Ask about this productRelated genes to: NSUN2 Blocking Peptide
- Gene:
- NSUN2 NIH gene
- Name:
- NOP2/Sun RNA methyltransferase 2
- Previous symbol:
- MRT5
- Synonyms:
- FLJ20303, TRM4, Misu
- Chromosome:
- 5p15.31
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-25
- Date modifiied:
- 2019-02-26
Related products to: NSUN2 Blocking Peptide
Related articles to: NSUN2 Blocking Peptide
- Colorectal cancer (CRC) is one of the leading causes of cancer-related mortality worldwide, largely due to therapeutic resistance and inefficient drug delivery. Here, we report the development of a targeted and biocompatible siRNA delivery platform designed to silence RNA methyltransferase NSUN2, a key regulator of mC RNA methylation implicated in CRC progression and immune evasion. Poly (lactic acid) (PLA)-based nanoparticles were engineered and functionalized with an RGD peptide for tumor-specific targeting and a cationic KA26 peptide to promote siRNA complexation and cellular internalization. The resulting PLA-RGD-KA26-siRNA nanocomplexes (PRR) exhibited uniform nanoscale dimensions, a positive surface charge, and high colloidal stability in aqueous solution. In vitro studies demonstrated significantly enhanced cellular uptake and efficient NSUN2 knockdown across multiple CRC cell lines, resulting in marked inhibition of cancer cell migration with negligible cytotoxicity to normal cells. In a CT-26-luciferase lung metastasis mouse model, PRR nanoparticles preferentially accumulated in metastatic lesions and achieved potent NSUN2 silencing, leading to substantial lung tumor regression. Combination therapy with PD-L1 blockade (PRRP) produces synergistic antitumor effects, including near-complete suppression of metastasis, increased CD4 and CD8 T-cell infiltration, reduced Ki67 proliferation, and enhanced apoptosis without detectable systemic or organ toxicity. These findings establish a rationally designed tumor-targeted RNA delivery system that effectively modulates NSUN2-driven epigenetic pathways and restores antitumor immune activity. This approach offers a promising therapeutic avenue for metastatic CRC by integrating RNA-based epigenetic regulation with immune checkpoint inhibition. - Source: PubMed
Publication date: 2026/04/20
Ali KamranLi YangBi QiuchenZhu XiaolinSun XiaoliZhu HepingZhang HuamiaoHuang LeyiHu HonghuaYang XiaohuiTang LongguangWang Jianwei - Radiotherapy is the primary treatment for nasopharyngeal carcinoma (NPC), yet radioresistance frequently develops and leads to the failure of treatment for NPC. NSUN2 acts as a potential oncogene in NPC, but its role in NPC radioresistance remains unclear. In this study, we revealed that NSUN2 was upregulated in radioresistant NPC tissues. Through a series of functional assays following radiotherapy, including CCK-8, colony formation, apoptosis analysis by flow cytometry, we demonstrated that NSUN2 promoted radioresistance and enhanced DNA damage repair in NPC cells. Mechanistically, NSUN2 negatively regulated TP53 expression and competitively enhanced the UCHL3-RAD51 interaction, thereby facilitating RAD51 deubiquitination and RAD51-mediated homologous recombination repair of DNA double-strand breaks. Moreover, the suppressive effect of NSUN2 knockdown on NPC radioresistance was reversed by TP53 knockdown. Furthermore, the small molecule GSK-F1 was found to directly bind to NSUN2 and promote its proteasomal degradation, consequently activating the downstream TP53/RAD51 signaling axis and increasing NPC cell cytotoxicity and radiosensitivity. In conclusion, our study elucidates that NSUN2 promotes NPC radioresistance by negatively regulating the TP53/RAD51 axis, and the NSUN2 inhibitor GSK-F1 functions as a radiosensitizer in NPC by disrupting the NSUN2/TP53/RAD51 signaling pathway, thereby providing a potential clinical strategy for the targeted therapy and radiosensitivity in NPC. - Source: PubMed
Publication date: 2026/03/30
