Ask about this productRelated genes to: OSBPL3 Blocking Peptide
- Gene:
- OSBPL3 NIH gene
- Name:
- oxysterol binding protein like 3
- Previous symbol:
- OSBP3
- Synonyms:
- ORP-3, ORP3, KIAA0704
- Chromosome:
- 7p15.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-10
- Date modifiied:
- 2015-11-16
Related products to: OSBPL3 Blocking Peptide
Related articles to: OSBPL3 Blocking Peptide
- Colorectal cancer (CRC) is the third most common cancer worldwide, with prognosis often limited by disease progression. The role of oxysterol-binding protein-like 3 (OSBPL3) in various cancers remains unclear. This study aimed to investigate the expression, biological function, and relationship of OSBPL3 with the tumor microenvironment (TME) in CRC, and to assess its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/04/24
Liang WeijunWang ChengxingWei JianchangZhou ChaorongHe CanxiuHe YaomingZhao JinglinLi ShangrenCao Jie - Fat deposition plays a crucial role in regulating the production performance and meat quality of broilers. Although the heterogeneity of mammalian adipocytes has been extensively studied, research on the molecular mechanisms underlying differences in lipid droplet accumulation in avian adipocytes remains limited. This study confirmed a significant positive correlation (R > 0.81, < 0.001) between the SSC signal and lipid droplet content via fluorescence staining of lipid droplets, Oil Red O staining, and triglyceride (TG) quantification. Based on this, a label-free sorting strategy using SSC signals was established to sort differentiated chicken preadipocytes, obtaining high lipid droplet (H) and low lipid droplet (L) subpopulations, which were subsequently subjected to transcriptome sequencing and differential gene expression (DEG) analysis, followed by GO and KEGG enrichment analysis. The results indicated no significant differences in the expression of adipogenesis marker genes (, , , , ) between the high lipid droplet (H) and low lipid droplet (L) groups, suggesting that both groups are at similar stages of differentiation. KEGG analysis revealed that both the H vs. NC and L vs. NC comparisons were enriched in common pathways, including the PPAR signaling pathway, ECM-receptor interaction, focal adhesion, cytokine-receptor interaction, and calcium-Apelin signaling pathway, suggesting that both groups of cells had activated the adipogenesis program. GO analysis showed that, in both H vs. NC and L vs. NC comparisons, differentially expressed genes (DEGs) were enriched in biological processes (BPs) related to cell adhesion, nucleosome assembly, chromatin remodeling, and receptor activity, as well as cellular components (CCs) such as the extracellular matrix, cytoskeleton, and nucleosome organization, indicating extensive gene reprogramming and activation of signaling transduction during differentiation. In the H vs. L comparison, enriched pathways included ABC transporters, ECM-receptor interaction, focal adhesion, gap junctions, microtubule-related processes, and neuroactive ligand-receptor interactions, involving lipid transmembrane transport, cytoskeleton stabilization, and signal transduction regulation, suggesting that high lipid droplet cells are more mature in lipid droplet transport, storage, and homeostasis maintenance. GO enrichment results further supported this conclusion, as H vs. L specifically enriched processes related to microtubule-related processes, cell cycle, and redox reactions (BPs), as well as chromosome organization, cytoskeleton, and motor activity (CC/MF), indicating that high lipid droplet cells maintain lipid droplet fusion and metabolic homeostasis via enhanced microtubule transport and antioxidant regulation. Differential gene analysis revealed that the L group upregulated genes associated with fatty acid synthesis and elongation (, , , , ), cholesterol and isoprenoid biosynthesis (, , , , , , ), and fatty acid oxidation (, , , ), reflecting a metabolic characteristic of concurrent lipid synthesis and mobilization; the H group, conversely, upregulated genes associated with lipid droplet formation and storage (, , , , ), lipid transport (, , , , ), and antioxidant defense (, , ), exhibiting a storage and homeostasis-oriented metabolic state. In the NC, L, and H groups, the expression of five genes-, , , , and -showed