SPARCL1 ELISA kit
- Known as:
- SPARCL1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-SPARCL1-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- SPARCL1 ELISA kit
Related genes to: SPARCL1 ELISA kit
- Gene:
- SPARCL1 NIH gene
- Name:
- SPARC like 1
- Previous symbol:
- -
- Synonyms:
- MAST9
- Chromosome:
- 4q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2016-10-05
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- Papillary thyroid carcinoma (PTC) is the most prevalent type of thyroid malignancy, where invasive growth and distant metastasis contribute to a worsened patient prognosis. SPARCL1, a known tumor suppressor gene in various cancers, encodes a secreted glycoprotein. Preliminary research suggests that elevated expression of SPARCL1 is correlated with a better prognosis in PTC, highlighting its potential as an innovative restorative therapeutic agent, but its specific role and underlying mechanisms remain unclear. This study aimed to investigate the impact of SPARCL1 on the invasion and metastasis of PTC cells by constructing an overexpression model of SPARCL1 in PTC cells through viral transduction, collecting the supernatant proteins from the PTC cell model and adding them to PTC cells, and introducing recombinant SPARCL1 protein into PTC cells. In addition, we also conducted animal experiments to detect the effects of SPARCL1 on the subcutaneous tumor formation and multi-organ metastasis of PTC cells in mice, as well as the inhibitory effect of recombinant SPARCL1 on tumors formed by PTC cells. The findings revealed that overexpression of the SPARCL1 gene, secretory form of SPARCL1 protein, and recombinant SPARCL1 protein all significantly inhibited the malignant biological behaviors of PTC cells. Overexpression of SPARCL1 can inhibit the subcutaneous growth of tumor cells and their metastasis to the lungs, liver, and kidneys of mice, and recombinant SPARCL1 protein can also inhibit the growth of subcutaneous tumors. Mechanistically, SPARCL1 appears to mediate its anti-tumor effects through the SLC3A2-mediated ferroptosis pathway, suggesting a novel mechanism by which SPARCL1 influences PTC progression. In summary, SPARCL1 inhibits the proliferation, invasion, and metastasis of PTC, highlighting its potential as a candidate for innovative restorative therapies in PTC treatment. - Source: PubMed
Publication date: 2026/05/20
Wu FengpingZhang JinkangZhang XiaoliXu DongkunCheng ShuanghuaLiu QianGan YuxinRen LifangYang HaochengZhang KunXia XuliangJiang ZhiqiangShi YuhongTu Wenling - Bone metastasis is a leading cause of death in prostate cancer (PC) patients. Although androgen-deprivation therapy (ADT) combined with novel androgen-targeted agents constitutes the cornerstone of systemic treatment, its efficacy is limited. We investigated the adrenal contribution in promoting progression of castration-resistant PC (CRPC) within bone using a preclinical intratibial xenograft model (VCaP, 22Rv1, and LNCaP cells). Mice underwent orchiectomy (ORX) to mimic ADT, with or without adrenalectomy (ORX+ADX) to eliminate adrenal contribution. A significant increase in bone mineral density (BMD) was observed in tumor-grafted tibiae in ORX-treated mice compared to controls (p<0.001), indicating a strong tumor-induced sclerotic response. In contrast, ORX+ADX reduced tumor take rate by approximately 50% and decreased tumor-induced BMD by over 80% (p<0.001). Transcriptomic analysis revealed that ADX downregulated tumor-induced transcripts in bone by over 90%, including osteogenic (Lox, Sparcl1, Bmp2, Postn, Col1a1) and pro-angiogenic (Bmper, Pecam-1, Esam) signatures. Additionally, BMP, PI3K/Akt and ERK1/2 signaling pathways were associated with the tumor-induced bone response. Both high serum progesterone and intratumoral levels of dihydrotestosterone (DHT) were associated with the sclerotic bone phenotype. ADX markedly reduced intratumoral DHT and downregulated glycolytic genes (HK2, PFK2, LDHA) and secretory proteins expressed by the tumor, including Stanniocalcin 2, potentially mediating paracrine effects in the sclerotic bone response. Altogether, these findings highlight the critical role of adrenal- dependent androgen synthesis, particularly via progesterone, in driving the sclerotic CRPC in bone. Our findings suggest that a comprehensive blockade of adrenal contribution is essential to prevent the sclerotic bone response associated with CRPC. - Source: PubMed
