Ask about this productRelated genes to: PIWIL1 Blocking Peptide
- Gene:
- PIWIL1 NIH gene
- Name:
- piwi like RNA-mediated gene silencing 1
- Previous symbol:
- -
- Synonyms:
- PIWI, HIWI, CT80.1
- Chromosome:
- 12q24.33
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-11
- Date modifiied:
- 2016-04-19
Related products to: PIWIL1 Blocking Peptide
Related articles to: PIWIL1 Blocking Peptide
- Treatment with immune checkpoint inhibitors in colorectal cancer (CRC) has largely benefited patients with microsatellite instability-high (MSI-H) and not the larger proportion of patient with microsatellite-stable (MSS) tumors. This clinical dichotomy has fueled the view that high mutational burden is the dominant driver of tumor immunogenicity and that MSS CRC fails to respond because it is "antigen poor". To directly test this premise and define the origins of presented tumor antigens, we integrated HLA class I immunopeptidomics and matched RNA-seq from 26 primary CRC tumors spanning MSI-H and MSS subtypes. Using patient-specific canonical and cancer-specific proteogenomic databases, we identified 115,292 unique MHC-associated peptides (MAPs) across 61 HLA alleles, with a mean of 9,292 MAPs per tumor and no significant difference in MAP counts between MSI-H and MSS tumors. In toto, we identified 266 tumor antigens, all coded by unmutated genomic sequences, comprising 70 aberrantly expressed tumor-specific antigens (aeTSAs) and 196 tumor-associated antigens (TAAs). In our cohort, MSS tumors presented more TAAs and a comparable number of aeTSAs per tumor relative to MSI-H tumors. In TCGA-COAD stratified analyses (483 tumors), MSS tumors yielded more presentable aeTSAs and TAAs per patient than MSI-H tumors. Across both subtypes, aeTSAs arose predominantly from intronic translation, UTR usage, retroelement activation, and germline-like transcription, including recurrent aeTSAs from PIWIL1, L1TD1, and endogenous retroviral loci. Together, these data demonstrate that MSS CRC is not antigen poor and highlight non-canonical translation as a major, previously underappreciated contributor to the CRC immunopeptidome. - Source: PubMed
Publication date: 2026/05/07
Courcelles MathieuHardy Marie-PierreDurette ChantalLanoix JoelMinati RobinLaverdure Jean-PhilippeVincent KrystelPerreault ClaudeThibault Pierre - In order to explore the role of piwil1 (Piwi-like RNA-mediated gene silencing 1) in sex differentiation and gonadal development of largemouth bass (Micropterus salmoides). To this end, we established a 17β-estradiol (E2)-treated pseudo-female group (XY-F, sex reversal rate 100%), a control female group (XX-F), and a control male group (XY-M). The full-length cDNA of piwil1 was obtained using the RACE technique, and its expression pattern, response to E2 treatment, and spatial localization were analyzed. The piwil1 cDNA is 3091 bp in length and encodes a protein of 855 amino acids. qRT-PCR showed that piwil1 was highly expressed in the gonads, with higher expression in mature testes than in ovaries (P < 0.05). During early gonadal differentiation, piwil1 expression increased in all groups (XY-M, XX-F, and XY-F). At 2 months old, piwil1 expression was significantly suppressed in E2-treated XY-F fish compared to XY-M and XX-F (P < 0.05). By 12 months old, piwil1 expression was highest in XY-M testes. Fluorescence in situ hybridization (FISH) results confirmed the differential expression pattern of the piwil1 gene, and strong signals were observed in oogonia (OG), primary oocytes (OC1), growing oocytes (GOC), vitellogenic oocytes (VO), primary spermatogonia (PSG), secondary spermatogonia (SSG), primary spermatocytes (PSC), and sperm (SP). In conclusion, piwil1 plays an important role in testis development and spermatogenesis, which exhibits a male-biased expression pattern in largemouth bass. These findings provide a potential molecular target for monosex male breeding in largemouth bass. - Source: PubMed
