ArticleLaboratory investigation; a journal of technical methods and pathology2020
Fatty acid beta oxidation enzyme HADHA is a novel potential therapeutic target in malignant lymphoma.
Article in Laboratory investigation; a journal of technical methods and pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- Fatty acid metabolic reprogramming in the tumor microenvironment: Unraveling mechanisms and therapeutic prospects.Genes & diseases · 2026Review
- A tryptophan metabolism-related gene signature predicts prognosis and immune features in cutaneous melanoma.Frontiers in immunology · 2026Article
- HADHA-mediated regulation of JAK/STAT3 signaling in glioblastoma: a metabolic-epigenetic axis.Cell death discovery · 2025Article
- Emerging roles for fatty acid oxidation in cancer.Genes & diseases · 2025Review
- Altered carnitine transporter genes (Translational lung cancer research · 2024Article
- HADHA promotes esophageal cancer progression by activating mTOR signaling and the SP1/MDM2 axis.Acta biochimica et biophysica Sinica · 2024Article
- HADHA promotes glioma progression by accelerating MDM2-mediated p53 ubiquitination.Cancer gene therapy · 2024Article
- Evolutionary proteogenomic landscape from pre-invasive to invasive lung adenocarcinoma.Cell reports. Medicine · 2024Article
- HADHA promotes ovarian cancer outgrowth via up-regulating CDK1.Cancer cell international · 2023Article
- Genetics of enzymatic dysfunctions in metabolic disorders and cancer.Frontiers in oncology · 2023Review
- Orchestral role of lipid metabolic reprogramming in T-cell malignancy.Frontiers in oncology · 2023Review
- Abnormal expression of HADH, an enzyme of fatty acid oxidation, affects tumor development and prognosis (Review).Molecular medicine reports · 2022Review
- UBE2O promotes lipid metabolic reprogramming and liver cancer progression by mediating HADHA ubiquitination.Oncogene · 2022Article
- Over-Reduced State of Mitochondria as a Trigger of "β-Oxidation Shuttle" in Cancer Cells.Cancers · 2022Review
- Progress of potential drugs targeted in lipid metabolism research.Frontiers in pharmacology · 2022Review
- Ferroptosis in lymphoma: Emerging mechanisms and a novel therapeutic approach.Frontiers in genetics · 2022Review
- HumanInternational journal of biological sciences · 2022Article
- Reprogramming lipid metabolism as potential strategy for hematological malignancy therapy.Frontiers in oncology · 2022Review
- A "Weird" Mitochondrial Fatty Acid Oxidation as a Metabolic "Secret" of Cancer.Oxidative medicine and cellular longevity · 2022Review
- Carnitine Traffic in Cells. Link With Cancer.Frontiers in cell and developmental biology · 2020Review
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells, including malignant lymphoma cells, alter their metabolism, termed "metabolic reprograming," on initiation of malignant transformation as well as upon accumulation of genetic abnormalities. Here, to identify a novel therapeutic target involved in the metabolic changes during malignant lymphoma, we performed global analyses combined with shotgun proteomics, in silico database analysis, and clinic-pathologic analysis of nonneoplastic lymphoid tissue and malignant lymphoma tissue and verified the molecular functions in vitro. In total, 2002 proteins were detected from both samples and proteins related to fatty acid beta-oxidation (FAO) were detected more frequently in malignant lymphoma tissue. Consequently, the most frequently detected protein, the mitochondrial trifunctional enzyme subunit-alpha (HADHA), was identified as a potential target. Immunohistochemical analyses revealed that HADHA tended to be overexpressed in a high-grade subtype of malignant lymphoma tissue. Clinicopathologic study revealed that HADHA overexpression was correlated with significantly worse overall survival (P = 0.013) and was an independent prognostic predictor in diffuse large B-cell lymphoma (P = 0.027). In vitro, downregulation of HADHA negatively regulated cell growth by causing G0/G1 arrest (P = 0.0008) similar to treatment with etomoxir, an inhibitor of FAO (P = 0.032). Moreover, downregulation of HADHA increased the susceptibility to doxorubicin (P = 0.002) and etoposide (P = 0.004). Moreover, these phenotypes were confirmed in an HADHA knockout system. Thus, we provide a basis for a novel therapeutic strategy through the regulation of HADHA and FAO in patients with refractory malignant lymphoma.
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