Ask about this productRelated genes to: LIX1L antibody
- Gene:
- LIX1L NIH gene
- Name:
- limb and CNS expressed 1 like
- Previous symbol:
- -
- Synonyms:
- MGC46719
- Chromosome:
- 1q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-02
- Date modifiied:
- 2015-09-03
Related products to: LIX1L antibody
Related articles to: LIX1L antibody
- Limb expression 1-like protein (LIX1L) is an essential player in liver disorders, but its function in metabolic dysfunction-associated steatohepatitis (MASH) and associated hepatocellular carcinoma (HCC) progression remains obscure. Here, we identify LIX1L as a key integrative regulator linking lipid metabolism and inflammation, adipose tissue and hepatic microenvironment, which promotes MASH progression. LIX1L significantly upregulates in MASH patients, mouse models, and palmitic acid-stimulated hepatocytes. Lix1l deletion inhibits hepatic lipid accumulation, inflammation, and fibrosis as well as adipocyte differentiation by downregulating CD36, alleviating MASH and associated HCC progression in mice. Mechanistically, metabolic stress promotes PARP1-mediated poly-ADP-ribosylation of LIX1L to increase stability and RNA binding ability of LIX1L. Subsequently, LIX1L binds to AU-rich element in the 3'UTR and CDS of CD36 mRNA, thus mitigating CD36 mRNA decay. Furthermore, LIX1L deficiency-mediated downregulation of CD36 reprograms the tumor-prone liver microenvironment with increased cytotoxic T lymphocytes and reduced immunosuppressive cell proportions. These data indicate a systematic function of LIX1L in the pathogenesis of MASH and underscore targeting PARP1/LIX1L/CD36 axis as a feasible strategy for treatment of MASH and associated HCC. - Source: PubMed
Publication date: 2024/12/25
Leng YingrongZhang YanqiuCheng YangYe ShengtaoZheng YingHe MengmengWu EnyiKong LingyiZhang Hao - With the advancement of RNA sequencing technology, there has been a drive to uncover and elucidate the pivotal role of A-to-I RNA editing events in tumorigenesis. However, A-to-I miRNA editing events have been clearly identified in bladder cancer, the molecular mechanisms underlying their role in bladder cancer remain unclear. In our investigation, we observed a notable under-expression of edited miR-154-p13-5p in bladder cancer (BC) tissues, in contrast to normal counterparts. Remarkably, heightened expression levels of edited miR-154-p13-5p correlated with improved survival outcomes. To assess the impact of modified miR-154-p13-5p, we conducted a string of cell phenotype assays through transfection of the corresponding miRNAs or siRNAs. The results unequivocally demonstrate that edited miR-154-p13-5p exerts a substantial inhibitory influence on proliferation, migration, and induces apoptosis by specifically targeting LIX1L in bladder cancer. Moreover, we observed that the editing of miR-154-p13-5p or LIX1L-siRNAs inhibits the expression of LIX1L, thereby suppressing EMT-related proteins and cell cycle protein CDK2. Simultaneously, an upregulation in the expression levels of Caspase-3 and Cleaved Caspase-3 were also detected. Our research findings suggest that the upregulation of edited miR-154-p13-5p could potentially enhance the prognosis of bladder cancer, thereby presenting molecular biology-based therapeutic strategies. - Source: PubMed
Publication date: 2024/05/13
Hu ZhengxiangLiu ChunhuiMei ZujunWang XinleiMa YuyangLiu XingXu HaoFang GaochuanLiu XinyuLi RuiWang JieShi ZhenduoHan Conghui - Limb expression 1-like protein (LIX1L) might be an RNA-binding protein involved in post-transcriptional regulation. However, little is known regarding the biological function and mechanism of LIX1L in cancer cells. Here we demonstrate a clear correlation between LIX1L expression and epithelial-mesenchymal transition (EMT) markers in 81 non-small cell lung cancer (NSCLC) tissues and The Cancer Genome Atlas database, suggesting that LIX1L is a mesenchymal marker. Besides, LIX1L expression is obviously elevated in TGFβ1-induced EMT NSCLC cells and enhances cell migration, invasion, anoikis resistance, epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) resistance, and proliferation. Interestingly, the increased LIX1L expression prominently localizes to the nucleoli, where it physically interacts with the key ribosome biogenesis regulator NCL protein, inducing ribosomal RNA (rRNA) synthesis in EMT NSCLC cells. NCL knockdown or inhibition of rRNA synthesis reverses the enhanced EMT functions and proliferation ability caused by LIX1L overexpression in NSCLC cells, indicating that NCL expression and rRNA synthesis participates in LIX1L-mediated biological functions during EMT. Collectively, our findings suggest that the LIX1L-NCL-rRNA synthesis axis is a novel EMT-activated mechanism. Targeting the pathway might be a therapeutic option for EMT and EGFR-TKI resistance in NSCLC. - Source: PubMed
Publication date: 2022/12/20
Li MingleiZhang JiaxiMeng XueLiu BeiXie Shelly MLiu FangYao DeminZhang JingguoShen HaitaoXing Lingxiao - The competing endogenous RNA (ceRNA) network plays an important role in the occurrence and development of a variety of diseases. This study aimed to construct a ceRNA network related to exosomes in diabetic retinopathy (DR). - Source: PubMed
Wang TongCheng Mao-YuanShan Meng-YaTang Cui-YaoPan Nai-JiaXu Zi-HuiTang Xian-Lun - Mitral valve prolapse (MVP) is a common cardiac valve disease that often progresses to serious secondary complications requiring surgery. MVP manifests as extracellular matrix disorganization and biomechanically incompetent tissues in the adult setting. However, MVP has recently been shown to have a developmental basis, as multiple causal genes expressed during embryonic development have been identified. Disease phenotypes have been observed in mouse models with human MVP mutations as early as birth. This study focuses on the developmental function of DCHS1, one of the first genes to be shown as causal in multiple families with non-syndromic MVP. By using various biochemical techniques as well as mouse and cell culture models, we demonstrate a unique link between DCHS1-based cell adhesions and the septin-actin cytoskeleton through interactions with cytoplasmic protein Lix1-Like (LIX1L). This DCHS1-LIX1L-SEPT9 axis interacts with and promotes filamentous actin organization to direct cell-ECM alignment and valve tissue shape. - Source: PubMed
Publication date: 2022/02/17
Moore Kelsey SMoore ReeceFulmer Diana BGuo LilongGensemer CortneyStairley RebeccaGlover JanieceBeck Tyler CMorningstar Jordan EBiggs RachelMuhkerjee RupakAwgulewitsch AlexanderNorris Russell A