Zheng LemeiLi MengnaLi XiaolongWei JianxiaXue ChangningWei QingqingDuan YumeiXin HuizhenWu ZubingZeng TingXiong WeiFan SongqingZhou MingDeng Hongyu - N-methyladenosine (mA) and 5-methylcytosine (mC) are dynamic and reversible RNA modifications that play important roles in cardiovascular diseases (CVDs). By regulating RNA stability, splicing, transport, translation, and degradation, mA and mC shape key pathological processes including endothelial dysfunction, inflammation, apoptosis, fibrosis, impaired contractility, and metabolic remodeling. Core regulators, including METTL3, METTL14, fat mass and obesity-associated protein (FTO), AlkB homolog 5 (ALKBH5), and YTH family proteins for mA, as well as NSUN2, DNMT2, TET2, and ALYREF YBX1 for mC related pathways, display disease stage specific and cell type-specific patterns across atherosclerosis, ischemic cardiomyopathy, heart failure, myocarditis, cardiomyopathy, and rheumatic heart disease, highlighting their potential as diagnostic and prognostic biomarkers. Therapeutically, pharmacological modulation of writers and erasers, adeno-associated virus-based gene delivery, and stem cell-based strategies show encouraging preclinical efficacy, while lifestyle interventions such as exercise may optimize the cardiac RNA methylation landscape. In addition, emerging RNA methylation marks, including N¹-methyladenosine (mA),7-methylguanosine (mG), N⁶,2'-O-dimethyladenosine (mAm), and oxidative cytosine derivatives such as 5-hydroxymethylcytosine (hmC) and 5-formylcytosine (fC), further expand the RNA modification landscape of cardiovascular remodeling by linking cap-dependent translation, mitochondrial protein synthesis, and stress adaptation. However, major challenges remain, including resolving RNA methylation dynamics at single-nucleotide and single-cell resolution, integrating RNA methylation with other regulatory layers, and achieving precise cardiac delivery with durable safety. With advances in multi-omics, spatial mapping, nanomedicine, and translational research, targeting RNA methylation offers a promising paradigm for improved diagnosis, risk stratification, and personalized therapy in cardiovascular disease. - Source: PubMed
Publication date: 2026/05/05
Li HuilinFan QimingSang JiajunKan ChengxiaSun XiaodongZhang Kexin - Renal fibrosis (RFib) is a final common pathway in chronic kidney disease (CKD) progression. Although 5-methylcytosine (m5C) RNA modification can regulate mRNA fate, its role in RFib and redox-regulated cell death remains incompletely defined. - Source: PubMed
Publication date: 2026/04/21
Zan YuxinChen LinMa LimingMeng PanpanMa ShinanLiu HuizhongTian YaqiHe XijuWang ZhixiaoDing Yan - Despite advances in immunotherapy, significant challenges remain in the treatment of esophageal cancer (EC), largely due to its molecular complexity and the immunosuppressive tumor microenvironment (TME). Recently, long non-coding RNAs (lncRNAs) have emerged as critical regulators of tumor immunity, influencing key pathways involved in inflammation, immune evasion, and therapeutic response. In this review, we examine the role of immune-related lncRNAs in modulating major immunological signaling pathways in EC, including Programmed Cell Death Protein 1/Programmed Death-Ligand 1 (PD-1/PD-L1), Toll-Like Receptor (TLR), Tumor Necrosis Factor-alpha (TNF-α), Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB), and Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathways. Oncogenic lncRNAs such as LINC02096, Cancer Susceptibility Candidate 9 (CASC9), and Small Nucleolar RNA Host Gene 20 (SNHG20) promote immune checkpoint expression, facilitating immune escape and resistance to checkpoint blockade. Other lncRNAs, including LINC02820, NSUN2-methylated lncRNA (NMR), and Myeloid-Associated Long Non-coding RNA (MALR), activate TNF-α/NF-κB signaling, contributing to inflammation-driven metastasis. Additionally, MALAT1 and FAM83H-AS1 regulate transforming growth factor-beta (TGF-β)-mediated epithelial-to-mesenchymal transition, enhancing tumor progression. Conversely, NF-κB Interacting Long Non-coding RNA (NKILA) functions as a tumor suppressor by inhibiting NF-κB activation. Importantly, lncRNA expression profiles correlate with immune checkpoint levels, immune cell infiltration, and patient survival, highlighting their potential as biomarkers for prognosis and therapeutic response. This review provides a framework for understanding lncRNA-mediated immune regulation and supports their translational potential in EC immunotherapy. - Source: PubMed
Publication date: 2026/04/17
Uttam VivekRana Manjit KaurSethi GautamJain Aklank