L-Lactate reprograms tumor-associated macrophages to drive pancreatic cancer progression via BCL3 lactylation

This repository contains the raw experimental data supporting the findings in the study investigating the metabolic-signaling axis between pancreatic ductal adenocarcinoma (PDAC) and tumor-associated macrophages (TAMs). Our study demonstrates that the uptake of tumor-derived L-lactate induces site-specific L-lactylation of the transcriptional co-regulator BCL3 at lysine 21 (K21) in TAMs, this modification functions as a molecular switch, driving BCL3 nuclear translocation and enhancing its binding to the NF-κB p50 subunit, which competitively displaces the pro-inflammatory p65 subunit, this mechanism rewires the transcriptional output to induce a pro-tumorigenic TAMs phenotype, facilitating PDAC progression. This dataset includes quantitative raw data in Excel/CSV files containing the raw numerical data used to generate all bar charts, statistical plots, and functional assay graphs in the manuscript (including qPCR results, tumor growth metrics, etc.).