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LGR5

LGR5, also known as leucine-rich repeat-containing G protein-coupled receptor 5, is a seven-transmembrane receptor protein that acts as a specific marker for adult stem cells in self-renewing tissues such as the intestinal crypts and hair follicles.^[1] It functions primarily as a high-affinity receptor for R-spondin (RSPO) proteins, which bind to its extracellular leucine-rich repeat domain to potentiate canonical Wnt/β-catenin signaling, thereby promoting stem cell proliferation, maintenance, and tissue homeostasis.^[2] Discovered as a Wnt target gene, LGR5 plays a critical role in postembryonic development and regeneration, with its expression tightly regulated in cycling stem cell populations.^[3] The structure of LGR5 features a large N-terminal extracellular domain composed of 17 leucine-rich repeats for ligand binding, followed by seven transmembrane helices characteristic of G protein-coupled receptors (GPCRs), and a short intracellular C-terminal tail that lacks typical G-protein activation motifs.^[4] Unlike classical GPCRs, LGR5 does not couple to heterotrimeric G proteins but instead enhances Wnt signaling by stabilizing the Wnt receptor complex on the cell surface, counteracting the inhibitory effects of E3 ubiquitin ligases such as RNF43 and ZNRF3 through RSPO-mediated interactions.^[5] This mechanism amplifies β-catenin accumulation and transcriptional activation of Wnt target genes, including LGR5 itself, forming a positive feedback loop essential for stem cell dynamics.^[6] LGR5 expression is highly specific to stem cell niches, with prominent localization in the base of intestinal crypts where it marks rapidly cycling columnar cells responsible for epithelial renewal, as well as in the bulge region of hair follicles and other sites like the stomach and ovary. In the intestine, LGR5-positive stem cells generate all cell lineages of the epithelium every 3–5 days, highlighting its role in continuous tissue turnover.^[3] Beyond normal physiology, dysregulated LGR5 signaling contributes to tumorigenesis, as it is overexpressed in various cancers including colorectal, ovarian, and pancreatic, where it identifies cancer stem cells capable of tumor initiation and metastasis.^[7] Therapeutic targeting of the LGR5/RSPO axis is emerging as a strategy to inhibit cancer progression while sparing normal stem cell function.^[8]

Molecular Biology

Gene Characteristics

The LGR5 gene, originally identified in 1998 as an orphan G protein-coupled receptor (initially termed HG38 or GPR49) within the glycoprotein hormone receptor subfamily, encodes a receptor with potential for binding novel ligands.^[9] This gene is situated on the long arm of human chromosome 12 at cytogenetic band 12q22-23, spanning approximately 145 kilobases from position 71,439,797 to 71,586,310 (GRCh38 assembly) and comprising 18 exons in its primary transcript (ENST00000266674).^[10]^[1]^[4] LGR5 encodes a precursor protein of 907 amino acids, which undergoes processing to form the mature receptor. Its promoter region, located upstream of exon 1, includes TCF/LEF-binding sites that enable direct transcriptional activation by canonical Wnt signaling, establishing LGR5 as a key Wnt target gene.^[11] Additional regulatory elements, such as enhancers identified through chromatin interaction analyses (e.g., GeneHancer regions at chr12:71,438,701–71,442,291), modulate its tissue-specific expression.^[4] In adult human tissues, LGR5 exhibits basal expression in organs including skeletal muscle, placenta, spinal cord, and brain, but demonstrates markedly elevated levels in restricted niches such as the crypt base of the small intestine and colon, as well as the bulge of hair follicles, where it serves as a marker for cycling stem cells.^[9]^[1]^[12]

Protein Structure

LGR5 is a class A G protein-coupled receptor (GPCR) featuring seven transmembrane α-helical domains that anchor the protein in the plasma membrane, a defining architectural element shared with rhodopsin-like GPCRs. The extracellular N-terminal ectodomain is composed of 17 leucine-rich repeats (LRRs), which fold into a β-sheet-rich horseshoe structure essential for ligand recognition and receptor activation. This LRR array, spanning approximately residues 22–541, positions the binding site away from the membrane, facilitating interactions with extracellular cues while the hinge region connects it to the first transmembrane helix.^[13] The protein includes an N-linked glycosylation site at asparagine 208 (Asn208) within the ectodomain, a conserved feature that supports proper folding, trafficking, and stability of the receptor, aligning with glycosylation patterns observed in related glycoprotein hormone receptors. Sequence conservation is high across mammals; for instance, human LGR5 shares about 90% amino acid identity with mouse Lgr5 in the extracellular domain, underscoring its evolutionary preservation for core receptor functions.^[14]^[15] At the intracellular C-terminus, LGR5 possesses a PDZ-binding motif (typically class I type, involving the terminal residues) that enables recruitment of PDZ-domain-containing scaffold proteins, such as DLG1, to regulate receptor localization and assembly of signaling complexes. Although no full-length crystal structure exists, insights from the crystallized LGR5 ectodomain (PDB: 4KNG) in complex with R-spondin 1 reveal a rigid, elongated horseshoe conformation of the LRRs, with low root-mean-square deviation (RMSD) values across structures, enabling accurate homology modeling of the transmembrane and intracellular regions based on related LGR family members like LGR4 and canonical class A GPCRs such as rhodopsin.67254-4/fulltext)00287-8)

