NSUN6 antibody
- Known as:
- NSUN6 (anti-)
- Catalog number:
- orb74297
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- NSUN6 antibody
Related genes to: NSUN6 antibody
- Gene:
- NSUN6 NIH gene
- Name:
- NOP2/Sun RNA methyltransferase 6
- Previous symbol:
- NOPD1, ARL5B-AS1
- Synonyms:
- FLJ23743
- Chromosome:
- 10p12.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-21
- Date modifiied:
- 2019-02-26
Related products to: NSUN6 antibody
Related articles to: NSUN6 antibody
- Ovarian cancer (OC) remains one of the most lethal gynecological malignancies, largely due to late diagnosis and high metastatic potential. RNA 5-methylcytosine (m⁵C) modification has emerged as a key regulatory mechanism in cancer biology, yet the role of m⁵C-related genes such as NSUN6 in OC remains poorly understood. In this study, we first obtained three OC datasets and one m5C-related dataset from the GEO database and identified differentially expressed genes (co-DEGs) using Venn diagram analysis. Kaplan Meier plotter showed that NSUN6 was the only regulator significantly associated with patient prognosis. Additionly, Western Blot, Online database analysis and immunohistochemical staining evaluation showed that NSUN6 was significantly downregulated in OC and negatively correlated with tumor stage, metastasis and survival. Next, we overexpressed NSUN6 in OC cell lines. CCK8, wound healing and Transwell assays demonstrated that NSUN6 overexpression inhibited OC cell proliferation, migration, and invasion. Rescue experiments confirmed NSUN6-mediated suppression of AKT phosphorylation. In vivo xenograft models confirmed the tumor-suppressive effect of NSUN6, showing reduced tumor burden in both intraperitoneal and subcutaneous models. Bioinformatic analyses revealed enrichment in immune-related pathways and correlations with immune infiltration markers, which were further validated using ovarian cancer clinical samples. Collectively, our results demonstrate that NSUN6 is downregulated in OC and suppresses OC proliferation, migration, and invasion by inhibiting AKT activity, highlighting its potential as a therapeutic target in OC. - Source: PubMed
Publication date: 2026/05/29
Hu KuanShi WenjingZhou ZongjiangDeng XinyueLi Juanni - Colorectal cancer (CRC) stands as a widespread gastrointestinal malignancy, marked by high morbidity and mortality, and poses a substantial threat to global public health. This research aims to explain the significance of NSUN6 in CRC progression. Tumor tissues were harvested from CRC patients, with subsequent analysis of the association between NSUN6 expression and clinical features. After intervening in NSUN6 expression in CRC cells and normal cells, cell proliferation, apoptosis, migration, and invasion were detected. m5C modification and ALYREF enrichment on KLF1 were analyzed. The binding of KLF1 to USP15 was detected. We found that NSUN6 expression was increased and correlated with the clinical characteristics of CRC patients. After downregulation of NSUN6, cell proliferation was decreased, apoptosis was increased, and cell migration and invasion were reduced. NSUN6 stabilizes KLF1 mRNA via ALYREF-dependent m5C modification, thereby enhancing KLF1 expression. KLF1 promotes USP15 expression. Overexpression of KLF1 or USP15 alleviated the suppressing effect of NSUN6 downregulation on the malignant progression of CRC cells. NSUN6 downregulation inhibited tumor growth and liver/lung metastasis, which were promoted upon KLF1 overexpression. In conclusion, NSUN6 mediates m5C modification and promotes the malignant progression of CRC cells via the KLF1/USP15 axis. - Source: PubMed
Dong ZhihongWang YonglingChen JiaxinYu WeibangChen YanPeng WenjianCheng Wei - Perioperative neurocognitive disorders (PND) are common in elderly patients, with emerging evidence linking their pathogenesis to abnormal cell death. PANoptosis is a newly identified inflammatory form of programmed cell death, but its role in PND remains unknown. Here, we employed animal behavioral tests, single-cell sequencing (scRNA-seq), methylated RNA immunoprecipitation-sequencing (meRIP-seq), RNA sequencing (RNA-seq), immunofluorescence, and TUNEL staining to investigate the role and underlying mechanisms of PANoptosis in PND. Y-maze and open-field experiments confirmed cognitive and locomotor deficits in a PND mouse model. scRNA-seq revealed altered cellular composition and neuronal heterogeneity in PND brain tissues, with elevated PANoptosis-related gene expression and scores in PND neurons. In vivo and in vitro assays confirmed increased expression of PANoptosis markers (ASC, AIM2, Pyrin) and neuronal apoptosis in PND. Based on the differentially expression gene (DEG) analysis conducted using scRNA-seq, we identified NSUN6 as a key gene that was significantly downregulated in neurons of the PND group, and overexpression of NSUN6 suppressed isoflurane-induced neuronal PANoptosis. RNA-seq and meRIP-seq further revealed that NSUN6 promoted m5C modifications enriched in CDSs and 3' UTRs, with pathway analysis implicating PANoptosis-associated signaling. OAS2 was identified as a direct substrate of NSUN6-mediated m5C modification, with NSUN6 overexpression enhancing both its m5C enrichment and expression. Collectively, our findings suggest that NSUN6 may be involved in OAS2-associated m5C modification and neuronal PANoptosis, supporting a potential role for the NSUN6/OAS2 axis in the pathogenesis of PND. - Source: PubMed
Publication date: 2026/05/07
Gong XinhaoLiu WenLuo HanqingA RunnaHu YulongHu YingchuanFeng XiaojinChen Shoulin - - Source: PubMed
Publication date: 2026/04/09
Chen CanPan Shi-YiXu JiaCao XinyuanZhang Wei-MingXu Hua-Guo - The epigenetic modification of transfer RNA (tRNA) and tRNA-derived small RNAs (tsRNAs) is associated with the initiation and development of cancer. However, the biological role of mC-modified tsRNAs, especially in bladder cancer (BC), and their regulatory mechanisms remain unclear. Here, we identify a novel mC-modified tsRNA, mC-tRF3b-Cys-23 (mtRC), whose expression is significantly downregulated in both tumor tissues and urine samples of BC patients and is strongly negatively correlated with the malignant progression of bladder cancer. In vitro and in vivo functional experiments reveal that mtRC, but not its unmodified counterpart (tRC), exhibits a tumor-suppressive role. Furthermore, NOP2/Sun RNA methyltransferase 6 (NSUN6) regulates mtRC abundance and suppresses cell proliferation. Mechanistically, mtRC directly binds the oncosuppressor protein RNA-binding motif 4 (RBM4) and improves its stability by preventing RBM4 ubiquitination, thereby upregulating RBM4 protein levels. RBM4 reduces the levels of glycolytic genes and decreases glycolysis, thereby inhibiting histone H3 lysine 18 lactylation (H3K18la). This reduction in H3K18 lactylation attenuates the transcriptional activation of the downstream oncogenes IL1RAP and VASH2, thereby ultimately suppressing tumor malignancy in BC. Together, our results not only underscore the critical role of mtRC in BC but also unravel a novel and coherent regulatory signaling axis-mtRC/RBM4/H3K18la/IL1RAP&VASH2-that orchestrates BC malignancy, suggesting mtRC may serve as a candidate therapeutic target for BC treatment. - Source: PubMed
Publication date: 2026/02/27
Ying XiaolingHuang YapengHuang JianCai QinyuZhang DanniChen CongNie YuxiYang BaotongLi ChuanHu WenyuXiong ChangZhang ChengchengJi DingLiang YaominYang MeiWu WenqiJi Weidong