Ask about this productRelated genes to: LCN2 protein
- Gene:
- LCN2 NIH gene
- Name:
- lipocalin 2
- Previous symbol:
- -
- Synonyms:
- NGAL, 24p3
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-29
- Date modifiied:
- 2016-10-05
Related products to: LCN2 protein
Related articles to: LCN2 protein
- Depression and obesity impair quality of life and burden economies. Growing evidence shows a strong link between these two diseases. The objective of this study is to identify the shared core genes associated with both depression and obesity and to evaluate their diagnostic potential. - Source: PubMed
Publication date: 2026/09/18
Wu WanrongChen HuiYan LiyingJiang LinboLuo TongZhang LijingXiang ChengAn SuYang YangXu Tian-Rui - Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by hepatic lipid accumulation, inflammation, and oxidative injury. However, the regulatory role of integrin beta-like 1 (ITGBL1) in MASH remains unknown. - Source: PubMed
Publication date: 2026/09/17
Dai WenRen Qi-QiGu HongHuang RongJi Yi-FeiLu Cui-HuaLiu Zhao-XiuHuang Wei - Cutaneous squamous cell carcinoma (cSCC) is a prevalent skin malignancy characterized by aggressive biological behaviors. Lipocalin 2 (LCN2) has been implicated in the progression of various cancers; however, the specific mechanisms by which LCN2 modulates malignant phenotypes of cSCC remain insufficiently understood. The expression levels of LCN2, ubiquitin specific peptidase 48 (USP48), and methyltransferase like 1 (METTL1) were analyzed in cSCC tissues, paracancerous tissues, and/or cell lines using western blotting and quantitative real-time PCR. Functional assays, including cell counting kit-8 (CCK-8), flow cytometry, wound healing, Transwell invasion, and colorimetric assays, were conducted to evaluate cell proliferation, apoptosis, migration, invasion, and ferroptosis indicators. The regulatory mechanisms were investigated via methylated RNA immunoprecipitation (MeRIP), dual-luciferase reporter, co-immunoprecipitation (Co-IP), and ubiquitination assays. Furthermore, in vivo tumorigenicity was assessed using a xenograft mouse model. LCN2 was significantly upregulated in cSCC tissues and cell lines. LCN2 expression was associated with clinical stage of cSCC patients. Knockdown of LCN2 suppressed cell proliferation, migration, and invasion, while promoting apoptosis and ferroptosis. Mechanistically, USP48 was found to interact with LCN2 and enhance its stability by removing K48-linked ubiquitin chains. Functionally, USP48 silencing inhibited the malignant behaviors of cSCC cells, whereas these effects were rescued by LCN2 overexpression. Upstream analysis revealed that METTL1 stabilized USP48 mRNA expression via m7G methylation modification. Knockdown of METTL1 inhibited the key malignant phenotypes of cSCC cells, however, these effects were effectively reversed by USP48 overexpression. Consistent with in vitro findings, USP48 silencing reduced tumor growth and LCN2 and Ki67 expression in vivo, but these inhibitory effects were attenuated by the restoration of LCN2. This study elucidated a novel oncogenic axis in cSCC, wherein METTL1 stabilized USP48 mRNA through m7G methylation modification, and USP48 in turn deubiquitinated and stabilized LCN2 protein. This axis promoted cSCC progression. Clinically, these findings identify the METTL1/USP48/LCN2 pathway as a potential therapeutic target for cSCC. - Source: PubMed
Publication date: 2026/09/22
Li XiuqiShu LinLi XiaoqianDu Min - Albuminuria reflects renal and cardiovascular damage in type 2 diabetes (T2D), but its association is not fully understood. We evaluated the association of macroalbuminuria with cardiac structure and function. - Source: PubMed
Publication date: 2026/09/21
Olloquiegui Xabier IrazustaAndueza Saioa EcheverriaIzco Marina PascualSalinas Gonzalo Luis AlonsoLorente Loreto FernándezAlbéniz Susana RavassaSolis-Barquero Sergio MAramendía-Vidaurreta VerónicaMora-Gutiérrez José MaríaOrbe JosuneFernández-Seara Maria AGarcía-Fernández Nuria - Cyclosporine A (CSA), a critical immunosuppressant, induces nephrotoxicity through oxidative stress and inflammatory pathways, limiting its clinical utility. Natural compounds like Nigella sativa oil (NSO) and Echinacea purpurea extract (EPE) possess antioxidant and immunomodulatory properties, but their combined mechanistic action against CSA toxicity is unexplored. This study investigated the protective mechanisms of NSO and EPE, individually and in combination, against CSA-induced renal and immunological toxicity in rats. Fifty male Wistar rats were divided into five groups (n = 10/group): Control, CSA (cyclosporine A, 15 mg/kg/day, i.p.), CSA + NSO (Nigella sativa oil, 200 mg/kg/day, p.o.), CSA + EPE (Echinacea purpurea extract, 200 mg/kg/day, p.o.), and CSA + NSO+EPE (100 mg/kg/day each, p.o.). After 30 days, renal and bone marrow tissues were analyzed for oxidative stress and redox status markers (malondialdehyde, MDA; reduced glutathione, GSH; oxidized glutathione, GSSG) and the antioxidant transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2), alongside the pro-inflammatory mediator TNF-α (tumor necrosis factor-alpha). Gene expression of renal injury biomarkers (Tlr4, toll-like receptor 4; Tgfb1, transforming growth factor-β1; Lcn2, lipocalin-2; Kim1, kidney injury molecule-1) and bone marrow immunomodulatory cytokines (Il2, interleukin-2; Il6, interleukin-6; Il17a, interleukin-17 A; Ifng, interferon-γ) was also assessed. Serum hepatic (AST, aspartate aminotransferase; ALT, alanine aminotransferase) and renal (creatinine, urea) function parameters, along with hematological parameters, were also evaluated. CSA significantly (p < 0.05) induced oxidative stress (↑MDA, ↑GSSG; ↓GSH, ↓Nrf2) and inflammation (↑TNF-α) in kidney and bone marrow. It upregulated renal pro-fibrotic and injury genes (Tlr4, ~ 2.9-fold; Tgfb1, ~ 4.9-fold; Lipocalin-2, ~ 3.9-fold; Kim1, ~ 4.3-fold) and severely downregulated bone marrow cytokines (Il2, Il6, Il17a, Ifng; up to ~ 80%). Co-treatment with NSO and EPE, particularly in combination, potently reversed these effects. The combination therapy most effectively normalized oxidative balance, suppressed TNF-α, enhanced Nrf2, mitigated the expression of renal injury genes, and significantly restored the expression of key bone marrow cytokines towards control levels, concurrently improving serum creatinine, urea, and hematological profiles. NSO and EPE confer protection against CSA toxicity through a multi-mechanistic approach: potentiation of the Nrf2 antioxidant pathway and concomitant suppression of TLR4-mediated inflammatory and TGF-β1-driven fibrotic signaling. Their combination offers a superior therapeutic strategy to harness CSA's immunosuppressive benefits while alleviating its detrimental renal and immunological side effects. - Source: PubMed
Publication date: 2026/09/18
Abdel-Maksoud Eman MLebda Mohamed ATharwat HanaaEl-Sayed YasserHashem Aml E