primed lysosome activation and promoted lysosomal degradation of B7-H4 independently of the tumor cell cycle. Treatment with abemaciclib resulted in T cell activation and mitigated B7-H4-mediated immune suppression via inducing B7-H4 degradation in preclinical tumor models. Thus, B7-H4 palmitoylation is an undocumented PTM controlling B7-H4 protein stability and abemaciclib may be repurposed to enhance B7-H4 degradation, thereby treating patients with B7-H4+ tumors.

2025-02-14 | PXD054393 | Pride

Abemaciclib differentially reshapes the immunopeptidome of breast cancer subtypes

Project description: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.

2026-02-25 | PXD060684 | Pride

Loss of Optineurin Drives Cancer Immune Evasion via Palmitoylation-Dependent IFNGR1 Lysosomal Sorting and Degradation.

Project description: Not available

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Circular RNA circEIF3C promotes intrahepatic cholangiocarcinoma progression and immune evasion via the miR-34a-5p/B7-H4 axis.

Project description: Not available

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Efficacy of abemaciclib in palbociclib-resistant hormone receptor positive organoids derived from patient derived xenografts from patients who progressed on palbociclib

Project description:Resistance to CDK4/6 inhibitors plus endocrine therapy, standard of care for HR+/HER2-neg metastatic breast cancer (MBC) patients, remains as a clinical problem with limited therapeutic options after disease progression. Treatment with abemaciclib after progression on a prior CDK4/6i has received increasing interest. However, molecular predictors of cross-resistance and unique mechanism of resistance to each CDK4/6i are unknown. In this study, multiomics analyses revealed ≥30 differentially altered pathways between palbociclib and abemaciclib resistant models. Mechanistic, preclinical and retrospective clinical evidence showed that HR+/HER2-neg MBC tumors refractory to palbociclib still may be responsive to abemaciclib. Based on the unique mechanisms of resistance to each CDK4/6i, we propose that patients who would benefit from abemaciclib treatment post progression on palbociclib could be selected based on the Hallmark gene set enrichment of G2/M pathway, while those who most probably would be refractory could be identified base on the gene set enrichment of OXPHOS pathway.

2023-07-10 | GSE229146 | GEO

Efficacy of abemaciclib in palbociclib-resistant hormone receptor positive breast cancer cell lines: MCF-7 and T47D

2023-07-10 | GSE222367 | GEO

RNA-seq analysis of MCF7 cells treated with abemaciclib, SR11302

Project description:We measured changes in gene expression in MCF7 with CDK4/6 and AP-1 inhibition by abemaciclib and SR11302, respectively.

2020-09-01 | GSE157214 | GEO

RNA-seq of detecting the effect of CDK4&6 inhibitor Abemaciclib and VSV-M51 in glioma

Project description:The RNA-seq data provided evidence that CDK4&6 inhibitor Abemaciclib and VSV-M51 increase the oncolytic effect in glioma

2022-06-01 | GSE166914 | GEO

Proteomics analysis of the molecular mechanism by which Antibody-drug conjugate Oba01 combined with Abemaciclib kills colorectal cancer organoids

Project description:Proteomics reveals the molecular mechanism by which the antibody-drug conjugate Oba01 and the CDK4/6 inhibitor Abemaciclib jointly kill colorectal cancer organoids

2025-05-03 | PXD063571 | JPOST Repository

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