PYCR1 Human Protein
- Known as:
- PYCR1 Human Protein
- Catalog number:
- GWB-BSP301
- Product Quantity:
- 10ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- PYCR1 Human Protein
Ask about this productRelated genes to: PYCR1 Human Protein
- Gene:
- PYCR1 NIH gene
- Name:
- pyrroline-5-carboxylate reductase 1
- Previous symbol:
- -
- Synonyms:
- P5C
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-24
- Date modifiied:
- 2015-09-07
Related products to: PYCR1 Human Protein
Related articles to: PYCR1 Human Protein
- Osteosarcoma treatment outcomes are compromised by increased drug resistance, distant metastasis, and tumor recurrence. While Pyrrolidine-5-carboxylic acid reductase 1(PYCR1) knockdown has been shown to inhibit tumor proliferation and migration in certain cancers. Its effects in osteosarcoma and regulatory mechanisms within osteosarcoma cells have not been explored. This study investigated the role of PYCR1 in osteosarcoma proliferation and its potential molecular mechanisms. The expression of PYCR1 was assessed in osteosarcoma tissues by immunohistochemistry and its correlation with clinical outcomes was determined. Subsequently, lentivirus-mediated knockdown and over expression of PYCR1 was achieved in osteosarcoma cells to evaluate its impact on proliferation, colony formation, and migration ability. The PI3K/Akt signaling pathway and its downstream effector COL1A1 were investigated using a combination of biomarker analysis, transcriptome sequencing, and co-immunoprecipitation assays. Subsequent silencing of COL1A1 induced phenotypic changes and confirmed tumorigenicity in vivo. The ferroptosis agonist Erastin and its specific antagonist Ferrostatin-1 (Fer-1) were combined with PYCR1 knockdown to explore their correlation with ferroptosis. By applying the pathway inhibitor LY294002, it was confirmed that the PI3K/Akt pathway is crucial for osteosarcoma proliferation. This study confirms that PYCR1 drives osteosarcoma cell proliferation and migration through three key mechanisms: regulating downstream genes, inhibiting ferroptosis, and activating the PI3K/Akt signaling pathway. - Source: PubMed
Publication date: 2026/06/19
Hu JianhuaHuang YiyuanChen HaomingXie ZehaoYan HanLi HaomiaoLi Runguang - Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Glutamine plays a critical role in the progression of LUAD. However, the function of pyrroline-5-carboxylate reductase 1 (PYCR1) and its regulatory role in glutamine metabolism remain unclear. Transcriptomic and clinical data for LUAD were obtained from The Cancer Genome Atlas (TCGA) and validated using Gene Expression Omnibus (GEO) datasets (GSE19188, GSE13213). Glutamine metabolism-related genes were analyzed for differential expression and prognostic significance. Functional enrichment was performed via gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) analyses. Single-cell RNA-seq data (GSE117570) were processed using Seurat, and cell-cell communication was inferred with CellChat. In vitro, lentiviral overexpression, Western blotting, EdU, CCK-8, and glutamine uptake assays were conducted. An orthotopic xenograft model was established in nude mice to assess tumor growth in vivo. Six glutamine-metabolism-related genes were found significantly overexpressed in LUAD tissues and associated with poor overall survival. Single-cell sequencing revealed predominant PYCR1 expression in malignant cells. Functional assays demonstrated that PYCR1 overexpression enhanced glutamine uptake, proliferation, and inhibited apoptosis in LUAD cells, effects mediated via suppression of the P53 pathway. PYCR1 promoted tumor growth in a xenograft model and was found to transcriptionally upregulate 5-oxoprolinase (OPLAH), which augmented its oncogenic effects. Our findings identify the PYCR1/OPLAH axis as a key driver of LUAD progression via p53 signaling, revealing a promising therapeutic target. - Source: PubMed
Publication date: 2026/06/15
Chen WeiWang KaiWang RenyuDeng XufengLiu XiaobingDai PengLiu Quanxing - Chronic Rhinosinusitis with Nasal polyps (CRSwNP) are characterized by chronic inflammation and occur in 1-4% of the population worldwide. Patients often have comorbid asthma, and standard treatments among them are hindered by significant recurrence and lack of durability. Currently, knowledge of the molecular circuitry and immune microenvironmental interplay that utilizes metabolic reprogramming within CRSwNP is incomplete. - Source: PubMed
Publication date: 2026/05/25
Zhao LiMeng Xiang JiangLiang XuYuan Guang MeiShi Li - Recent advances in next-generation sequencing have revealed that long non-coding RNAs (lncRNAs) can encode functional micropeptides through small open reading frames (sORFs), altering the perception of the non-coding genome. In this study, we identified a 48-amino acid micropeptide named PAMP (proline-associated micropeptide), encoded by the lncRNA PSMA3-AS1, as a novel tumor suppressor in lung adenocarcinoma (LUAD). PAMP is significantly downregulated in LUAD tissues and positively correlates with favorable prognosis. Functional assays demonstrated that PAMP inhibits LUAD cell proliferation in vitro and suppresses tumor growth in vivo. Mechanistically, PAMP directly interacts with PYCR1, a key enzyme in proline biosynthesis. Structural modeling and mutagenesis revealed that the PAMP-F16 and PYCR1-N123 residues are critical for the interaction, resulting in the inhibition of PYCR1 enzymatic activity and decreased proline accumulation. Notably, synthetic PAMP administration recapitulates these anti-tumor effects, effectively reducing intracellular proline levels and impairing tumor progression in cellular and animal models. Together, our findings uncover a previously uncharacterized lncRNA-encoded micropeptide that orchestrates proline metabolic reprogramming to restrain LUAD development, offering new opportunities for metabolic intervention in precision oncology. - Source: PubMed
Publication date: 2026/06/09
Ma YunYi JianiZheng ChengcaiYang JuzeLi JiaYu MengqianQian XinyiRen JiayiWu XiaofanLu YanLiu Pengyuan - Osteosarcoma (OS) is a malignant tumor originating in the bones, predominantly affecting children and adolescents, characterized by high aggressiveness and poor prognosis. Identifying new prognostic biomarkers is crucial for improving the diagnosis and treatment of OS. - Source: PubMed
Publication date: 2026/05/27
Xu GuoyongLiu ChongXue JiangChen JiaruiZou ZhuanMo SenZhou ZhongxianZhan Xinli