LRRC15 antibody
- Known as:
- LRRC15 (anti-)
- Catalog number:
- orb101141
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- LRRC15 antibody
Related genes to: LRRC15 antibody
- Gene:
- LRRC15 NIH gene
- Name:
- leucine rich repeat containing 15
- Previous symbol:
- -
- Synonyms:
- LIB
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-25
- Date modifiied:
- 2015-08-27
Related products to: LRRC15 antibody
Related articles to: LRRC15 antibody
- Metastatic breast cancer remains incurable, underscoring the need for novel therapeutic strategies. Epidemiological and preclinical evidence suggests statins suppress metastatic outgrowth, however the underlying mechanisms remain unclear. We employed high-resolution spatial transcriptomics (ST) to explore the cellular composition and differentially expressed genes (DEGs) in the metastatic microenvironment following atorvastatin treatment. Formalin-fixed, paraffin-embedded breast cancer liver metastases from control and atorvastatin-treated mice were analyzed by Nanostring CosMx Spatial Molecular Imager (SMI)/Bruker using a 973-gene panel, profiling 212 and 207 tumor-adjacent field of views (FOVs) (TAFs) respectively, which identified eight cell clusters, while non-tumor FOVs (NTFs) were sparse. Preferential depletion of LRRC15⁺ myofibroblastic cancer associated fibroblasts (CAFs), CXCL8⁺ inflammatory CAFs, and C1QC⁺/SPP1⁺ tumor associated macrophages (TAMs) subsets were revealed by harmony-assisted cell annotation and Seurat label transfer, which further separated CAFs and TAMs into discrete functional subpopulations. Immunohistochemistry (IHC) was also performed to validate cell types in both the tissues. Wilcoxon-based DEG analysis identified metastasis-associated gene expression changes between groups. Atorvastatin treatment reduced CAFs, Hepatic stellate cells (HSCs) (significantly), and macrophages (trending) in TAFs, with no changes in NTFs. These findings were supported by IHC (n = 4), which confirmed prominent reductions in these cell types while hepatocyte and endothelial markers remained unchanged. DEG analysis revealed coordinated downregulation of metastasis and extracellular matrix- associated transcripts in atorvastatin-treated TAFs. Our findings suggest that atorvastatin alters the cellular milieu in the disseminated microenvironment towards one in which pro-tumorigenic CAF and HSC populations are reduced, to create a microenvironmental niche favorable for maintaining metastatic dormancy and preventing relapse. - Source: PubMed
Publication date: 2026/09/12
Atale NehaChen JieIsett Brian RBao RiyueMeyer Ernest MWells Alan - Fibroblasts are essential for tissue repair, but persistent activation of matrix-remodelling myofibroblasts can promote fibrosis, tissue stiffening and immune dysfunction. LRRC15 is a leucine-rich repeat-containing cell-surface protein enriched in selected activated mesenchymal compartments, with the strongest functional evidence arising from cancer-associated stroma. State-level evidence also links LRRC15 to a TGF-β-regulated extracellular matrix-remodelling myofibroblast state in idiopathic pulmonary fibrosis and to disease-specific myofibroblast programs in human skin, including inflamed hidradenitis suppurativa associated with scarring risk. However, LRRC15-specific causal evidence in physiological wound repair and pathological scarring remains limited. This review therefore considers LRRC15 positivity a context-dependent stromal state rather than a universal fibroblast lineage or intrinsically pathological identity. Focusing on pulmonary fibrosis and tumour stroma, with skin repair as a comparative framework, we integrate single-cell transcriptomics, spatial mapping, matrix biology and cancer immunology. Current evidence supports LRRC15 as a marker of activated stromal programs and, in selected tumour models, as a contributor to immunoregulatory stromal function, but does not establish universal control of fibroblast contractility, matrix persistence, or scar formation. We propose that temporal persistence and anatomical context may distinguish adaptive from maladaptive LRRC15-associated remodelling. Across tissues, these observations suggest related or convergent programs rather than a demonstrated conserved molecular identity. The proposed repair-to-pathology spectrum is therefore hypothesis-generating and requires validation through temporal lineage tracing, tissue-relevant LRRC15 perturbation, spatial protein analysis, and stage-specific therapeutic studies. LRRC15 is best viewed as a biological readout and potential targeting handle whose significance must be defined in each tissue context. - Source: PubMed
