Prognostic and Immune Infiltration Analysis of Transaldolase 1 (TALDO1) in Hepatocellular Carcinoma

Abstract

Background

Transaldolase 1 (TALDO1) deficiency was associated with hepatocellular carcinoma (HCC), but the association between TALDO1 and prognosis in HCC remains unclear.

Material and Methods

RNA-seq and clinical data of HCC from The Cancer Genome Atlas (TCGA) database and Gene Expression Omnibus (GEO) database were analyzed. CCK8 and EdU assays were utilized to examine the effect of TALDO1 on HCC proliferation. Transwell assay was used to explore the effect of TALDO1 on HCC migration. Western Blot was applied to detected the expression levels of pathway-related proteins.

Results

TALDO1 mRNA level was higher in HCC tissues than in control normal tissues in TCGA and GEO databases (P<0.001, P<0.001). Expression of TALDO1 mRNA was associated with histologic grade (P=0.021). Multivariate regression analysis revealed that high TALDO1 mRNA expression was an independent risk factor for prognosis (P<0.001). High expression of TALDO1 had poor overall survival (OS) (P=0.046). Additionally, Nomogram prognostic model of TALDO1 and clinicopathological parameters could predict the prognostic OS of HCC patients. Functional enrichment and immune infiltration analysis revealed that TALDO1 negatively regulates immune response. Furthermore, knockdown TALDO1 expression suppressed the proliferation and migration ability of HCC cells. Mechanistically, TALDO1 leaded to activation of the mitogen-activated protein kinase (MAPK) pathway and enhancement of epithelial-mesenchymal transition (EMT).

Conclusion

Our findings demonstrated that TALDO1 could serve as a promising novel biomarker for HCC patients, which might modulate the immune microenvironment resulting in a poor prognosis.

Keywords:

• transaldolase 1
• prognosis
• immune infiltration
• proliferation
• migration

Ethics Approval

This study was conducted in accordance with the Declaration of Helsinki and approved by Ethics Committee of Lihuili Hospital (No. KY2022SL389-01).

Disclosure

The authors report no conflicts of interest in this work.

Additional information

Funding

Our research was funded by the Ningbo Medical and Health Brand Discipline (PPXK2018-03).