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.), as well as original, uncropped chemiluminescence raw Western Blot (WB) images for all immunoblots presented in the main figures and supplementary materials.