Abstract:

Background:TSC22D domain family genes, including TSC22D1-4, have been extensively reported to be involved in tumors. However, their expression profiles and prognostic significance in acute myeloid leukemia (AML) remain unknown.

Methods:The present study investigated the expression profiles and prognostic significance of TSC22D domain family genes in AML through the use of multiple online databases, including the CCLE, EMBL-EBI, HPA, Oncomine,GEPIA2, UALCAN, BloodSpot, and GSCALite databases. The cBioPortal and GSCALite databases were used to explore the genetic alteration and copy number variation (CNV) of TSC22D3. TRRUST Version 2 was used to explore the gene ontology biological process, disease ontology, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways associated with TSC22D3. The AnimalTFDB3.0, STRING, and Harmonizome databases were used to investigate the protein–protein interaction (PPI) network of TSC22D3. Harmonizome was used for TSC22D gene regulatory kinase analysis. The TargetScanHuman 8.0, MiRDB, and ENCORI databases were used to execute the analysis of TSC22D3 regulatory miRNAs. Then, the GSCALite and GEPIA2021 databases were used to investigate the correlation between TSC22D3 expression and immune infiltration.

Results:The expression of TSC22D3 was upregulated markedly in AML cells relative to normal hematopoietic stem cells. The expression of TSC22D3 was increased in AML group compared with normal control group. And overexpression of TSC22D3 was associated with poor OS in AML patients.Furthermore, gene ontology analysis revealed that TSC22D3 was involved in leukemia. Functional enrichment analysis indicated that TSC22D3 has many biological functions, including the regulation of many genes, kinases, miRNAs, signaling pathways, and immune infiltration.

Conclusions:TSC22D3 expression was upregulated in AML, and overexpression was associated with poor OS in AML patients. Therefore, TSC22D3 may serve as a novel prognostic biomarker for AML.

Journal Link: 10.21203/rs.3.rs-1209284/v2 Journal Link: Publisher Website Journal Link: Download PDF Journal Link: Google Scholar