ArticleCancer genomics & proteomics
Exosomes Transfer ST6GAL1-mediated Therapeutic Resistance in Rectal Cancer Cells.
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Article
- Tissue-specific factors that govern the sialoglycan-Siglec axis in cancer.Bioscience reports · 2026Review
- Beta-site Amyloid Precursor Protein Cleaving Enzyme 1 Overexpression Abrogates ST6GAL1 Mediated Rectal Cancer Chemoradiation Resistance.Cancer genomics & proteomicsArticle
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Authors and funding
9 authors.
Funding
Abstract
BACKGROUND/
aimLocally advanced Rectal cancer (RC) is treated with neoadjuvant chemoradiation, but treatment resistance is common. We have previously shown that ST6GAL1 causes RC chemoradiation resistance. Exosomes are small particles that can transfer proteins between cells. We hypothesized that exosomes transfer ST6GAL1 between RC cells, spreading treatment resistance. MATERIALS AND
methodsWe characterized exosomes isolated from multiple ST6GAL1-expressing colorectal cancer (CRC) cell lines. Treatment response was assessed in ST6GAL1-knockdown (KD) cells treated with these exosomes. Single cell RNA sequencing (scRNA-seq) and flow cytometry for surface sialylation were performed on CRC organoids to compare presence of ST6GAL1 RNA and protein activity.
resultsExosomes from multiple CRC cell lines contained ST6GAL1 protein and ST6GAL1 KD cells treated with these exosomes demonstrated transfer of ST6GAL1 with increase in protein in treated cells, but not mRNA, and the protein localized to the Golgi complex. In addition, treated cells demonstrated increased resistance to chemoradiation-induced apoptosis (
conclusionThese findings demonstrate that ST6GAL1-containing rectal cancer exosomes transfer ST6GAL1 between cells causing treatment resistance.
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