Ask about this productRelated genes to: ALDH1A1 antibody
- Gene:
- ALDH1A1 NIH gene
- Name:
- aldehyde dehydrogenase 1 family member A1
- Previous symbol:
- PUMB1, ALDH1
- Synonyms:
- RALDH1
- Chromosome:
- 9q21.13
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2015-11-18
Related products to: ALDH1A1 antibody
Related articles to: ALDH1A1 antibody
- Glucocorticoids are frequently used in the management of brain tumours to control tumour-associated cerebral oedema and symptoms related to mass effect. Because glucocorticoid exposure may increase the risk of upper gastrointestinal complications in selected patients, proton pump inhibitors (PPIs) are often prescribed prophylactically. Emerging evidence suggests that exposure to PPIs with potent aldehyde dehydrogenase 1A1-activating properties (PA-PPIs) such as omeprazole may be associated with worse progression-free and overall survival in newly diagnosed glioblastoma (GBM). Routine reflexive PPI prophylaxis may therefore not be justified. When acid suppression is clinically indicated, the choice of agent should be individualized, with consideration of H₂ receptor antagonists or antacids where appropriate. These findings support an acid-suppressive stewardship approach in the management of patients with GBM. - Source: PubMed
Sabahat Noor UsNisar FareehaShamim Muhammad Shahzad - The activation of the Wnt/β-catenin pathway with chemoresistance in colorectal cancer has been hypothesized. However, the use of specific inhibitors for targeting this pathway has not been well explored. In the present study, we analyze the activation of this pathway and its role in the stemness phenotype acquisition to regulate chemoresistance using our long-term 5-fluorouracil (5-FU) - resistant model of colorectal cancer cells, known to present epithelial-mesenchymal transition and enhanced migration and invasion. - Source: PubMed
Publication date: 2026/09/04
Ramos Diego Alfonso Arreguide Pina Daniela Filomena TavaresSousa-Squiavinato Annie Cristhine Moraesde Araújo Wallace MartinsRocha Murilo RamosMorgado-Diaz Jose Andres - Minichromosome maintenance protein 2 (MCM2) is a key regulator of DNA replication and has been implicated in tumor progression. While previous studies have demonstrated its role in lung cancer stem cells (CSCs), its role in breast cancer remains unclear. This study aimed to investigate whether MCM2 regulates CSCs and epithelial-mesenchymal transition (EMT) in breast cancer. - Source: PubMed
Publication date: 2026/08/31
Kim Rae-Kwon - Lung cancer remains the leading cause of cancer-related mortality worldwide, largely due to therapeutic resistance and tumor recurrence. In non-small cell lung cancer (NSCLC), cancer stem cells (CSCs) have emerged as key contributors to tumor persistence and progression. However, accelerated CSC-targeted drug discovery is limited by the lack of scalable and quantitative screening systems capable of capturing stemness-associated phenotypes. Conventional two-dimensional (2D) assays often fail to reflect the architectural and molecular complexity of CSC-enriched tumor populations. Here, we report the establishment of a luciferase-based three-dimensional (3D) NSCLC spheroid platform integrating CSC-like enrichment with a high-throughput quantitative readout. The luminescent signal strongly correlated with spheroid burden and viable cell content. Compared with 2D monolayers, 3D NSCLC spheroids exhibited elevated expression of pluripotency-associated factors, including OCT4, NANOG, and SOX2, and CSC-associated markers, namely CD44, ALDH1A1, and ABCG2, supporting the enrichment of CSC-like subpopulations. As a proof-of-concept, screening of renieramycin T right-half derivatives identified DH_18 as a lead compound in the established 3D NSCLC spheroid model, exhibiting greater potency than DH_19, accompanied by increased apoptosis and reduced CSC-associated proteins in follow-up experimental validation. Integrated network pharmacology incorporating enrichment and protein-protein interaction analyses further mapped DH_18-NSCLC targets to lung CSC-associated networks and pathways related to stemness and aggressive tumor phenotypes, reinforcing the biological relevance of the 3D screening context. Collectively, these findings present a quantitative and scalable 3D NSCLC spheroid platform suitable for CSC-targeted drug screening and nominate DH_18 as a candidate compound with potential activity against stemness-linked molecular networks. - Source: PubMed
Publication date: 2026/09/01
Samart ParinyaChanthateyanonth SupasornRodboon NapachaiCharoenvitayavorakul NititYamada TatsukiYokoya MasashiChanvorachote PithiIssaragrisil SurapolLuanpitpong Sudjit - Colorectal cancer (CRC) remains a major cause of cancer-related mortality due to therapeutic resistance. Because colorectal cancer stem-like cells (CRCSCs) play a central role in tumor initiation and progression, therapeutic strategies addressing CSC-enriched populations are urgently needed. In this study, we investigated the anticancer effects of emodin, a natural anthraquinone, in CSC-enriched tumorsphere models. Emodin significantly suppressed the viability and self-renewal capacity of HCT116- and SW480-derived CSCs. It induced G0/G1 cell cycle arrest and markedly downregulated stemness-associated markers (CD44, CD133, ALDH1A1, SOX2, NANOG, and OCT4). Importantly, emodin-induced cell death was characterized by mitochondrial dysfunction, increased mitochondrial reactive oxygen species, loss of membrane potential, and nuclear translocation of apoptosis-inducing factor (AIF). This cytotoxicity was not rescued by the pan-caspase inhibitor Z-VAD-FMK, confirming caspase-independent apoptosis. Furthermore, network pharmacology and experimental validation identified GSK3β as a key target. Emodin reduced Wnt/β-catenin signaling by decreasing β-catenin stabilization and nuclear accumulation. Crucially, a rescue experiment utilizing LiCl confirmed that emodin's suppressive effects are mechanistically dependent on the GSK3β/Wnt/β-catenin axis. Collectively, emodin suppresses CRCSC characteristics by downregulating Wnt/β-catenin signaling and inducing AIF-associated caspase-independent apoptosis, highlighting its therapeutic potential against CRC. - Source: PubMed
Publication date: 2026/08/31
Ahmadi MahdiehKim Hong LaeJung Hye Jin