Ask about this productRelated genes to: LRRC59 antibody
- Gene:
- LRRC59 NIH gene
- Name:
- leucine rich repeat containing 59
- Previous symbol:
- -
- Synonyms:
- PRO1855, FLJ21675
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-12
- Date modifiied:
- 2014-11-19
Related products to: LRRC59 antibody
Related articles to: LRRC59 antibody
- Leucine-rich repeat-containing protein 59 (LRRC59) has been implicated in the pathogenesis of various human cancers, but its functional role and underlying molecular mechanisms in cervical carcinogenesis and progression remain unknown. In this study, LRRC59 expression was assessed in cervical cancer (CC) and normal cervical tissues using public databases and clinical specimens. Correlations between LRRC59 expression and clinical characteristics were analyzed using data from our institutional cohort and The Cancer Genome Atlas (TCGA). The functional effects of LRRC59 on CC cell proliferation, apoptosis, invasion, and migration were evaluated through in vitro assays and xenograft tumor models. Potential mechanisms were identified by integrated bioinformatics analysis and subsequently validated experimentally. LRRC59 was significantly upregulated in CC tissues, and elevated LRRC59 expression correlated with poor prognosis. Knockdown of LRRC59 suppressed CC cell proliferation, invasion, and migration, while promoting apoptosis. Mechanistically, LRRC59 knockdown downregulated total β-catenin, nuclear β-catenin, and the expression of downstream targets c-Myc and cyclin D1. Treatment with SKL2001, a Wnt/β-catenin pathway agonist, partially reversed the inhibitory effects of LRRC59 knockdown on proliferation, invasion, and migration, as well as its pro-apoptotic effect. Furthermore, LRRC59 knockdown led to reduced expression of Y-box binding protein 1 (YBX1). Collectively, these findings demonstrate that LRRC59 promotes CC progression likely via YBX1-mediated Wnt/β-catenin signaling, identifying LRRC59 as a promising prognostic biomarker and potential therapeutic target in cervical cancer. - Source: PubMed
Publication date: 2026/04/28
Zhu QianXu GuiqinWang TianmingDing ZhuyunLiu LianhuaLing LingYing Xiaoyan - Nuclear envelope (NE) rupture is a hallmark of cancer cells, and persistent NE damage drives genome instability and inflammation. NE repair relies on activation of the endosomal sorting complex required for transport (ESCRT)-III repair machinery by the LEMD2-CHMP7 compartmentalization sensor, but little is known beyond these core factors. Here, we use convergent proximity proteomics to inventorise proteins mobilized to the NE upon assembly of LEMD2-CHMP7 and activation of ESCRT-III. Within this NE repairome, we identify LRRC59 as a critical regulator of LEMD2 accumulation at NE ruptures. We find that LRRC59, together with the nuclear transporters KPNB1 and XPO1, restricts the assembly of LEMD2-CHMP7 complexes to the site of rupture. Disruption of this regulatory axis escalates LEMD2-CHMP7 spreading across the NE, driving torsional DNA damage in ruptured nuclei and micronuclei. Thus, our work identifies a central regulatory layer of NE repair centered on LRRC59 and KPNB1. We propose that altered LRRC59 levels and deregulated nuclear transport coordinately compromise NE repair, driving genome instability and cancer development. - Source: PubMed
Publication date: 2025/12/12
