Glypican-3, GPC3 recombinant protein
- Known as:
- Glypican-3, GPC3 Rec. protein
- Catalog number:
- BRP1021
- Product Quantity:
- 100 μg
- Category:
- -
- Supplier:
- Biospect
- Gene target:
- Glypican-3 GPC3 recombinant protein
Related genes to: Glypican-3, GPC3 recombinant protein
- Gene:
- GPC3 NIH gene
- Name:
- glypican 3
- Previous symbol:
- SDYS
- Synonyms:
- OCI-5, SGBS, SGBS1, SGB, DGSX
- Chromosome:
- Xq26.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-08
- Date modifiied:
- 2019-04-23
Related products to: Glypican-3, GPC3 recombinant protein
Related articles to: Glypican-3, GPC3 recombinant protein
- To develop a microbubble-based contrast agent using light-activated site-specific conjugation (LASIC) for targeted molecular ultrasound imaging of glypican-3 (GPC3) positive hepatocellular carcinoma (HCC). - Source: PubMed
Publication date: 2026/08/11
Hui JamesShin YonghwanPham JanetChen Po-ChunRuppa AravinthHankil VeronicaGuo LeaKalamullah Hanif SaifurrahmanKaneko NaokiChiang Jason - Alternative polyadenylation (APA) generates mRNA isoforms with distinct 3' untranslated regions (3'UTRs), thereby influencing transcript stability and translation. In cancer, 3'UTR shortening can activate oncogenes by escaping microRNA (miRNA)-mediated repression, but its role in hepatocellular carcinoma (HCC) remains poorly defined. Here, we profiled mRNA length alterations in multistage human HCC transcriptome datasets and investigated their functional consequences. Approximately 77% of mRNAs with altered length exhibited 3'UTR shortening. Glypican-3 (GPC3) was the most prominently upregulated shortened transcript, and high GPC3 expression was associated with poor prognosis in HCC. GPC3 knockdown reduced proliferation and induced apoptosis, whereas GPC3 overexpression promoted cell growth. Among APA regulators, Cleavage Stimulation Factor 2 (CSTF2) was upregulated in HCC, correlated positively with GPC3 expression, and predicted adverse clinical outcomes. Modulation of CSTF2 expression altered GPC3 3'UTR length, with CSTF2 overexpression promoting GPC3 3'UTR shortening, increasing GPC3 protein expression, enhancing proliferation, and suppressing apoptosis. Further analysis revealed that GPC3 3'UTR shortening removed binding sites for miR-96-5p and miR-140-5p, relieving miRNA-mediated translational repression. These findings identify CSTF2-driven APA as a mechanism of oncogenic GPC3 activation in HCC and suggest the CSTF2-GPC3 axis as a potential therapeutic target. - Source: PubMed
Publication date: 2026/08/10
Jeon SoyoungShin EunbiHa Jin WoongNa Min JeongKim Sang YeanNam Suk Woo - Hepatocellular carcinoma (HCC) remains a global health challenge with limited treatment efficacy despite advances in immune checkpoint blockade (ICB). The low immunogenicity of HCC tumors and impaired dendritic cell (DC) function contribute to suboptimal therapeutic outcomes. To address these limitations, we developed a synergistic nanoparticle dyad combining tumoricidal and immunomodulatory components. Specifically, an anti-GPC3-antibody-conjugated, emodin-loaded spiky mesoporous silica nanoparticle (E-SMSNα) selectively targets HCC cells to induce immunogenic cell death, while a matured DC-membrane-camouflaged, c-di-AMP-loaded nanoparticle (A-MSNm) reprograms dysfunctional DCs, bridging innate and adaptive immunity. This combinatorial approach synergistically promotes antitumor immunity, significantly suppressing primary tumor growth and inducing durable protection against tumor rechallenge. Moreover, it shows strong synergy with PD-1 checkpoint blockade, positioning it as a promising strategy for HCC immunotherapy. - Source: PubMed
Publication date: 2026/07/23
Liu ChangZhao XiejunSong HuiYuan YiwenMa JiaDong YingtongXu TianzhaoLi XiaojiaoLiu Xinghui - Chimeric antigen receptor T-cell (CAR-T) therapy has produced remarkable therapeutic results in blood cancers, while its application to solid malignancies remains limited by a pooled objective response rate of approximately 9%. This gap stems from core biological obstacles: heterogeneous antigen expression, physical inaccessibility within dense stromal architectures, and immunosuppressive microenvironments that drive T-cell exhaustion through epigenetically fixed transcriptional programs. The period spanning 2024-2025 represents a pivotal turning point. GD2-targeting CAR-T cells delivered intracerebroventricularly achieved durable complete responses (including one sustained beyond 30 months) in H3K27M-mutated diffuse midline gliomas. CLDN18.2-targeting satricabtagene autoleucel demonstrated randomized superiority over physician's choice in advanced gastric cancer (progression-free survival HR 0.37). GPC3-targeting CAR-T cells armored with a dominant-negative TGF-β receptor achieved objective response rates of 50-57% in hepatocellular carcinoma, representing a three- to four-fold improvement over unarmored predecessors. These breakthroughs reflect a paradigm shift from potency-driven engineering toward resilience-based design: metabolic armoring via autocrine IL-10 and IL-15, epigenetic protection through DNMT3A disruption and c-Jun overexpression, logic-gated targeting via synNotch circuits, and microenvironmental shielding through dominant-negative receptors. Beyond the local microenvironment, emerging recognition of systemic neuroendocrine-immune dysregulation further informs CAR-T persistence and fitness considerations. This review synthesizes the mechanistic insights, engineering strategies, clinical evidence, and emerging platforms, including lentiviral CAR-T generation, that define the current landscape, and proposes a tiered framework for next-generation solid tumor CAR-T development, while explicitly acknowledging the limitations and unknowns that persist. - Source: PubMed
Publication date: 2026/07/29
Onyekweli Samuel ObiosaOmoruyi Gloria OsayamenAkintayo Christopher OloruntobaOlaniyi Samuel Kehinde - Glypican-3 (GPC3) is a heparan sulfate proteoglycan that is highly expressed in hepatocellular carcinoma and promotes tumor progression through Wnt3a/β-catenin signaling. However, how the nanoscale organization of GPC3 at the cell surface controls signaling remains unclear. Here, we combined nano-resolution MINFLUX imaging, single-molecule tracking, and functional assays to define the spatial architecture and dynamics of GPC3 on hepatoma cells. We found that GPC3 exists as both single molecules and nanoscale clusters and switches between confined and free diffusions on the plasma membrane. Heparan sulfate (HS) chains create nanoscale corrals that limit GPC3 movement, whereas removal of HS increases diffusive heterogeneity and disrupts confinement. Wnt3a stimulation induces the formation of higher-order GPC3 assemblies and enhances β-catenin signaling, while loss of HS markedly reduces this response. MINFLUX DNA-PAINT further revealed that HS chains orchestrate the spatial distribution of Wnt3a and promote its association with the Wnt receptor, Frizzled-1, an essential step for pathway activation. Collectively, these findings reveal that HS controls the nanoscale organization and dynamics of GPC3 to promote Wnt receptor assembly and efficient β-catenin signaling in hepatoma cells. - Source: PubMed
Publication date: 2026/07/22
Lin ShaoliBall David AFazel MohamadrezaKarpova Tatiana SHo Mitchell