Ask about this productRelated genes to: PRR11 Blocking Peptide
- Gene:
- PRR11 NIH gene
- Name:
- proline rich 11
- Previous symbol:
- -
- Synonyms:
- FLJ11029
- Chromosome:
- 17q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-12-13
- Date modifiied:
- 2016-04-01
Related products to: PRR11 Blocking Peptide
Related articles to: PRR11 Blocking Peptide
- Long noncoding RNAs (lncRNAs) play critical roles in regulating stemness signature genes (SSGs) and tumor immunity, thereby shaping the tumor microenvironment and antitumor immune responses. Increasing evidence suggests that cancer stem cell traits are closely associated with immune evasion and therapeutic resistance, underscoring the need to systematically characterize the pan-cancer interplay among SSGs, lncRNAs, and tumor immunity. Here, we developed an integrative analytical framework that combines network-based modeling with Bayesian network inference to identify core regulatory triplets (STEM-LncCRTs), each consisting of an lncRNA, an SSG, and an immune gene. We demonstrate that specific stemness-related lncRNAs can distinguish cancer subtypes, and that common stemness-related lncRNAs correlate significantly with immune cell infiltration. Notably, the ATAD5/PRR11-AS1/SKP2 triplet exhibits favorable prognostic potential across multiple cancers and consistently outperforms individual gene markers in predicting 1-, 3-, and 5-year overall survival. Furthermore, using four machine learning algorithms across three independent immunotherapy cohorts, we validate the predictive value of STEM-LncCRTs for immune checkpoint inhibitor response. Importantly, integrating STEM-LncCRTs with tumor mutation burden further improves predictive accuracy. Collectively, this study provides a systems-level view of stemness-related lncRNA regulation in tumor immunity and offers practical biomarkers for predicting immunotherapy efficacy. - Source: PubMed
Qian ZhipengYin JiaqiZhang ChunlongWang GuohuaWang ChunyuLi YangZhao Yuming - Colorectal cancer (CRC) and atherosclerosis (AS) share pathological phenotypes and clinical links, but their shared pathogenic mechanisms are unclear. This study aimed to identify shared genetic drivers, construct a CRC risk model using AS-related genes, and validate expression via multi-omics. - Source: PubMed
Publication date: 2026/01/12
Li YuqingWei JinhongXu YuanyuanWu ZhenyuHe SaiqiZhu YuhangNi WenZhang DiXu HuiyaZhang ChuanjieZhou AijunShen TongLi Jianming - Retinoblastoma (RB) is the most common pediatric intraocular malignancy and seriously threatens vision and survival if not treated early. However, effective targeted therapies remain unavailable owing to the lack of well-defined molecular targets beyond RB1 gene mutations. There is a critical need to identify novel therapeutic targets. Through transcriptomic analysis of four RB-related datasets (GSE125903, GSE110811, GSE97508, and GSE24673) from the Gene Expression Omnibus (GEO) database, we identified proline-rich 11 (PRR11) as a significantly overexpressed gene in RB. Single-cell transcriptomic analysis revealed that PRR11 exhibits heterogeneous expression in different RB cell types, at particularly high levels in tumor-related populations such as cone precursor-like cells and MKI67 photoreceptorness-decreased cells. Functional studies demonstrated that PRR11 promotes RB cell proliferation and tumor growth both in vitro and in vivo. Coimmunoprecipitation mass spectrometry (co-IP/MS) revealed that OTUB1, a deubiquitinase, interacts with and stabilizes PRR11, sustaining its high expression in RB cells. The proteomic analysis further revealed that Dickkopf WNT signaling pathway inhibitor 3 (DKK3) is a downstream adaptor downregulated by PRR11. Suppression of DKK3 by PRR11 leads to aberrant activation of the Wnt/β-catenin signaling pathway, thereby upregulating cyclin D1 and promoting S/G2M cell cycle progression. These findings establish PRR11 as an oncogenic driver in RB and highlight the OTUB1-PRR11-DKK3 axis as a regulatory mechanism of Wnt/β-catenin signaling in RB tumorigenesis. Targeting PRR11 and its downstream pathways provides a potential and novel therapeutic strategy for RB treatment. - Source: PubMed
Publication date: 2026/01/14
He YuJu XuemingLi HuanLi MingzeZhang DanXiao JialingWu YixiaoZhang PuYang ZhenglinGong Bo - The long-term immunological effects of prior Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection in people living with Human Immunodeficiency Virus (HIV) remain poorly understood. This study aimed to characterize plasma proteomic alterations associated with previous SARS-CoV-2 infection in HIV-infected individuals and to identify potential biomarkers and affected pathways. High-throughput liquid chromatography–tandem mass spectrometry (LC–MS/MS) was performed on plasma obtained from three groups: HIV-infected individuals with documented prior SARS-CoV-2 infection, HIV-monoinfected individuals, and healthy controls. A total of 13,675 proteins were identified. Hierarchical clustering and sparse partial least squares discriminant analysis revealed distinct proteomic profiles in the prior-SARS-CoV-2 group. Ten proteins with the highest discriminatory power—PRR11, TEX14, METTL9, NMD3, PXT1, CRISP2, MELK, SPF27, GCP6, and GTPBP8—were associated with cell cycle regulation, RNA processing, apoptosis, mitochondrial function, and cytoskeletal organization. Subcellular localization indicated predominant nuclear and cytoplasmic involvement, suggesting alterations in transcriptional regulation and intracellular structural dynamics. These signatures imply that preceding SARS-CoV-2 exposure may compound HIV-associated immune dysregulation and disrupt cellular homeostasis. The findings offer novel molecular insights into the persistent biological impact of SARS-CoV-2 in the context of HIV and identify candidate proteomic biomarkers with potential utility for risk stratification and targeted intervention in immunocompromised populations. - Source: PubMed
Publication date: 2025/12/09
Chanthara ChayaninKhattiya JanyaRoytrakul SittirukAkekawatchai ChareepornPhaonakrop NarumonNiyomdecha Nattamon - Gene pairing is a highly conserved and special mode of eukaryotic gene organization, and critically implicated in development and diseases including cancer. We previously found that PRR11 and SKA2 constitute a classic head-to-head gene pair. Here, we further demonstrate that PRR11, SKA2, and its intronic miR301a and miR454 constitute a more exquisite bidirectional transcription unit that are overexpressed in various types of cancers. Functional studies using lung cancer as a model system reveal that co-overexpression of PRR11, SKA2, miR301a and miR454 together remarkably accelerates cell growth, cell cycle progression and cell motility in lung cancer cells, and promotes tumor growth in mouse models in vivo, whereas CRISPRi-mediated repression of the entire transcription unit inhibits these malignant phenotypes. Mechanistically, the four component genes do not display any additive or synergistic effect, but rather compensate for each other for robustly sustained activation of PI3K-AKT pathway, with PRR11 interacting with GRB2, and SKA2 with EGFR. Notably, miR301a and miR454 exert their oncogenic functions at least partially via repressing PTEN translation. Moreover, the transcription unit presents as a prominent prognostic meta-marker for lung cancer. Collectively, these findings demonstrate the essential and coordinated roles of PRR11-SKA2-miR301a/454 bidirectional transcription unit in lung cancer progression, highlighting its potential diagnostic and therapeutic values in cancers. - Source: PubMed
Publication date: 2025/11/27
Liu TaoZuo XiaofengSun ShijieDu KailongTao ChuntaoXia XingYu LinliZhang ChunxueYang ZhengmeiWang YitaoYe JunhongBu Youquan