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ACILAN AYHAN, C.

Publications and source records attributed to ACILAN AYHAN, C..

2 recordsLinked to original sources

GLproxScape reconstructs spatial chromatin occupancy landscapes from tiled genomic locus proteomics

Genomic locus proteomics combines proximity labeling with mass spectrometry to identify the proteins associated with user-defined genomic loci. However, per-region enrichment values from tiled guide designs are typically pooled before hit calling, collapsing the latent spatial structure encoded by overlapping measurements. Here, we describe GLproxScape, an R package that treats per-region enrichments as indirect spatial measurements and reconstructs latent chromatin occupancy landscapes through a Gaussian labeling-kernel forward model. Sequence-specific transcription factors are resolved by motif-anchored non-negative least-squares deconvolution against JASPAR or HOCOMOCO position weight matrices, while chromatin regulators which lack defined DNA-binding motifs are inferred as broad occupancy zones, enabling recovery of overlapping members of multi-subunit complexes. Applied to published genomic locus proteomics datasets at the human TERT, MYC, FOXP2, and FOXQ1 loci and the mouse Ripk3 locus, GLproxScape recovered known regulators with predicted positions independently supported by ChIP-Atlas peaks, reconstructed candidate co-binding relationships, and identified chromatin complexes inaccessible to pooled analyses. Systematic sgRNA-ablation experiments further showed that densely tiled designs improve event recovery and positional stability, providing concrete experimental guidance for future genomic locus proteomics studies.

bioinformatics↗

Chromatin-focused genetic and chemical screens identify BRPF1 as a targetable vulnerability in Taxol-resistant triple-negative breast cancer

Triple-negative breast cancer (TNBC) stands out as a particularly aggressive and frequently recurring form of breast cancer. Due to the absence of hormone receptors, the available treatment avenues are constrained, making chemotherapy the primary approach. Unfortunately, the development of resistance to chemotherapy poses a significant challenge, further restricting the already limited therapeutic alternatives for recurrent cases. Understanding the molecular basis of chemotherapy resistance in TNBC is pivotal for improving treatment outcomes. Here, we generated two different Taxol-resistant TNBC cell lines with a dose-escalation method to mimic chemotherapy resistance in vitro. These cells exhibited hallmark features of resistance, including reduced cell growth, altered morphology, and evasion of apoptosis. Transcriptome analysis uncovered elevated ABCB1 expression and multidrug-resistant phenotype in the resistant cells. To comprehensively investigate the key epigenetic regulators of Taxol resistance, we conducted chromatin-focused genetic and chemical screens and pinpointed Bromodomain and PHD Finger Containing 1 (BRPF1) as a novel regulator of Taxol resistance in TNBC cells. Knockout of BRPF1, the reader protein in the MOZ/MORF histone acetyl-transferase complex, but not the other complex members, sensitized resistant cells to Taxol. Additionally, BRPF1 inhibitors, PFI-4 and OF-1, in combination with Taxol significantly reduced cell viability. Transcriptome analysis upon BRPF1 loss or inhibition revealed a negative impact on ribosome biogenesis-related gene sets, resulting in a global decrease in protein translation in Taxol-resistant cells. Our ChIP-qPCR analysis demonstrated that active BRPF1 directly interacts with the ABCB1 promoter, enhancing its expression towards inducing a multidrug-resistant phenotype. Conversely, knockout or inhibition of BRPF1 leads to decreased ABCB1 expression. This dual mechanism critically sensitizes Taxol-resistant TNBC cells to chemotherapy. Our findings uncover a comprehensive molecular framework, highlighting the pivotal role of epigenetic reader protein BRPF1 in Taxol resistance and providing potential avenues for therapeutic intervention in TNBC.

cancer biology↗