Open Access

ARTICLE

Increased MAD2L2 expression predicts poor clinical outcome in Colon Adenocarcinoma

by HAOTONG SUN^1,2, HEYING WANG^1,3, XIN LI^1,2, YANJIE HAO^1,2, JUN LING^1,2, HUAN WANG^1,2, FEIMIAO WANG^1,2, FANG XU^1,2,*

1 School of Basic Medicine, Medical Genetics and Cell Biology, Ningxia Medical University, Yinchuan, 750004, China
2 Key Laboratory of Reproduction and Genetics, Ningxia Medical University, Yinchuan, 750004, China
3 Department of Human Anatomy and Histology Embryology, Ningxia Medical University, Yinchuan, 750004, China

* Corresponding Author: FANG XU. Email:

(This article belongs to the Special Issue: Bioinformatics Study of Diseases)

BIOCELL 2023, 47(3), 607-618. https://doi.org/10.32604/biocell.2023.026445

Received 06 September 2022; Accepted 15 November 2022; Issue published 03 January 2023

Abstract

Background: Colon adenocarcinoma (COAD) is the second leading cause of cancer death worldwide thus, identification of COAD biomarkers is critical. Mitotic Arrest Deficient 2 Like 2 (MAD2L2) is a key factor in mammalian DNA damage repair and is highly expressed in many malignant tumors. This is a comprehensive study of MAD2L2 expression, its diagnostic value, prognostic analysis, potential biological function, and impact on the immune system of patients with COAD. Methods: Gene expression, clinical relevance, prognostic analysis, diagnostic value, GO/KEGG cluster analysis, data obtained from TCGA, and bioinformatics statistical analysis were performed using the R package. Immune responses to MAD2L2 expression in COAD were analyzed using TIMER. The expression of MAD2L2 in HCT116 cells induced by the inflammatory factor TNF-α was detected using Western blot. Results: Our results underscore the clinical diagnostic value and potential biological significance of MAD2L2 in patients with COAD. A high level of MAD2L2 expression has been found in COAD and correlated with tumor status and colon polyps. ROC curve analysis showed that MAD2L2 expression has high diagnostic value in COAD. Analysis of immune infiltration results showed that MAD2L2 expression was positively correlated with neutrophil levels. The western blot results demonstrated that MAD2L2 was dose-dependently present with TNF-α. GO/KEGG revealed that MAD2L2 overexpressed and coexpressed genes were mostly involved in biological functions, including hypoxia response, response to reduced oxygen levels, mitochondrial translation elongation, and other processes. Conclusion: MAD2L2 as a new COAD biomarker contributes to our understanding of how alterations in gene expression and the immunological environment contribute to the development of colon cancer. Following further investigation, MAD2L2 may prove to be a viable target factor for clinical diagnosis and therapy of COAD.

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