Timmer RomyBellanger AuréliePeeters SarahKim Herade la Ballina Laura RodriguezEikvar SisselArns Annemijn JOortgijs EsméeSekulić NikolinaDe Vos Winnok HCampsteijn Coen - Leucine‑rich repeat‑containing protein 59 (LRRC59), a 244‑amino‑acid endoplasmic reticulum membrane protein, is implicated in the tumorigenesis of multiple malignancies. However, its functional significance in colorectal cancer (CRC) remains poorly understood. In the present study, LRRC59 expression in CRC tissues was evaluated using immunohistochemistry and western blotting. Colony formation, Cell Counting Kit‑8, wound healing and Transwell assays, in xenograft models, were used to evaluate the effect of LRRC59 on CRC progression. Apoptosis was analyzed using flow cytometry and western blotting. The interaction between LRRC59 and the protein kinase RNA‑like endoplasmic reticulum kinase (PERK) pathway was verified using the starBase database and western blotting. It was found that LRRC59 expression was significantly higher in CRC tissues than in normal tissues. LRRC59 knockdown in HCT116 and LoVo cells inhibited proliferation, migration and invasion and promoted apoptosis, and the PERK pathway was significantly activated. subcutaneous tumorigenesis assays corroborated these findings. Treatment with a PERK pathway‑specific inhibitor reduced the apoptosis of HCT116 and LoVo cells with LRRC59 knockdown. These findings suggest that LRRC59 is not only significantly upregulated in CRC but also mechanistically drives tumor progression by coordinating pro‑oncogenic processes, including enhanced proliferation, migration and invasion. Importantly, mechanistic evidence was provided that LRRC59 inhibits apoptosis by suppressing the PERK signaling axis, identifying this molecule a target in the development of CRC therapeutic strategies. - Source: PubMed
Publication date: 2025/10/24
Hou XingdongWang YutingChen YuzhuoZhong PeiyanWang GuangzhiLi BaichengLu BoweiJiang HanyuNing Shili - The potency of T cell-mediated responses is a determinant of immunotherapy effectiveness in treating malignancies; however, the clinical efficacy of T-cell therapies has been limited in hepatocellular carcinoma (HCC) owing to the extensive immunosuppressive microenvironment. - Source: PubMed
Publication date: 2024/12/10
Chen JiananJiang YouhaiHou MinghuiLiu ChunliangLiu ErdongZong YaliWang XiangMeng ZhengyuanGu MingyeSu YuWang HongyangFu Jing - Endoplasmic reticulum stress may affect the occurrence and development of cancer. However, its effect on the prognosis of colon cancer (CC) patients is not clear yet. Herein, based on TCGA database, we screened 15 endoplasmic reticulum stress responsive genes (ERSRGs) associated with the prognosis of CC patients by Cox regression. By LASSO and multivariate Cox regression analyses, a prognostic risk assessment model involving 12 genes (DNAJB2, EIF4A1, YPEL4, COQ10A, IRX3, ASPHD1, NTRK2, TRIM39, XBP1, GRIN2B, LRRC59, and RORC) was built. The survival curves indicated that patients in the low-risk group had good prognosis. ROC curves demonstrated a good performance of this 12-gene prognostic model, and the Riskscore could be considered as an independent prognostic factor. Patients in low-risk group benefit more from immune checkpoint inhibitor and immune checkpoint blockade (ICB) treatment. Besides, the enrichment analysis suggested a remarkable difference in Ca signaling in both groups. Finally, based on the cMAP database, we identified several potential drugs that could target high-risk groups, such as Dasatinib, GNF-2, Saracatinib, and WZ-1-84. To sum up, our research constructed an ERSRGs-characteristic prognostic model. The model is a promising biomarker for prediction of clinical outcomes and immune therapy response of CC patients. SIGNIFICANCE: Based on the transcriptomic data of colon cancer in the TCGA database, this study screens 12 endoplasmic reticulum stress-related genes (ERSRGs), including DNAJB2, EIF4A1, YPEL4, COQ10A, IRX3, ASPHD1, NTRK2, TRIM39, XBP1, asphD1, NTRK2. GRIN2B, LRRC59, and RORC, and a prognostic model was constructed. This model can be used as a predictor of prognosis and immunotherapy response in colon cancer patients. At the same time, model-based prediction of drugs can also be a potential option for colon cancer treatment in the future. - Source: PubMed
Publication date: 2024/08/17
Yuan ZhibinWang YiXu SongZhang MengTang Jianjun