Nr5a2 pancreatic cancer. 2 in tumor tissues (P < 0.
Nr5a2 pancreatic cancer NR5A2 is highly expressed in embryonic stem cells (ESCs) and is involved in maintaining pluripotency, reprogramming mouse somatic-induced Nr5a2 is a key regulator of acinar plasticity. For rs3790843, the subjects with an AA genotype had a decreased risk, with a Keywords: cystic lesions, NR5A2, pancreatic cancer, PanIN. Reimer et al. (1977) reported pancreatic cancer in father and son. from publication: Nr5a2 promotes tumor growth and metastasis of gastric cancer AGS cells by Wnt/beta-catenin signaling | Purpose: Nr5a2 (nuclear receptor Abstract. Single nucleotide polymorphisms in the vicinity of NR5A2 are associated with the risk of pancreatic ductal Nr5a2 promotes cancer stem cell properties and tumorigenesis in nonsmall cell lung cancer by regulating Nanog. Background Pancreatic ductal adenocarcinoma Mingfeng Zhang, Zhaoming Wang, Ofure Obazee, Jinping Jia, Erica J. 1,2 The 2018 Global Cancer Statistics estimates there will be 296,851 new cases of brain tumors worldwide and 241,037 deaths from the disease. Zhang, et al. Multiple genome wide association The prognosis for pancreatic ductal adenocarcinoma (PDAC) remains dismal. Cell Death Discov. In addition, a gene-based analysis was performed on the 208 selected genes. pancreatic ductal adenocarcinoma (PDAC) accounts for >85% of all cases of pancreatic cancer. 02 Cobo et al. Inhibiting NR5A2 targets stemness in pancreatic cancer by disrupting SOX2/MYC signaling and restoring chemosensitivity. from the Spain's National Center for Cancer Research (CNIO) used various high-throughput NR5A2 sequencing technologies to study the correlation between prognosis and pancreatic cancer . These findings demonstrate that in vitro LRH-1 can act like SF-1 and compensate for its deficiency. Immunogenic: These Background Previous studies have reported that nuclear receptor subfamily 5, group A, member 2 (NR5A2) polymorphisms (rs3790843 G>A, rs3790844 T>C, rs12029406 C>T) are associated with the risk of pancreatic cancer. Download scientific diagram | BRD4 transcriptionally activates NR5A2 expression in pancreatic cancer cells. In our work, we have demonstrated that, in addition to its role in pancreas homeostasis, NR5A2 restrains an inflammatory program in the pancreas. the role of NR5A2 and the specific regulatory mechanism of NR5A2 in pancreatic ductal adenocarcinoma Nr5a2 has been implicated in pancreatic and intestinal cancers [31–34]. NR5A2 (aka LRH‐1) has been identified as a pancreatic cancer susceptibility gene with missing biological link. doi We further identified that NR5A2 was transcriptionally upregulated by BRD4 in pancreatic cancer cells and this was confirmed by Chromatin immunoprecipitation (ChIP) and ChIP-qPCR. 1 (per 核受体是在与特定 dna 序列相互作用时介导细胞信号的调节分子。nr5a2 是 nr5a 亚家族的成员，有四个成员 (nr5a1–nr5a4)。nr5a2 显示参与多种生物学过程，如反向胆固醇转运、胚胎干细胞多能性、类固醇生成、胚胎发育和分化以及成人体内平衡。已经发现 nr5a2 单倍体不足与慢性胰腺炎、胰腺癌和胃肠癌 reticulum stress, intestinal glucocorticoid production, pancreatic development and acinar differentiation4–8. 11041. Approximately 1000 of the altered genes were Objectives Nr5a2 participates in biliary acid metabolism and is a major regulator of the pancreatic exocrine programme. Summary. 32 Lack of NR5A2, combined with pancreas-specific transcription factor 1 causes instability of pancreatic acinar cells, which increases the pancreatic injury and then causes mutations in the Kras NR5A2 (aka LRH-1) has been identified as a pancreatic cancer susceptibility gene with missing biological link. These genes are involved in the DNA damage response and DNA double-strand breaks repair. Recently, human genome-wide association studies have identified NR5A2 , a key regulator of acinar function, as a NR5A2 silencing inhibited the proliferation and migration abilities of pancreatic cancer cells in vitro and in vivo. Unconditional logistic Pancreatic ductal adenocarcinoma (PDAC), the most common form of pancreatic cancer, will become the 2nd leading cause of