Ask about this productRelated genes to: PTTG1 antibody
- Gene:
- PTTG1 NIH gene
- Name:
- PTTG1 regulator of sister chromatid separation, securin
- Previous symbol:
- TUTR1
- Synonyms:
- PTTG, HPTTG, EAP1, securin
- Chromosome:
- 5q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-23
- Date modifiied:
- 2019-03-07
Related products to: PTTG1 antibody
Related articles to: PTTG1 antibody
- Intrahepatic cholangiocarcinoma (iCCA) is characterized by heterogeneity and poor survival. It remains unclear how telomere maintenance programs influence the prognosis and immune microenvironment in iCCA, and clinically applicable, telomere‑anchored transcriptomic tools are currently lacking. - Source: PubMed
Publication date: 2026/05/30
Wang LihuaZhao WenjingCui ZhongfengLi Guangming - Liver hepatocellular carcinoma (LIHC) is a leading cause of cancer-related mortality worldwide, with limited therapeutic options and poor prognosis, particularly at advanced stages. Identifying key molecular drivers involved in LIHC progression is critical for improving diagnosis and treatment strategies. In this study, we performed an integrated bioinformatics analysis using four independent GEO datasets (GSE19665, GSE54236, GSE55092, and GSE84598) to identify differentially expressed genes (DEGs) associated with LIHC. A total of 147 common DEGs were identified, and protein-protein interaction network analysis revealed CCNA2, MAD2L1, AURKA, and PTTG1 as central hub genes. Functional enrichment analyses indicated that these genes are primarily involved in cell cycle regulation, mitosis, and chromosomal stability. Expression analyses using TCGA-based databases demonstrated significant upregulation of these hub genes at both mRNA and protein levels in LIHC tissues compared with normal liver tissues. Elevated expression was associated with advanced tumor stage, poor overall survival, immune cell infiltration, and altered drug sensitivity, highlighting their clinical relevance. Promoter methylation analysis suggested that epigenetic regulation may contribute to gene dysregulation, while genetic alterations were infrequent. Experimental validation using RT-qPCR confirmed overexpression of hub genes in LIHC cell lines. Furthermore, siRNA-mediated knockdown of these genes significantly suppressed proliferation, colony formation, and migration in HepG2 and Huh7 cells. Collectively, these findings identify CCNA2, MAD2L1, AURKA, and PTTG1 as key oncogenic drivers and potential biomarkers and therapeutic targets in LIHC. - Source: PubMed
Publication date: 2026/05/28
Jinli WangShiping Hu - Ovarian endometriosis (OE) is a chronic, inflammatory gynecological disorder associated with sterility and an elevated risk of ovarian cancer. Despite its high prevalence, the complex molecular mechanisms governing OE pathogenesis remain poorly investigated. We conducted a comprehensive histopathological and molecular investigation of OE in a cohort of 188 Saudi women (88 patients with OE and 100 healthy controls) using histopathological, qRT-PCR, immunostaining, and Western blot techniques. Histopathological analysis confirmed significant stromal fibrosis and chronic inflammation in endometriotic lesions. Gene expression profiling revealed a pro-proliferative, anti-apoptotic signature, marked by the upregulation of and the downregulation of , , and . Interestingly, we identified a post-transcriptional regulatory paradox in the inflammatory response: while mRNA was significantly upregulated, its corresponding protein level was downregulated, suggesting a novel, tightly controlled mechanism to limit excessive local inflammation. Besides the increased autophagic activity and decreased Ubiquitin mRNA levels, epigenetic dysregulation was prominent, characterized by the upregulation of DNA methyltransferase DNMT3B and the downregulation of the histone variant H3.1. These findings elucidate novel molecular pathways underlying OE pathogenesis as evidenced by a post-transcriptional paradox in IL-6 expression, and uncover key dysregulations spanning cell proliferation, apoptosis, inflammation, autophagy, and epigenetic regulation. - Source: PubMed
Publication date: 2026/05/20
Nahdi SaberArafah MariaPetraglia FeliceJalouli MarouaAlamri AbdullahAlanazi MohammadRahman Md AtaurAlwasel SalehHarrath Abdel Halim - Lung adenocarcinoma (LUAD) remains a leading cause of cancer mortality, and the molecular drivers that promote its malignant progression are not fully characterized. This study aimed to define the oncogenic function of pituitary tumor transforming gene 1 () in LUAD and to elucidate its mechanistic relationship with distal-less homeobox 2 () and the WNT/β-catenin signaling pathway. - Source: PubMed
Publication date: 2026/04/27
Chen HuiliZhang XinyuLian XiaofuWang ZiqiangZhang FeiyueZhang JingMin ShengpingYang ShashaWang XiaojingLian Chaoqun - Pericyte loss is an early and critical event in the pathogenesis of diabetic retinopathy (DR), yet the molecular mechanisms underlying pericyte dysfunction remain incompletely understood. Using single-cell RNA sequencing, we generated a retinal cellular overview comprising 37,982 cells from diabetic and nondiabetic mice. We identified a previously unrecognized pericyte subpopulation defined by high expression of pituitary tumor-transforming gene 1 (), which was enriched in diabetic retina. Functional studies demonstrated that CRISPR-Cas9- or small interfering RNA-mediated silencing of restored pericyte stability and barrier-supporting function under high-glucose stress. In vivo, silencing via viral or pericyte-specific adeno-associated virus delivery improved retinal vascular integrity and reduced retinal vascular dysfunction in diabetic mice. Integrated transcriptomic and metabolomic profiling revealed that silencing reprogrammed metabolism, modulating glycolytic flux and attenuating oxidative stress. Furthermore, a therapeutic strategy using spherical nucleic acid-based si nanocarriers (sTDN-si) substantially ameliorated retinal vascular dysfunction in DR model. These findings suggest that PTTG1 is a critical regulator of pericyte metabolic homeostasis and microvascular function in DR, highlighting its translational potential as a therapeutic target for diabetic microvascular complications. - Source: PubMed
Publication date: 2026/05/15
Zhang LinyuRen LingZhang JingyueZhao YaXia MinLi XiaosaYao MudiMa FanfeiJiang ChangMu WanXia JiaoYao JinYan Biao