Integrated profiling identifies DXS253E as a potential prognostic marker in colorectal cancer

TL;DR

This study identifies DXS253E as a potential marker for predicting outcomes in colorectal cancer and shows it promotes cancer progression through the AKT/mTOR pathway.

Contribution

The study reveals DXS253E's role in CRC progression and its association with prognosis and immune infiltration, suggesting it as a potential therapeutic target.

Findings

DXS253E is upregulated in CRC tissues and linked to poor patient survival.

High DXS253E methylation correlates with better CRC prognosis.

DXS253E promotes CRC cell proliferation and glycolysis via the AKT/mTOR pathway.

Abstract

Increasing evidence suggests that DXS253E is critical for cancer development and progression, but the function and potential mechanism of DXS253E in colorectal cancer (CRC) remain largely unknown. In this study, we evaluated the clinical significance and explored the underlying mechanism of DXS253E in CRC.

DXS253E expression in cancer tissues was investigated using the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. The Kaplan-Meier plot was used to assess the prognosis of DXS253E. The cBioPortal, MethSurv, and Tumor Immune Estimation Resource (TIMER) databases were employed to analyze the mutation profile, methylation, and immune infiltration associated with DXS253E. The biological functions of DXS253E in CRC cells were determined by CCK-8 assay, plate cloning assay, Transwell assay, flow cytometry, lactate assay, western blot, and qRT-PCR.

DXS253E was upregulated in CRC tissues and high DXS253E expression levels were correlated with poor survival in CRC patients. Our bioinformatics analyses showed that high DXS253E gene methylation levels were associated with the favorable prognosis of CRC patients. Furthermore, DXS253E levels were linked to the expression levels of several immunomodulatory genes and an abundance of immune cells. Mechanistically, the overexpression of DXS253E enhanced proliferation, migration, invasion, and the aerobic glycolysis of CRC cells through the AKT/mTOR pathway.

We demonstrated that DXS253E functions as a potential role in CRC progression and may serve as an indicator of outcomes and a therapeutic target for regulating the AKT/mTOR pathway in CRC.

The online version contains supplementary material available at 10.1186/s12935-024-03403-4.

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