a gradual increase, suggesting that these genes were associated with preadipocyte differentiation and lipid droplet deposition. In summary, although the high and low lipid droplet subpopulations of chicken preadipocytes exhibit similar differentiation states, they form distinct metabolic orientations. The L group is characterized by active lipid synthesis, fatty acid oxidation, and membrane lipid remodeling, while the H group predominantly features lipid droplet storage, lipid transport, and antioxidant homeostasis. This study highlights the molecular mechanisms underlying the metabolic heterogeneity of avian adipocytes and provides a theoretical basis for poultry fat deposition regulation and genetic improvement. - Source: PubMed
Publication date: 2026/03/12
Wang BoyuLi YantaoWang YakeChen JiayiWang JialiLi XiaopingLi Zhenhui - As a member of the oxysterol-binding protein-like (OSBP) family, which is primarily involved in lipid transport and metabolic regulation, Oxysterol-binding protein-like protein 3 (OSBPL3), has garnered increasing attention due to its abnormal expression and functional roles in various cancers. However, the specific role and molecular mechanisms of OSBPL3 in pancreatic cancer (PDA) remain unclear. - Source: PubMed
Publication date: 2026/02/18
Sun QihuiLi XiaojiaZou QiChen YangZhu XiaoqiJiang HailinJiang TingtingWei FangXie Keping - Colorectal cancer progression involves dysregulated signaling pathways such as Hippo-YAP, but upstream regulators remain poorly defined. Here we demonstrate that oxysterol-binding protein-like 3 (OSBPL3) modulates Hippo-YAP signaling to drive tumor aggressiveness. Analysis of clinical specimens and experimental models shows that elevated OSBPL3 levels in colorectal cancer tissues correlate with shortened patient survival. Depleting OSBPL3 impairs cancer cell proliferation and invasion and induces cell cycle arrest, while its overexpression accelerates tumor growth. Mechanistic studies reveal that OSBPL3 binds 14-3-3 proteins to promote YAP1 nuclear translocation, activating downstream oncogenic pathways. Notably, tumors with high OSBPL3 expression exhibit resistance to MEK inhibitors, but this resistance is overcome by YAP1 suppression or combined YAP/MEK inhibition in patient-derived organoids. These results establish OSBPL3 as a critical Hippo-YAP pathway regulator and propose targeting OSBPL3-mediated signaling as a therapeutic strategy for colorectal cancers with Hippo pathway alterations. - Source: PubMed
Publication date: 2026/03/07
Zhong YuchenZheng ChaojingWang ZitongZhang WeiyuanWu HongyuLuo JunZhang HaoWang ChunlinZhang ChenkaiHu HanqingYuan ZimingWang MengZhang QianWang Guiyu - The progression of lung adenocarcinoma (LUAD) involves multiple molecular determinants, among which Oxysterol-binding protein-like 3 (OSBPL3) has been suggested to contribute to tumorigenesis, though its functional significance in LUAD remains poorly characterized. In this study, we elucidate the oncogenic functions and underlying mechanisms of OSBPL3 in LUAD pathogenesis. Analysis of clinical specimens revealed upregulated OSBPL3 expression in LUAD, which correlated with unfavorable patient outcomes. Genetic depletion of OSBPL3 in vitro impeded cellular proliferation, migratory capacity, and cell cycle progression, while inducing apoptotic cell death. Mechanistically, OSBPL3 was found to interact with the transcription factor NFE2L2, promoting its nuclear translocation and enhancing the transcriptional activation of PLAU, a downstream target gene. Upregulation of PLAU subsequently stimulated expression of key glycolytic enzymes through PI3K/AKT pathway activation, resulting in increased glucose consumption and lactate secretion. This metabolic reprogramming toward aerobic glycolysis facilitated malignant progression. Both genetic inhibition of PLAU and pharmacological blockade of AKT signaling abrogated the tumor-promoting phenotypes induced by OSBPL3. In vivo, OSBPL3 silencing significantly attenuated tumor growth and promoted apoptosis. Collectively, these findings identify an OSBPL3-NFE2L2-PLAU-AKT signaling axis that drives glycolytic metabolism and LUAD progression, showing its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/02/12
Zhang QingqiongZhang JingshunLi JunxianChen ShuangLiu YijunLi KaidiGuo Minzhang