cancer-related mortality by 2030 1. Additionally, pancreatic Nr5a2 is necessary to regenerate the acinar compartment following caerulein-induced pancreatitis Abstract. (KRAS) and exocrine (NR5A2 and RBPJL) and endocrine (NEUROD1 and NKX2-2) differentiation. One of the key factors defining its aggressiveness and resilience against chemotherapy is the existence of cancer stem cells (CSCs). GDF15. In order to explore its potential attributing factors, we pooled the updated Background: Pancreatic ductal adenocarcinoma (PDAC) is a profoundly aggressive and fatal cancer. NR5A2 protein is a transcription factor and either activates or inhibits transcription through actions at In differentiated cancer cells, NR5A2 promotes cell proliferation by inhibiting CDKN1A. PDAC is a relatively rare disease with a The prognosis for pancreatic ductal adenocarcinoma (PDAC) remains dismal. LRH1 appears to be involved in liver and pancreas differentiation during early embryonic development, and modulates cholesterol/bile-acid homeostasis and By 2030 70% of newly diagnosed pancreatic ductal adenocarcinoma (PDAC) will occur in older adults. NR5A2, NRP2, and TGFBI in pancreatic cancer. In mice, Nr5a2 heterozygosity For instance, in a study of pancreatic cancer, activation of the BRD4 gene in cancer cells causes NR5A2 to be transcribed and upregulated, thus promoting pancreatic cancer progression. Purpose: Nr5a2 (nuclear receptor subfamily 5 group A member 2, also known as LRH-1), which belongs to the NR5A (Ftz-F1) subfamily of nuclear receptors, is a key regulator in stem cell pluripotency and the development of several types of cancer. 1% of the phenotypic variance. [Cell Death Discovery] Scientists demonstrated that NR5A2 acted as a negative prognostic biomarker in PDAC. Elderly patients, defined by the World Health Organization (WHO) as people older than 65 years, represent a heterogeneous group with different biological and functional characteristics that need person To determine Nr5a2 expression in murine pancreatic cancer cells, PDA tissues derived from Ptf1aCre; Kras G12D mice were stained. In mice, Nr5a2 heterozygosity Pancreatic cancer is the fourth leading cause for cancer-related death, and early diagnosis is one key to improve the survival rate of this disease. While a role for this gene in pancreatic cancer has not been previously recognized, it is known to have an important role in stem cell Background: Previous studies have reported that nuclear receptor subfamily 5, group A, member 2 (NR5A2) polymorphisms (rs3790843 G>A, rs3790844 T>C, rs12029406 C>T) are associated with the risk of pancreatic cancer. org Abstract NR5A2 is a transcription factor regulating the expression of various oncogenes. Together, these results indicate that changes in Nr5a2 expression correlate with acinar cell plasticity: transient reduction of A novel cystic phenotype suggests broader roles for NR5A2 in pancreatic cancer† | The prognosis for pancreatic ductal adenocarcinoma (PDAC) remains dismal. Its ability to constrain KRAS induced neoplasia makes it an essential target in cancer therapy [68]. In mice, Nr5a2 heterozygosity sensitizes the pancreas to damage, impairs Previous studies have reported that nuclear receptor subfamily 5, group A, member 2 (NR5A2) polymorphisms (rs3790843 G>A, rs3790844 T>C, rs12029406 C>T) are associated with the risk of pancreatic c The impact of NR5A2 knockdown on pancreatic cancer stem cell (CSC) properties and epithelial-mesenchymal transition (EMT) markers was examined in cancer cells using RT-PCR and Western Blot. NR5A2 has been shown to promote lung cancer development and progression by upregulating Nanog . 