Biological Function

Ligand Interactions

LGR5 serves as a receptor for the R-spondin family of ligands, specifically RSPO1 through RSPO4, which bind to its extracellular domain with high affinity to potentiate Wnt/β-catenin signaling.^[2] Among these, RSPO1 demonstrates the highest binding affinity for LGR5, with a dissociation constant (Kd) of approximately 3.1 nM as determined by surface plasmon resonance assays. The other RSPOs (RSPO2-4) also bind LGR5, albeit with slightly lower affinities in the low nanomolar range, enabling selective enhancement of Wnt pathway activity in a ligand-dependent manner.^[13] The binding mechanism involves the formation of an RSPO-LGR5 complex that stabilizes interactions between Frizzled (FZD) receptors and low-density lipoprotein receptor-related proteins 5 and 6 (LRP5/6), thereby promoting the assembly of the Wnt signalosome without LGR5 directly binding Wnt ligands. LGR5 functions exclusively as a co-receptor in this context, relying on RSPO ligation to counteract the inhibitory effects of E3 ubiquitin ligases such as RNF43 and ZNRF3, which otherwise degrade FZD and LRP5/6 from the cell surface.^[6] This initial ligand-receptor interaction is crucial for amplifying low-level Wnt signals in stem cell niches. Experimental validation of these interactions comes from radioligand binding assays and cell-based functional studies, which show that RSPO binding to LGR5 directly correlates with increased Wnt reporter activity and is absent in LGR5-deficient cells.^[2] Furthermore, genetic knockout studies in mice reveal the ligand dependency of LGR5-mediated signaling; while single Lgr5 knockouts exhibit only mild intestinal phenotypes, combined Lgr4/Lgr5 double knockouts completely abolish crypt proliferation and organoid formation in vitro, underscoring RSPO's essential role in sustaining Lgr5+ stem cell expansion.00287-8)

Signaling Pathways

LGR5 primarily functions as a receptor for R-spondin (RSPO) ligands, potentiating the canonical Wnt/β-catenin signaling pathway by forming a complex that inhibits the E3 ubiquitin ligases ZNRF3 and RNF43.^[6] This LGR5-RSPO complex binds to and neutralizes ZNRF3/RNF43, preventing their ubiquitination and subsequent degradation of Wnt receptors such as Frizzled (FZD) and low-density lipoprotein receptor-related protein 6 (LRP6) on the cell surface.^[16] By stabilizing these receptors, LGR5 enhances the sensitivity of cells to Wnt ligands, thereby amplifying downstream signaling without directly initiating the pathway.^[17] Upon Wnt ligand binding to the stabilized FZD/LRP6 receptors, LGR5 facilitates the recruitment of intracellular effectors to the plasma membrane, including Dishevelled (DVL) and AXIN, which are critical for β-catenin stabilization.^[18] The formation of a supercomplex involving LGR5, FZD, LRP6, and DVL promotes the phosphorylation of LRP6 at key residues, such as serine 1490, which in turn recruits and sequesters AXIN from the β-catenin destruction complex (comprising AXIN, APC, GSK3β, and CK1).^[18] This inhibition disrupts β-catenin ubiquitination and degradation, allowing its accumulation in the cytoplasm and subsequent nuclear translocation to activate transcription factors like TCF/LEF.^[19] LGR5-mediated signaling operates independently of heterotrimeric G-proteins, distinguishing it from other G-protein-coupled receptors, and relies predominantly on LRP6 phosphorylation for signal transduction.^[6] Studies indicate that while LGR5 can interact with G-proteins in vitro, physiological Wnt potentiation does not require G-protein activation, as evidenced by the lack of effect from G-protein inhibitors on RSPO-LGR5-induced LRP6 phosphorylation and β-catenin stabilization.^[20] Evidence from genetic models underscores LGR5's essential role in Wnt signaling integrity, particularly in intestinal crypts. Lgr5 null mice exhibit defective Wnt/β-catenin signaling, manifested as deregulated pathway activity leading to precocious Paneth cell differentiation and impaired crypt homeostasis.^[21] These disruptions culminate in 100% perinatal lethality, characterized by gastrointestinal distension and failure to thrive due to insufficient suckling from ankyloglossia.^[22]

