Publications by authors named "Shaojia Wu"
Alternative cleavage and polyadenylation (APA) have gained increasing attention in cancer biology, yet its role in modulating anti-tumor immune response remains largely unexplored. Here, we identify the cleavage stimulation factor 2 (CSTF2), an APA-related gene, as a pivotal suppressor of anti-tumor immunity in pancreatic ductal adenocarcinoma (PDAC). CSTF2 promotes tumor development by inhibiting the infiltration and cytotoxic immune cell recruitment function of TCRαβCD4CD8NK1.
View Article and Find Full Text PDFBackground: The resistance of pancreatic ductal adenocarcinoma (PDAC) to trametinib therapy limits its clinical use. However, the molecular mechanisms underlying trametinib resistance in PDAC remain unclear.
Objective: We aimed to illustrate the mechanisms of resistance to trametinib in PDAC and identify trametinib resistance-associated druggable targets, thus improving the treatment efficacy of trametinib-resistant PDAC.
Article Synopsis
- - The study focuses on understanding how diverse cancer cells in primary colorectal cancer (CRC) lead to metastasis, particularly to the liver and ovary, which remain largely unexplored.
- - Using advanced techniques like single-cell RNA sequencing and spatial transcriptomics, researchers identified a stem-like cell cluster that drives metastasis, with specific subpopulations targeting the liver or ovary.
- - They found that interactions with surrounding cells and metabolic support from myofibroblasts are crucial for the cancer cells' ability to migrate and establish in the ovary, highlighting a new mechanism for organ-specific CRC metastasis.
The biological functions of noncoding RNA N-methyladenosine (mA) modification remain poorly understood. In the present study, we depict the landscape of super-enhancer RNA (seRNA) mA modification in pancreatic ductal adenocarcinoma (PDAC) and reveal a regulatory axis of mA seRNA, H3K4me3 modification, chromatin accessibility and oncogene transcription. We demonstrate the cofilin family protein CFL1, overexpressed in PDAC, as a METTL3 cofactor that helps seRNA mA methylation formation.
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