Publication date: 2026/05/18
Thulin Malin HagbergLi LeiAbrahamsson SannaLandin AndreasHorkeby KarinWu JianyaoLagerquist Marie KOhlsson ClaesPoutanen Matti - Astrocytes regulate key aspects of the neural microenvironment that can be co-opted by cancer to support tumor growth and invasion. Secreted protein acidic and rich in cysteine-like 1 (SPARCL1) is a matricellular glycoprotein expressed by astrocytes and stromal cells, whose expression varies across cancer types. While SPARCL1 is downregulated in many peripheral cancers, reports of its expression in gliomas, specifically glioblastoma (GBM), are inconsistent. The biological context underlying these divergent findings, and the role of SPARCL1 in GBM malignancy, remains unclear. Publicly available transcriptomic datasets from the Ivy Glioblastoma Atlas Project (Ivy GAP), GlioVis, and TCGA were analyzed to evaluate SPARCL1 expression across GBM cohorts. Spatially resolved gene expression data from Ivy GAP were used to assess SPARCL1 expression from defined tumor regions. Microarray and RNA sequencing datasets from GlioVis and TCGA, respectively, were used to assess SPARCL1 expression across whole-tumor samples. Spatial transcriptomics from Ivy GAP show SPARCL1 expression was upregulated along the leading edge and in infiltrating tumor regions. Microarray datasets showed greater SPARCL1 expression in tumors of astrocyte lineage as opposed to oligodendrocyte lineage. Bulk RNA sequencing showed high SPARCL1 expression in low-grade gliomas, which is consistent with astrocytic lineage, IDH mutation, and spatial averaging effects that might obscure regional associations. These findings demonstrate that SPARCL1 expression in GBM is shaped by tumor architecture, molecular classification, and microenvironment interactions. Enrichment of SPARCl1 at invasive tumor margins is consistent with prior studies linking SPARCL1 to neuron-glioma synapse formation and angiogenesis. - Source: PubMed
Publication date: 2026/04/30
Allgood JuliAnne EJohnson TorrancePullan Jessica E - Astrocyte-derived extracellular matrix (ECM) proteins are critical for synaptic development and glutamatergic signaling, yet their role in attention deficit hyperactivity disorder (ADHD) remains poorly understood. This study examined serum levels of Thrombospondin-1 (Tsp-1), Sparc, and Sparcl-1 in children with ADHD and explored their associations with behavioral symptoms, executive dysfunction, and social impairments. Eighty-six children aged 6-12 years participated: 46 medication-naive with ADHD and 40 age- and sex-matched neurotypical controls. Clinical measures included the Conners' Parent Rating Scale-Revised: Long Form (CPRS-R:L), Social Responsiveness Scale (SRS), and Behavior Rating Inventory of Executive Function (BRIEF). Serum levels of Tsp-1, Sparc, and Sparcl-1 were quantified via ELISA. Children with ADHD exhibited significantly lower serum levels of Tsp-1 (p < 0.001), Sparc (p = 0.020), and Sparcl-1 (p = 0.049) than controls. Lower Sparc levels were associated with poorer executive functioning and reduced social responsiveness, while lower Tsp-1 levels were positively associated with higher ADHD symptom severity. This study provides the first evidence of reduced serum astrocyte-derived ECM proteins in children with ADHD, implicating glia-mediated synaptic dysregulation in the disorder's pathophysiology. These findings suggest a novel glia-centered mechanism and support the potential of ECM proteins as biomarkers for ADHD subtypes and as targets for future therapeutic interventions. - Source: PubMed
Publication date: 2026/05/05
Kısmet Nilüfer YıldızGökçearslan Selen SezenÜlkar Serenay ElgünAçıkel Sadettin Burak - Secreted protein acidic and rich in cysteine-like 1 (SPARCL-1) is an extracellular matrix-associated matricellular protein involved in endothelial stability and vascular homeostasis. Given the central role of endothelial dysfunction in preeclampsia, we hypothesized that circulating SPARCL-1 levels would differ between early- and late-onset preeclampsia. Accordingly, this study aimed to evaluate maternal serum SPARCL-1 levels in women with early- and late-onset preeclampsia and to assess its diagnostic performance by disease onset. - Source: PubMed
Publication date: 2026/04/17
Shirinova SevinjÖzalp MiraçToplu Murat İbrahimAydoğdu Burak DenizMihmanlı Veli