Code for the analysis of splicing in KRAS inhibited cell line
KRAS mutations are found in approximately 40% of colorectal cancers (CRCs) and are associated with poor clinical outcomes. While targeting KRAS has shown some therapeutic promise, treatment resistance remains a major challenge. Previous transcriptomic analyses revealed that the unfolded protein response and WNT/Ξ²-catenin signaling pathways are selectively upregulated in KRAS-silencing-sensitive cell lines, suggesting distinct molecular responses to oncogene inhibition.
However, the impact of KRAS inhibition on alternative splicing remains underexplored. Given that aberrant splicing is a known driver of tumor progression and cell dedifferentiation, this pilot project investigates splicing entropy as a proxy for transcriptomic diversity following KRAS knockdown.
- KRAS-silencing sensitive:
HCT116,SW480 - KRAS-silencing resistant:
LS174T,SW837
Each cell line was analyzed under control and KRAS-inhibited conditions to compare splicing entropy levels and evaluate reproducibility across replicates and cell line groupings.
- Splicing Entropy Analysis: Quantifies transcript diversity within each sample.
- Pairwise Comparisons: Control vs. KRAS-silenced samples for each cell line.
- Group-Level Analysis: Combined comparison of sensitive vs. resistant cell lines.
For questions or collaborations, please reach out to [rogerio.e.ramos.ribeiro@gmail.com].