Physiological Roles

Intestinal Stem Cells

LGR5-positive (LGR5+) cells, located at the base of intestinal crypts, function as crypt base columnar (CBC) stem cells that drive the homeostatic renewal of the intestinal epithelium.^[23] These cells undergo rapid division to replenish the epithelial lining, which turns over completely every 3-5 days in mammals.^[24] Positioned between Paneth cells, LGR5+ CBC stem cells maintain their stemness through interactions with the niche environment, ensuring continuous production of differentiated progeny that migrate upward along the crypt-villus axis.^[25] Lineage tracing experiments have confirmed the multipotency and long-term self-renewal capacity of LGR5+ cells. In seminal studies using Cre-inducible reporters targeted to the Lgr5 locus, individual LGR5+ cells generated all major epithelial lineages—including enterocytes, goblet cells, enteroendocrine cells, and tuft cells—over extended periods, demonstrating their role as the primary source of intestinal epithelial cells during steady-state conditions.^[23] These findings established LGR5 as a definitive marker for active intestinal stem cells, distinguishing them from more quiescent populations.^[26] In response to injury, such as radiation exposure, LGR5+ progenitors exhibit temporary expansion to facilitate epithelial regeneration. Ablation of LGR5+ cells impairs recovery from damage, underscoring their indispensability for restoring tissue integrity after acute insults, though other progenitor pools may contribute under severe stress.^[27] This regenerative plasticity allows LGR5+ cells to proliferate robustly in the altered niche, supporting rapid repopulation of the crypts.^[28] LGR5+ stem cells rely on Paneth cells for niche signaling, which provide essential factors like EGF and Wnt ligands to sustain their function. Paneth cells secrete Wnt3a to establish a high Wnt signaling gradient at the crypt base, promoting LGR5-mediated β-catenin stabilization and stem cell maintenance, while EGF supports proliferation.^[29] Competition for these limited niche signals among LGR5+ cells and Paneth cells regulates stem cell numbers and positioning within the crypt.^[25]