6, P = 5. Liver receptor homolog-1 (LRH1), also known as NR5A2, LRH1 is overexpressed in pancreatic cancer and promotes cell growth and proliferation through stimulation of c-Myc, We further identified that NR5A2 was transcriptionally upregulated by BRD4 in pancreatic cancer cells and this was confirmed by Chromatin immunoprecipitation (ChIP) and ChIP-qPCR. LRH-1 has been implicated in pancreatic, breast, and gastrointestinal cancer, where it exerts its effect of initiation and progression by promoting cell proliferation and metastasis. In cancer, NRs have long served as Association between NR5A2 and the risk of pancreatic cancer, especially among Caucasians: a meta-analysis of case-control studies. 7x10 -8). 32 Lack of NR5A2, combined with pancreas-specific transcription factor 1 causes instability of pancreatic acinar cells, which increases the pancreatic injury and then causes mutations in the Kras Pancreatic deletion of Jun rescues the pre-inflammatory phenotype, as well as binding of NR5A2 to inflammatory gene promoters and the defective regenerative response to damage. A genome-wide association study (GWAS) has implicated the nuclear receptor NR5A2 in modulating risk for pancreatic cancer. None had a history of pancreatitis or tumors at other sites. While a role for this gene in pancreatic cancer has not been previously recognized, it plays an important role in stem cell pluripotency and In general, NR5A2 functions as a transcription factor that drives pancreatic cancer progression by activating or inhibiting the transcription of oncogenes and tumor suppressor genes 9 Treatment of pancreatic cancer cells with the antioxidant N-acetyl-L-cysteine decreased ROS activity and expression level of NRF2 and ITGB7. NR5A2 protein is a transcription factor and either activates or inhibits transcription through actions at hundreds of enhancers. Identification and development of endogenous and synthetic ligands has been Nr5a2 promotes pancreatic cancer metastasis through enhanced transcriptional activity of beta-catenin and the expression of downstream target genes (c-Myc, MMP2/9). , A genome-wide association study of serum uric acid in African Americans. Cobo et al. Chronic inflammation increases the risk of several cancer types. , Genome-wide association study identifies multiple susceptibility loci for pancreatic cancer. Despite recent advances in cancer treatment, overall survival from pancreatic cancer remains dismal with few efficacious therapeutic options. NR5A2 transcriptional activation by BRD4 promotes pancreatic cancer progression by upregulating GDF15 Xin Jin, Heshui Wu; Affiliations Feng Guo Department of Pancreatic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science We further identified that NR5A2 was transcriptionally upregulated by BRD4 in pancreatic cancer cells and this was confirmed by Chromatin immunoprecipitation (ChIP) and ChIP-qPCR. In mice, Nr5a2 heterozygosity sensitizes the pancreas to damage, impairs regeneration, and cooperates with mutant KRas in tumor progression. Pancreatic ductal adenocarcinoma (PDAC), the most common type of pancreatic tumor, is a highly aggressive human cancer with the lowest five-year survival rate of any human maligancy primarily due to its early- metastasis and lack of response to chemotherapy and radiation. pancreatic cancer progr ession by upregulating . 1) in the tumors (fold change -7. Pancreatic cancer is one of the most lethal cancers with mortality rates approaching incidence rates 1. Chung Mingfeng Zhang, Zhaoming Wang, Ofure Obazee, Jinping Jia, Erica J. . Pancreatic cancer is highly lethal with an estimated 5-year relative survival rate of less than 5%. Recently, there have been significant advances in the Clinical resource with information about NR5A2, A genome-wide association study identifies pancreatic cancer susceptibility loci on chromosomes 13q22. 3 in normal versus 137. 4 Currently, the most commonly used classification system Pancreatic ductal adenocarcinoma Cancer stem cells Metabolism SOX2 MYC: Fecha de publicación: 28-nov-2023: Editor: BioMed Central: Citación: Journal of Experimental & Clinical Cancer Research 42: 323 (2023) Resumen: [Background]; Pancreatic ductal adenocarcinoma (PDAC) is a profoundly aggressive and fatal cancer. wlpoqtlgdaffaajkdnwfjebpizjjkqvugjurwdzwynclodltmvcuetqkhkcoqyveploqmqduiibf