ALDH3B1

Last update 08 May 2025

Basic Info

Synonyms

aldehyde dehydrogenase 3 family member B1, Aldehyde dehydrogenase 7, Aldehyde dehydrogenase family 3 member B1

+ [2]

Introduction

Oxidizes medium and long chain saturated and unsaturated fatty aldehydes generated in the plasma membrane into non-toxic fatty acids (PubMed:17382292, PubMed:23721920). May have a protective role against the cytotoxicity induced by lipid peroxidation (PubMed:17382292). Short-chain fatty aldehydes are not good substrates (PubMed:17382292). Can use both NADP(+) and NAD(+) as electron acceptor in vitro, however in vivo preference will depend on their tissue levels (PubMed:17382292). Low activity towards acetaldehyde and 3,4-dihydroxyphenylacetaldehyde (PubMed:17382292, PubMed:23721920). Able to metabolize aromatic aldehydes such as benzaldehyde to their acid form (PubMed:17382292).

100 Clinical Results associated with ALDH3B1

100 Translational Medicine associated with ALDH3B1

0 Patents (Medical) associated with ALDH3B1

Literatures (Medical) associated with ALDH3B1

01 Mar 2025·Experimental Cell Research

Phthalocyanine and photodynamic therapy relieve albumin paclitaxel and gemcitabine chemoresistance in pancreatic cancer

Article

Author: Li, Zeru ; Yang, Xiaoying ; Qin, Cheng ; Zhao, Bangbo ; Li, Tianyu ; Zhang, Xiangyu ; Zhao, Yutong ; Wang, Weibin

Pancreatic cancer (PCa) is a solid tumor with extremely high malignancy and poor prognosis. Chemotherapy is an important treatment option. Compared with gemcitabine alone, albumin paclitaxel plus gemcitabine (AG) is more effective in the treatment of advanced PCa. The NCCN guidelines also list AG regimen as one of the first-line recommended schemes for PCa. As for the mechanism of drug resistance of AG regimen, there is no relevant literature report at present. MIA PaCa-2 and BxPC-3, two PCa cell lines, were utilized to construct stable cell lines (AG-resistant cell lines) resistant to paclitaxel plus gemcitabine via gradually increased drug concentration of gemcitabine and albumin paclitaxel. AG-resistant cell lines are more malignant than parental cell lines in proliferation, invasion and chemoresistance. 5 genes, including ALDH3A1, ALDH3B1, CDA, MUC1, C15orf48 were found significantly high expression in AG-resistant cell lines. By utilizing PDB database and drugbank, a large-scale virtual screening of target drugs is carried out to screen for possible small molecule targeted drugs, and phthalocyanine was selected and proved to sensitize AG-resistant cell lines. We also validated the mechanism of phthalocyanine sensitizing chemoresistance, demonstrating that it leads to cell death by stimulating intracellular ROS level.

01 Jan 2025·Translational Cancer Research

Establishment and validation of a prognostic prediction model for glioma based on key genes and clinical factors

Article

Author: Ge, Qiang ; Lin, Yu ; Li, Huining ; Hua, Dan

BackgroundGlioma is a common brain tumour that is associated with poor prognosis. Immunotherapy has shown significant potential in the treatment of gliomas. Herein, we proposed a new prognostic risk model based on immune- and mitochondrial energy metabolism-related differentially expressed genes (IR&MEMRDEGs) to enhance the accuracy of prognostic assessment in patients with glioma.MethodsData from samples from 671 glioma patients and 5 normal controls with available follow-up data and prognostic outcomes were downloaded from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. All data were downloaded on 13 November 2023. IR&MEMRDEGs were screened from the GeneCards website and published literature. Prognostic prediction models were constructed and analysed using Cox and Least Absolute Shrinkage and Selection Operator (LASSO) regression, Kaplan-Meier (KM) curve, and receiver operating characteristic (ROC) curve analyses. Single-sample gene set enrichment analysis (ssGSEA) was further performed to ascertain the percentage of immune cell infiltration in the glioma specimens.ResultsBioinformatics analysis of the GEO and TCGA databases identified eleven MEMRDEGs with dysregulated expression in gliomas: EIF4EBP1, TP53, IDH1, PRKCZ, CD200, GPI, PGM2, PKLR, AK2, ATP4A, and ALDH3B1. Further analysis identified EIF4EBP1, TP53, IDH1, PRKCZ, CD200, GPI, PGM2, AK2, and ALDH3B1 as separate predictive factors for glioma, among which PGM2 and AK2 exhibited superior accuracy [area under the ROC curve (AUC) >0.9], while EIF4EBP1, TP53, IDH1, PRKCZ, GPI, and ALDH3B1 demonstrated slightly lower accuracy (0.7< AUC <0.9), and CD200 displayed poor accuracy (0.5< AUC <0.7). Among these genes, the levels of AK2, ALDH3B1, EIF4EBP1, GPI, IDH1, PGM2, and TP53 were significantly higher in the high-risk group (HRG) compared with the low-risk group (LRG) (P<0.001), indicating a negative association with patient prognosis. In contrast, CD200 and PRKCZ were significantly downregulated in the HRG compared to the LRG (P<0.05), indicating a potential correlation with patient outcomes. Subsequently, prognostic models were constructed based on IR&MEMRDEG and MEMRDEGs to anticipate the outcomes of glioma patients, while the predictive efficacy of the model was validated via KM and ROC curve analysis. The results revealed that EIF4EBP1, TP53, IDH1, PRKCZ, GPI, PGM2, ALDH3B1, and AK2 had superior accuracy in predicting glioma prognosis. The ssGSEA results showed that only IDH1 was negatively linked to the amount of immune cell infiltration in the LRG, while displaying a positive connection in the HRG (r value>0), indicating that the expression levels of IDH1 may have a distinct influence on the tumour immune microenvironment.ConclusionsThe present study confirmed the significant predictive value of IDH1 for glioma prognosis, which may guide immunotherapy for glioma treatment.

01 Dec 2024·European Journal of Pharmacology

Are we better together? Addressing a combined treatment of pitavastatin and temozolomide for brain cancer

Article

Author: Vitorino, Rui ; Basso, João ; Fortuna, Ana ; Vitorino, Carla ; Ghavami, Saeid ; Matos, Ana Miguel

Pitavastatin is commonly prescribed to treat hypercholesterolemia through the regulation of cholesterol biosynthesis. Interestingly, it has also demonstrated a great potential for treating brain tumors, although the detailed cytotoxic mechanism, particularly in glioblastoma, remains incompletely understood. This work explores the activity of pitavastatin in 2D and 3D glioblastoma models, in an attempt to provide a more representative and robust overview of its anticancer potential in glioblastoma. The results show that not only is pitavastatin 10-1000 times-fold more effective in reducing tumoral metabolic activity than temozolomide, but also demonstrate a synergistic activity with this alkylating drug. In addition, low micromolar concentrations of this statin strongly impair the growth and the invasion ability of multicellular tumor spheroids. The obtained qRT-PCR and proteomics data highlight the modulation of cell death via apoptosis (BAX/BCL2, CASP9) and autophagy (BECN1, BNIP3, BNIP3L and LC3B), as well as an epithelial to mesenchymal transition blockage (HTRA1, SERPINE1, WNT5A, ALDH3B1 and EPHA2) and remodeling of the extracellular matrix (VCAN, SERPINE1 and TGFBI). Overall, these results lay the foundation for further investigations on the potential combinatory clinical treatment with temozolomide.

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ALDH3B1

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