ArticleCurrent gene therapy2023
SFXN3 is Associated with Poor Clinical Outcomes and Sensitivity to the Hypomethylating Therapy in Non-M3 Acute Myeloid Leukemia Patients.
Article in Current gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- An Integrative Methylation-Metabolism Gene Signature Defines Prognosis and Immunosuppressive Microenvironment in Prostate Cancer.Chemical biology & drug design · 2026Article
- REST-driven upregulation of SFXN3 promotes AML progression via Wnt/β-catenin activation and confers decitabine resistance.Translational oncology · 2026Article
- PRR22: A Novel Prognostic Indicator and Therapeutic Target for Prostate Cancer.Anti-cancer agents in medicinal chemistry · 2026Article
- Solute carrier-correlated gene signature in predicting the prognosis and immunity in patients with acute myeloid leukemia.European journal of medical research · 2025Article
- Sideroflexin family genes were dysregulated and associated with tumor progression in prostate cancers.Human genomics · 2025Article
- Comprehensive Analysis and Experimental Validation of HEPACAM2 as a Potential Prognosis Biomarker and Immunotherapy Target in Colorectal Cancer.Current gene therapy · 2025Article
- SFXN3 is a Prognostic Marker and Promotes the Growth of Acute Myeloid Leukemia.Cell biochemistry and biophysics · 2024Article
- ZNF695, A Potential Prognostic Biomarker, Correlates with Im mune Infiltrates in Cervical Squamous Cell Carcinoma and Endoce rvical Adenocarcinoma: Bioinformatic Analysis and Experimental Verification.Current gene therapy · 2024Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDNA hypermethylation plays a critical role in the occurrence and progression of acute myeloid leukemia (AML). The mitochondrial serine transporter, SFXN3, is vital for onecarbon metabolism and DNA methylation. However, the impact of SFXN3 on the occurrence and progression of AML has not been reported yet.
objectiveIn this study, we hypothesized that SFXN3 indicates a poor prognosis and suggested tailored treatment for AML patients.
methodsWe used GEPIA and TCGA repository data to analyze the expression of SFXN3 and its correlation with survival in AML patients. RT-qPCR was used to detect the SFXN3 level in our enrolled AML patients and volunteers. Additionally, Whole Genome Bisulfite Sequencing (WGBS) was used to detect the genomic methylation level in individuals.
resultsThrough the TCGA and GEPIA databases, we found that SFXN3 was enriched in AML patients, predicting shorter survival. Furthermore, we confirmed that SFXN3 was primarily overexpressed in AML patients, especially non-M3 patients, and that high SFXN3 in non-M3 AML patients was found to be associated with poor outcomes and frequent blast cells. Interestingly, non-M3 AML patients with high SFXN3 levels who received hypomethylating therapy showed a higher CR ratio. Finally, we found that SFXN3 could promote DNA methylation at transcription start sites (TSS) in non-M3 AML patients. These sites were found to be clustered in multiple vital cell functions and frequently accompanied by mutations in DNMT3A and NPM1.
conclusionIn conclusion, SXFN3 plays an important role in the progression and hypermethylation in non-M3 AML patients and could be a potential biomarker for indicating a high CR rate for hypomethylating therapy.
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