Roles in Other Tissues

Beyond the intestinal epithelium, LGR5 expression is observed in various other tissues, where it marks stem or progenitor cell populations adapted to tissue-specific regenerative demands, such as injury-induced repair or developmental maintenance. These LGR5-positive (LGR5+) cells often respond to Wnt signaling via R-spondin ligands, enabling proliferation and differentiation in contexts distinct from the continuous renewal of the gut.^[30] In the liver, LGR5 is expressed at low levels in pericentral hepatocytes during homeostatic adult tissue but is rapidly upregulated in biliary epithelial cells within ductules and pericentral hepatocytes following injury, such as partial hepatectomy or toxin-induced damage. These LGR5+ cells, derived from bile ductules, serve as facultative progenitors that contribute to hepatocyte regeneration by proliferating and differentiating into parenchymal cells during the recovery phase. For instance, in mouse models of liver damage, single LGR5+ cells isolated from injured livers can be expanded in vitro as organoids under Wnt/R-spondin conditions, demonstrating their stem-like potential and ability to generate functional liver tissue.^[31] Pericentral hepatocytes express LGR5 during homeostasis and contribute to zonal regeneration, with their role complementing that of ductular cells post-injury. Recent studies (as of 2025) highlight LGR5+ hepatocytes' contributions to liver zonation and replenishment during specific injuries.^[32] No overt liver phenotype is observed in homeostatic Lgr5 knockouts, consistent with its low basal expression.^[33] During kidney development, LGR5 marks a subset of nephron progenitor cells in the cap mesenchyme of the embryonic mouse kidney, where it supports the maintenance and expansion of these progenitors essential for nephron formation. Lineage tracing in Lgr5 reporter mice reveals that LGR5+ cells contribute to the generation of specific nephron segments, including the thick ascending limb and distal convoluted tubule, with expression peaking during the proliferative phase of nephrogenesis around embryonic days 12.5–14.5. R-spondin signaling through LGR5 is critical for sustaining this progenitor pool, as its disruption impairs distal nephron segment formation.^[34] In postnatal kidneys, LGR5 expression diminishes after the first week, reflecting the cessation of nephrogenesis in mammals.^[35] In the stomach, LGR5 primarily identifies active stem cell populations at the base of gastric glands in the antrum (pylorus), driving epithelial renewal through self-renewal and multipotent differentiation. In the antrum, LGR5+ cells in the pyloric glands undergo symmetric divisions during homeostasis, enabling rapid clonal expansion to replenish the epithelium every few days; these cells give rise to all glandular lineages, including mucus-secreting cells and enteroendocrine cells.^[36] In the corpus, LGR5 expression is lower and inducible upon injury or Helicobacter pylori infection, activating reserve progenitors to support oxyntic gland maintenance.^[37] Lineage tracing confirms their long-term contribution to antral unit renewal.^[38] LGR5+ progenitors also play roles in cyclic regeneration within sensory and integumentary structures. In the inner ear, LGR5 marks supporting cells in the cochlear sensory epithelium of neonatal mice, which act as Wnt-responsive progenitors capable of proliferating and transdifferentiating into hair cells following ototoxic damage. Activation of β-catenin signaling in these LGR5+ cells enhances mitotic regeneration, partially restoring auditory function in damage models, though this capacity wanes in adults.^[39] In hair follicles, LGR5 expression labels bulge stem cells that orchestrate the hair growth cycle, with these cells mobilizing during anagen phase to regenerate the follicle structure; they contribute to epithelial compartments of the follicle in a multipotent manner.^[30] Across these tissues, LGR5 expression levels vary, with high basal expression in the rapidly renewing stomach and hair follicles (comparable to intestinal crypts) but inducible or developmental-restricted patterns in liver and kidney, as quantified by RNA sequencing and reporter mice showing 10–100-fold upregulation post-injury or during embryogenesis.^[40] Knockout studies in mice reveal tissue-specific phenotypes: Lgr5-null mutants exhibit perinatal lethality due to gut defects, but conditional knockouts in non-intestinal tissues show milder effects, such as delayed hair follicle cycling leading to progressive hair loss and thinned pelage, impaired nephron segment specification in embryos, and reduced gastric gland regeneration upon challenge, underscoring LGR5's non-redundant role in progenitor dynamics.^[21]

Clinical Relevance

Regenerative Medicine Applications

LGR5-positive (LGR5+) stem cells serve as foundational elements in organoid cultures, enabling the in vitro generation of complex, self-organizing tissue structures that mimic native organ architecture. In intestinal organoid protocols, single Lgr5+ crypt stem cells can clonally expand to form crypt-villus structures, recapitulating epithelial turnover and differentiation under defined growth factors like R-spondin-1, EGF, and Noggin.^[41] Similarly, for gastric organoids, isolated Lgr5+ cells from the pyloric gland generate long-lived structures resembling mature antral epithelium, demonstrating multipotency and self-renewal in a three-dimensional matrix.^[42] Hepatic organoids derived from Lgr5+ biliary cells, activated during injury, propagate as ductal cysts that differentiate into hepatocyte-like cells, providing a platform for modeling liver regeneration.^[43] In embryonic development, LGR5 plays a critical role in gut formation by modulating Wnt signaling to regulate progenitor cell fate, with its deficiency leading to deregulated Paneth cell differentiation in the small intestine.^[21] Lgr5 knockout mice exhibit normal embryonic gut morphogenesis but display severe perinatal defects, including gastrointestinal dilation and an inability to suckle, resulting in 100% neonatal lethality.^[22] Although direct evidence for LGR5 in mammalian limb embryogenesis is limited, its interaction with R-spondin enhances Wnt activity in limb bud progenitors during developmental patterning in model organisms.^[44] LGR5 targeting holds promise for gene therapy in regenerative contexts, particularly for expanding stem cell populations to treat fibrotic diseases. In liver fibrosis models, combined administration of hepatocyte growth factor and R-spondin-1 induces Lgr5+ progenitor proliferation, reducing fibrosis and restoring hepatic function without tumorigenic risks.^[45] Activated hepatic stellate cells in fibrotic human livers further promote LGR5+ cell expansion, suggesting therapeutic strategies to harness these interactions for tissue remodeling.^[46] Post-2023 advances have integrated CRISPR editing with LGR5+ stem cells to advance personalized regenerative approaches. For instance, CRISPR-generated Lgr5 reporter pig models facilitate in vivo studies of LGR5+ cell contributions to tissue repair, enabling tailored interventions for organ-specific regeneration.^[47] These edited organoids also support patient-derived modeling for drug screening, enhancing precision in treating developmental and injury-related disorders.