Hamad Rabab SElmorsy Elsayed AEl-Kott Attalla FAlShehri Mohammed ANegm SallyEltantawy WaleedAli Mohamed A MChaudhary Anis AhmadSaber Sameh - Osteosarcoma (OS) is the most common human primary bone cancer, primarily affecting children and young adults. While the survival rate of patients diagnosed with localized OS is ∼65%, this decreases to ∼20% for patients with metastatic disease, and recurrent disease remains largely incurable. Therefore, identifying new therapeutic strategies is urgently needed for metastatic and refractory OS. This study analyzes the surfaceomes and global proteomes of 22 unique OS patient-derived xenografts (PDXs) using mass spectrometry to identify surface proteins for potential immunotherapeutic targeting. Both methods identify known OS-associated surface candidates including LRRC15, MMP14, MRC2, and CADM1, and several poorly characterized targets, including ROR2 and TMEM119. Both ROR2 and TMEM119 display robust expression in OS tissues but only limited or no expression in normal pediatric tissues, and loss of both targets reduces the migration of OS cells. These data provide a resource of surface proteins as potential immunotherapeutic targets in OS. - Source: PubMed
Publication date: 2026/08/26
Mooney BrianChu XiaojieNegri Gian LucaLizardo Michael MSong HarleyMarsh AlisonDelaidelli AlbertoHuang Yue ZRouleau MelanieSpencer Sandra EShraim RawanHamilton Amber KMagesh SruthiZhang WendongBudhathoki YogeshCannon Matthew VRoberts RyanGorlick RichardSweet-Cordero AlejandroDiskin Sharon JMaris John MLi WeiMorin Gregg BSorensen Poul H - The fourth Paediatric Therapeutic Development Workshop focused on osteosarcoma, the most common primary bone cancer in children and young adults. Current treatment of osteosarcoma comprises surgery and chemotherapy. Outcome has shown very little improvement over the last four decades and there are substantial unmet needs including improving survival, especially in metastatic or relapsed disease, and reducing treatment toxicity. There is a lack of new therapeutics in osteosarcoma, with the evaluation of new treatments challenged by complex biology and variation in chemotherapy standard of care regimens. An antibody-drug conjugate (ADC) targeting LRRC15 with an osteosarcoma-relevant payload is a promising therapeutic approach. Small molecule inhibitors and degraders targeting SMARCAL1 should be considered as a very high priority, as it is a target applicable to several high unmet need malignancies. Preclinical evaluation of KIF18A in osteosarcoma models is required. An early phase study of an eIF4A1 inhibitor is warranted. Further preclinical validation of RUNX2 using PROTACs or ADCs is required. Targeting MYC, either indirectly or directly is a high priority. Osteosarcomas have significant genomic instability and impaired DNA repair mechanisms and efforts are ongoing to exploit this vulnerability therapeutically. The goal is that these therapeutic developments will improve survival for patients with osteosarcoma. - Source: PubMed
Publication date: 2026/08/18
Baxter Joseph SMontiel Equihua ClaudiaMolenaar Jan JBerlanga PabloBishop Michael WBlanc PatriciaCampbell-Hewson QuentinCasanova MichelaCortes-Ciriano IsidroCrompton BrianDaems SamDanielson LauraDela Cruz FilemonFlanagan AdrienneGorlick RichardGraham AnnGuenther Lillian MHecker-Nolting StefanieHelman LeeKavanagh-Williamson MaiaKearns PamelaLass GeffenIp-Toma ChristinaLigon JohnLewin JeremyLivingston J AndrewMarchais AntoninMcCabe Martin GMittnacht SybilleNathrath MichaelaPalmerini EmanuelaPantziarka PanPatel SeemaPatel SheenaReed DamonRoberts RyanScotlandi KatiaSlotkin EmilyTseng MandySmallwood WalkerSorensen Poul HValverde ClaudiaWane MadinaWilson Gemma APearson Andrew D JJenkinson DavidGaspar NathalieStrauss Sandra J - The 15-leucine-rich repeat containing membrane protein (LRRC15) is a transmembrane protein derived from the leucine-rich repeat (LRR) superfamily that participates in various cell-cell and cell-extracellular matrix interactions, regulating fibrogenesis, vascular invasion, tumorigenesis, and the formation of the innate immune barrier to drive specific antiviral responses. LRRC15, whose expression is reportedly induced by TGF-β and IL-1β stimulation, was recently found to be associated with the development of skeletal diseases, and its presence has been related to the pathophysiological processes of osteoporosis, osteoarthritis and rheumatoid arthritis. Various transmembrane and intracellular signaling transductions are involved in LRRC15-mediated molecular functions, including integrin, NF-κB, Wnt/β-catenin, etc. Additionally, LRRC15 is considered a novel mesenchymal protein and an important biomarker for the occurrence and development of osteosarcoma. Understanding the role of LRRC15 in the bone, joint and tumor microenvironment will facilitate the development of new therapeutic options-particularly LRRC15-based target therapies-for skeletal diseases. - Source: PubMed
Publication date: 2026/07/24
Lin Zi-HaoHu Zhi-ChaoZhang Chang-QingZhu Zhen-ZhongTang Qian