Publication date: 2026/04/29
Zhang JialeMa MingchenLi ShengjieTian TaihangDu JinxingLei CaixiaZhu TaoTian JingSong Hongmei - [This retracts the article DOI: 10.1016/j.omtn.2017.12.020.]. - Source: PubMed
Publication date: 2026/04/15
Shen ShuyuanYu HaiLiu XiaobaiLiu YunhuiZheng JianWang PingGong WeiChen JiajiaZhao LiniXue Yixue - Cancer claims nearly 10 million lives yearly, demanding innovative diagnostics and therapies beyond surgery and chemotherapy's limitations, such as resistance and toxicity. Next-generation sequencing has unveiled PIWI-interacting RNAs (piRNAs), 26-31 nucleotide small non-coding RNAs, as pivotal regulators in cancer pathogenesis, offering fresh biomarkers and targets from a molecular biosciences lens. Once deemed germline-exclusive for transposon silencing via PIWI proteins (PIWIL1-4), piRNAs exhibit somatic dysregulation across malignancies, driving hallmarks like proliferation, metastasis, and chemoresistance. In colorectal cancer, piR-823 fosters invasion by stabilizing HIF-1α and G6PD, correlating with poor prognosis. Gastric cancers overexpress piR-651, promoting G2/M arrest evasion; lung cancers feature PMLCPIR enhancing ITGB1-PI3K-AKT signaling; multiple myeloma leverages piR-823 for proliferation; and hepatocellular carcinoma shows PIWIL1 upregulation tied to stemness. PiRNAs' tissue-specific signatures enable liquid biopsy detection, with panels predicting recurrence-free survival (e.g., piR-54265/STAT3 axis in CRC). Therapeutically, piRNA mimics/inhibitors (e.g., LNA-antisense against piR-L-138 in lung squamous cell carcinoma) sensitize tumors to cisplatin, while PIWI knockdown curbs metastasis preclinically. This review dissects piRNA biogenesis, oncogenic/suppressive duality, and translational promise. By bridging molecular mechanisms to clinical utility, encompassing diagnostics via plasma profiling and therapeutics like nanoparticle-delivered piRNA therapeutics, piRNAs herald a paradigm shift in precision oncology. - Source: PubMed
Publication date: 2026/04/07
Yang QianqianWu JingpingSu Yu - PIWI proteins, a subfamily of the PAZ-PIWI domain (PPD) protein family, are traditionally regarded as germline factors that partner with PIWI-interacting RNAs (piRNAs) to silence transposons and regulate gene expression. However, growing evidence implicates PIWI proteins as oncogenic drivers in diverse somatic cancers, often acting through piRNA-independent mechanisms that remain incompletely understood. Here, we integrate transcriptomic, translatomic, and proteomic profiling of wild-type versus PIWIL1-knockout gastric cancer cells to uncover a non-canonical, translational role for PIWIL1, one of the four human PIWI proteins. We find that PIWIL1 selectively enhances the translation of 5'-terminal oligopyrimidine (TOP) mRNAs by activating mTOR complex 1 (mTORC1). Mechanistically, PIWIL1 interacts with the R2TP chaperone complex (RUVBL1-RUVBL2-RPAP3-PIH1D1) and promotes its association with TELO2, facilitating mTOR-RAPTOR assembly and mTORC1 activation. Functionally, PIWIL1 deficiency sensitizes gastric cancer cells to mTOR inhibition, and in clinical samples, PIWIL1 expression positively correlates with mTORC1 pathway activity. Together, these findings define a novel piRNA-independent mechanism through which PIWIL1 contributes to tumor progression, extend PIWI-mediated translational control from the germline to human cancers, and establish PIWIL1 as a potential therapeutic target for gastric cancer in synergy with mTOR inhibition. - Source: PubMed
Publication date: 2026/04/22
Fan TianquZhao JiangshaLi LingCui MeihuaZhang JiaweiChi TianShi Shuo