Cancer Associations

LGR5 serves as a prominent marker for cancer stem cells (CSCs) across multiple malignancies, particularly in colorectal, gastric, and liver cancers, where its overexpression drives tumor progression and metastasis. In colorectal cancer, elevated LGR5 expression correlates with lymph node metastasis, larger tumor size, and advanced disease stages, facilitating cancer cell migration and invasion through enhanced Wnt/β-catenin signaling. Similarly, in gastric cancer, LGR5+ cells promote dedifferentiation and distant metastasis, with high expression observed in progressive lesions. In hepatocellular carcinoma (HCC), LGR5 marks liver CSCs that exhibit increased proliferation and clonogenicity, contributing to metastatic spread via similar pathway activation. Recent studies from 2024 and 2025 highlight the role of LGR5+ cells in chemoresistance; for instance, in gastric cancer, LGR5 co-expression with CD44 identifies CSCs resistant to cisplatin and oxaliplatin by activating Wnt, Hedgehog, and Notch pathways, while in colorectal and liver cancers, LGR5+ populations evade 5-fluorouracil and doxorubicin through sustained stemness. LGR5 exhibits a dual function in tumorigenesis, promoting cancer development via Wnt hyperactivation in many contexts while exerting tumor-suppressive effects upon its loss in others. High LGR5 levels amplify Wnt signaling to foster CSC maintenance and tumor growth in colorectal and gastric cancers, yet its knockdown in colorectal cell lines upregulates Wnt target genes like WISP1 and Wnt5a, enhancing invasion and anchorage-independent growth. In intestinal adenomas, LGR5 acts as a negative regulator of tumourigenicity by antagonizing excessive Wnt activity; its selective loss in regions of hyperactivated Wnt signaling facilitates epithelial-mesenchymal transition (EMT) and progression to carcinoma, as evidenced by reduced LGR5 positivity in invasive areas compared to adenomas. High LGR5 mRNA expression serves as a prognostic indicator of poor outcomes, particularly in early-stage gastric cancer. In stage I/II gastric cancer patients, elevated LGR5 levels are associated with significantly worse overall survival (5-year rate: 60.6% vs. 100% in LGR5-negative cases) and progression-free survival, independent of other clinicopathological factors in multivariate analysis. A 2025 meta-analysis in colorectal cancer further confirms that LGR5 overexpression correlates with reduced overall survival, underscoring its value in risk stratification. Therapeutic strategies targeting LGR5 have shown promise in overcoming CSC-driven resistance, including antibody-drug conjugates (ADCs) and combinations with EGFR inhibitors. LGR5-directed ADCs, such as those using the 8E11 antibody conjugated to payloads like CPT2, effectively shrink tumors in colorectal cancer patient-derived xenografts by depleting LGR5+ CSCs without severe off-target toxicity to normal stem cells. In 2025 preclinical studies, combining these ADCs with cetuximab— an EGFR monoclonal antibody—upregulates LGR5 expression in both RAS wild-type and mutant models, leading to enhanced tumor regression and prolonged survival compared to monotherapy, with complete responses observed in resistant PDX lines. Ongoing clinical trials include a phase I/II study of the LGR5-targeted CAR-T therapy CNA3103 for metastatic colorectal cancer, and bispecific antibodies like petosemtamab (EGFR x LGR5) in early-phase testing for gastrointestinal cancers.^[48]^[49] Additionally, inhibiting the LGR5/mTORC2 axis addresses metabolic plasticity in HCC; LGR5 activates mTORC2 via RAC1/AKT/FOXO3a to boost aerobic glycolysis, enabling resistance to glucose starvation, and mTORC2 blockade with agents like metformin suppresses this adaptation, reducing tumor growth in vitro and in vivo. Recent 2024-2025 investigations reveal LGR5's contributions to tumor microenvironment interactions, including glioma stiffness, extracellular matrix (ECM) adhesion, and metabolic resilience. In brain cancers like glioma, LGR5+ CSCs contribute to tumor progression and invasion through mechanisms such as EMT activation. Furthermore, LGR5 drives glucose starvation resistance in cancer cells by enhancing glycolytic capacity through mTORC2, a mechanism particularly relevant in nutrient-poor tumor niches.

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