# BRD4 Regulation of p53 in MCF-7 Breast Cancer Cells Study
> PhD thesis analysis on BRD4-mediated post-translational regulation of p53 in breast cancer cells and rMATS pipeline for alternative splicing analysis.

Tags: breast-cancer-research, p53-protein, brd4-inhibitor, mcf-7-cells, oncology, epigenetics, molecular-biology, biomedical-science
## PhD Thesis: BRD4 and p53 Regulation in Breast Cancer

## Introduction to Global Cancer Burden
* Breast cancer affects 2.3 million women annually with 685,000 deaths worldwide.
* BRD4 upregulation is a known epigenetic driver in aggressive cancer subtypes.

## Molecular Biology: BRD4 & p53 Axis
* p53 is the 'Guardian of the Genome', mutated in ~50% of all cancers.
* BRD4 occupancy at super-enhancers is required for baseline TP53 transcription in Luminal A breast cancer models like MCF-7.

## Experimental Design and Methodology
* **Model:** MCF-7 cells treated with MZ1 (PROTAC BRD4 degrader) and 2 Gy ionizing radiation.
* **Techniques:** Western Blotting for protein expression, RT-PCR for transcript analysis, and BCA assays for quantification.
* **Bioinformatics:** Implementation of rMATS pipeline on Ubuntu 20.04 (WSL) for differential alternative splicing detection.

## Key Results
* **Protein Levels:** BRD4 degradation via MZ1 consistently elevates p53 protein levels, peaking at 2 hours post-radiation.
* **Transcript Levels:** RT-PCR shows a fold change of 0.68, indicating MZ1 does not significanty alter TP53 mRNA levels.
* **Conclusion:** BRD4 regulates p53 at the post-translational level, likely affecting protein stability.

## Future Research Directions
* Co-immunoprecipitation (Co-IP) to confirm BRD4-MDM2 interactions.
* Extension of the study to Triple-Negative Breast Cancer (TNBC) models like MDA-MB-231.
* Exploring MZ1 as a potential radiosensitizer in clinical settings.
---
This presentation was created with [Bobr AI](https://bobr.ai) — an AI presentation generator.