Published online Apr 15, 2024. doi: 10.4251/wjgo.v16.i4.1344
Peer-review started: December 20, 2023
First decision: December 27, 2023
Revised: January 9, 2024
Accepted: February 25, 2024
Article in press: February 25, 2024
Published online: April 15, 2024
Processing time: 112 Days and 19 Hours
Cholangiocarcinoma (CCA) is a highly malignant cancer, characterized by frequent mucin overexpression. MUC1 has been identified as a critical oncogene in the progression of CCA. However, the comprehensive understanding of how the mucin family influences CCA progression and prognosis is still incomplete.
To investigate the functions of mucins on the progression of CCA and to establish a risk evaluation formula for stratifying CCA patients.
Single-cell RNA sequencing data from 14 CCA samples were employed for elucidating the roles of mucins, complemented by bioinformatic analyses. Subse
CCA tumor cells with elevated levels of MUC1 and MUC4 showed activated nucleotide metabolic pathways and increased invasiveness. MUC5AC-high cells were found to promote CCA progression through WNT signaling. MUC5B-high cells exhibited robust cellular oxidation activities, leading to resistance against antitumoral treatments. MUC13-high cells were observed to secret chemokines, recruiting and transforming macrophages into the M2-polarized state, thereby suppressing antitumor immunity. MUC16-high cells were found to promote tumor progression through interleukin-1/nuclear factor kappa-light-chain-enhancer of activated B cells signaling upon interaction with neutrophils. Utilizing the expression levels of these mucins, a risk factor evaluation formula for CCA was developed and validated across multiple cohorts. CCA samples with higher risk factors exhibited stronger metastatic potential, chemotherapy resistance, and poorer prognosis.
Our study elucidates the functional mechanisms through which mucins contribute to CCA development, and provides tools for risk stratification in CCA.
Core Tip: In this study, we have conducted a comprehensive investigation of mucins in cholangiocarcinoma (CCA) using a combination of bioinformatics analysis, including single-cell RNA sequencing and spatial transcriptomics, along with experimental validations. Our findings highlight the significant roles of MUC1, MUC4, and MUC5B in CCA metabolism, contributing to tumor progression and therapy resistance. Additionally, MUC5AC has been identified as a regulator of CCA invasiveness through the WNT signaling. MUC13 and MUC16 are found to play critical roles in tumor-immune interactions, regulating antitumoral immune defense. The collect impact of these mucins enables the development of a CCA prognosis evaluation model that effectively predicts tumor malignancy, treatment effectiveness, and prognosis in CCA cases.