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Identification of disulfidptosis-related subtypes, characterization of tumor microenvironment infiltration, and development of a prognosis model in colorectal cancer

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Abstract

Background

Colorectal cancer is the second leading cause of cancer-related deaths, which imposes a significant societal burden. Regular screening and emerging molecular tumor markers have important implications for detecting the progression and development of colorectal cancer. Disulfidptosis is a newly defined type of programmed cell death triggered by abnormal accumulation of disulfide compounds in cells that stimulate disulfide stress. Currently, there is no relevant discussion on this mechanism and colorectal cancer.

Methods

We classified the disulfidptosis-related subtypes of colorectal cancer using bioinformatics methods. Through secondary clustering of differentially expressed genes between subtypes, we identified characteristic genes of the disulfidptosis subtype, constructed a prognostic model, and searched for potential biomarkers through clinical validation.

Results

Using disulfidptosis-related genes collected from the literature, we classified colorectal cancer patients from public databases into three subtypes. The differentially expressed genes between subtypes were clustered into three gene subtypes, and eight characteristic genes were screened to construct a prognostic model.

Conclusion

The disulfidptosis mechanism has important value in the classification of colorectal cancer patients, and characteristic genes selected based on this mechanism can serve as a new potential biological marker for colorectal cancer.

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Availability of data and materials

The datasets used and/or analyzed during the current study are available from the corresponding author.

Abbreviations

CRC:

Colorectal cancer

SLC7A11:

Solute carrier family 7 member 11

NADPH:

Nicotinamide adenine dinucleotide phosphate

SLC3A2:

4F2 cell-surface antigen heavy chain

RPN1:

Dolichyl-diphosphooligosaccharide-protein glycosyltransferase subunit 1

NCKAP1:

Nck-associated protein 1

DRG:

Disulfidptosis-related genes

DEGs:

Differentially expressed genes

TCGA:

The Cancer Genome Atlas

GEO:

The Gene Expression Omnibus

LASSO:

Least absolute shrinkage and selection operator

OS:

Overall survival

HPA:

The Human Protein Atlas database

CIBERSORT:

Cell-type identification by estimating relative subsets of RNA transcript

TME:

Tumor microenvironment

CSC:

Cancer stem cell index

TMB:

Tumor mutation burden

MSI:

Microsatellite instability

CNV:

Copy number variation

PCA:

Principal component analysis

GOCC:

GO cellular component

GOMF:

GO molecular function

MDSCs:

Myeloid-derived suppressor cells

CDF:

Cumulative distribution function

MXRA8:

Matrix remodeling-associated protein 8

IGFBP5:

Insulin-like growth factor-binding protein 5

MRC2:

C-type mannose receptor 2

HTRA1:

Serine protease HTRA1

TNFAIP6:

Tumor necrosis factor-inducible gene 6 protein

SLC2A3:

Solute carrier family 2, facilitated glucose transporter member 3

GRP:

Gastrin-releasing peptide

APOD:

Apolipoprotein D

PCD:

Programmed cell death

ACD:

Accidental cell death

GLUT3:

Glucose transporter-3

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Funding

The authors declare that no funds, grants, or other support were received during the preparation of this manuscript.

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Authors and Affiliations

Authors

Contributions

LY was responsible for designing the study, analyzing the data, and was the main author of the manuscript. ZS and WYP provided guidance and revised the manuscript. TMY and DW were responsible for organizing the images. All authors read and approved the final manuscript.

Corresponding authors

Correspondence to Shu Zhu or Yunpeng Wang.

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Conflict of interest

The authors have no relevant financial or non-financial interests to disclose.

Ethics approval and consent to participate

This study only involved secondary analysis of publicly available data from databases. Not applicable.

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Li, Y., Tang, M., Dang, W. et al. Identification of disulfidptosis-related subtypes, characterization of tumor microenvironment infiltration, and development of a prognosis model in colorectal cancer. J Cancer Res Clin Oncol 149, 13995–14014 (2023). https://doi.org/10.1007/s00432-023-05211-1

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  • DOI: https://doi.org/10.1007/s00432-023-05211-1

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