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Last update 08 May 2025

ALDH3A1

Last update 08 May 2025

Basic Info

Synonyms

Aldehyde dehydrogenase 3, aldehyde dehydrogenase 3 family member A1, Aldehyde dehydrogenase family 3 member A1

+ [4]

Introduction

ALDHs play a major role in the detoxification of alcohol-derived acetaldehyde (Probable). They are involved in the metabolism of corticosteroids, biogenic amines, neurotransmitters, and lipid peroxidation (Probable). Oxidizes medium and long chain aldehydes into non-toxic fatty acids (PubMed:1737758). Preferentially oxidizes aromatic aldehyde substrates (PubMed:1737758). Comprises about 50 percent of corneal epithelial soluble proteins (By similarity). May play a role in preventing corneal damage caused by ultraviolet light (By similarity).

Drugs associated with ALDH3A1

CB29

Target

ALDH3A1

Mechanism

ALDH3A1 inhibitors

Active Org.-

Originator Org.

The Indiana University School of Medicine

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ALDH3A1

100 Translational Medicine associated with ALDH3A1

0 Patents (Medical) associated with ALDH3A1

530

Literatures (Medical) associated with ALDH3A1

01 Jul 2025·The Ocular Surface

Pard3 promotes corneal epithelial stratification and homeostasis by regulating apical-basal polarity, cytoskeletal organization and tight junction-mediated barrier function

Article

Author: Kaur, Satinder ; Vohra, Mehak ; Sohnen, Peri ; Swamynathan, Shivalingappa K ; Hirose, Tomonori ; Swamynathan, Sudha ; Kumar, Simran ; Kozmik, Zbynek

PURPOSETo document the expression of apical-basal polarity (ABP) determinants in the mouse corneal epithelium (CE) and elucidate the functions of Pard3 in establishment and maintenance of ABP, stratification, homeostasis, and barrier function in the CE.METHODSPard3^Δ/ΔC mice (Pard3^LoxP/LoxP; Aldh3A1-Cre/+) with cornea-specific Pard3 ablation were generated by breeding Aldh3A1-Cre/+ with Pard3^LoxP/LoxP mice. The control (Aldh3A1-Cre/+ or Pard3^LoxP/LoxP alone) and Pard3^Δ/ΔC corneal histology, ocular surface properties, barrier function, and actin cytoskeleton were assessed by Haematoxylin and Eosin staining of paraformaldehyde-fixed, paraffin-embedded tissues, scanning electron microscopy, fluorescein staining, and phalloidin staining, respectively. The expression of specific markers of interest was evaluated by qRT-PCR, immunoblots and immunofluorescent staining.RESULTSDynamic changes were observed in the expression and localization of ABP determinants as the CE stratified and matured between post-natal day 5 (PN5) and PN52. Adult Pard3^Δ/ΔC CE contained fewer cell layers with rounded basal cells, and loosely adherent superficial cells lacking microplicae. Adult Pard3^Δ/ΔC CE also displayed impaired barrier function with decreased expression of tight junction, adherens junction, and desmosome components, disrupted actin cytoskeletal organization, increased proliferation, and upregulation of transcription factors that drive epithelial-mesenchymal transition (EMT).CONCLUSIONSDisruption of ABP in Pard3^Δ/ΔC CE, altered expression of cell junction complex components and disorganized actin cytoskeleton, increased cell proliferation, and upregulated EMT transcription factors suggest that the ABP-determinant Pard3 promotes CE features while suppressing mesenchymal cell fate. Collectively, these results elucidate that Pard3-mediated ABP is essential for CE stratification, homeostasis and barrier function.

28 Apr 2025·Oncogene

Targeting aldehyde dehydrogenase ALDH3A1 increases ferroptosis vulnerability in squamous cancer

Article

Author: Wang, Boshi ; Dong, Jinxiu ; Wu, Jiaqi ; Lu, Yan ; Fang, Jinman ; Han, Wei ; Ge, Dianlong ; Koeffler, H Phillip ; Jiang, Yan-Yi ; Kong, Shuai ; Ma, Junboya ; Zhou, Jianian ; Zhang, Yuan-Wei ; Pan, Huaguang ; Wei, Dan-Dan ; Wang, Fei ; Jiang, Yuan ; Zhou, Dan ; Chen, Jian ; Peng, Jingyi ; Yin, Chuntong ; Shen, Chengyin

Ferroptosis is a unique modality of regulated cell death induced by excessive lipid peroxidation, playing a crucial role in tumor suppression and providing potential therapeutic strategy for cancer treatment. Here, we find that aldehyde dehydrogenase-ALDH3A1 tightly links to ferroptosis in squamous cell carcinomas (SCCs). Functional assays demonstrate the enzymatic activity-dependent regulation of ALDH3A1 in protecting SCC cells against ferroptosis through catalyzing aldehydes and mitigating lipid peroxidation. Furthermore, a specific covalent inhibitor of ALDH3A1-EN40 significantly enhances the ferroptosis sensitivity induced by the ferroptosis inducer. The combination of EN40 and a ferroptosis inducer exhibits a synergistic effect, effectively inhibiting the proliferation of SCC cells/organoids and suppressing tumor growth both in vitro and in vivo. On mechanism, high expression of ALDH3A1 is transcriptionally governed by TP63, which binds to super-enhancer of ALDH3A1. Collectively, our findings reveal a yet-unrecognized function of ALDH3A1 exploited by SCC cells to evade ferroptosis, and targeting ALDH3A1 may enhance the effect of ferroptosis-induced therapy in SCCs.

03 Apr 2025·Carcinogenesis

Establishing a new-onset diabetes-related metabolism signature for predicting the prognosis and immune landscape in pancreatic cancer

Article

Author: Cheng, Bin ; Wang, Ronghua ; Chen, Wei ; Peng, Wang ; Li, Yanling ; Chen, Shiru ; Wang, Jinlin ; Cao, Mengdie ; Liu, Luyao ; Bai, Shuya ; Cui, Haochen ; Zhao, Yuchong ; Liang, Jingwen ; Yang, Yilei

AbstractNew-onset diabetes (NOD) is a common condition among patients with pancreatic adenocarcinoma (PAAD) and is related to poor clinical outcomes. The potential impact of NOD on PAAD progression and the tumor microenvironment remains unclear. Here, we revealed that NOD in PAAD was associated with metabolic disorders. Utilizing three machine-learning algorithms, an NOD-related metabolism signature (NRMS) was established. Validated in three independent cohorts, patients with a high NRMS score exhibited a worse prognosis. Moreover, an elevated NRMS score was associated with an immunosuppressive microenvironment and diminished response to immunotherapy. Further experiments demonstrated that ALDH3A1, a key feature in NRMS, was significantly upregulated in tissues from PAAD patients with NOD and played a crucial role in tumor progression and immune suppression. Our findings highlight the potential of NRMS as a prognostic biomarker and an indicator of immunotherapy response for patients with PAAD.

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ALDH3A1

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