Human Testican 1 / SPOCK1 Protein
- Known as:
- Human Testican 1 / SPOCK1 Protein
- Catalog number:
- SP1-H5248
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human Testican 1 / SPOCK1 Protein
Related genes to: Human Testican 1 / SPOCK1 Protein
- Gene:
- SPOCK1 NIH gene
- Name:
- SPARC (osteonectin), cwcv and kazal like domains proteoglycan 1
- Previous symbol:
- TIC1, SPOCK
- Synonyms:
- testican-1
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-10-02
- Date modifiied:
- 2018-02-23
Related products to: Human Testican 1 / SPOCK1 Protein
Related articles to: Human Testican 1 / SPOCK1 Protein
- Head and Neck Squamous Cell Carcinoma (HNSCC) diagnosis remains a challenge for clinicians, with human papillomavirus (HPV) status long associated with HNSCC prognosis and response to therapy. Small non-coding molecules, such as microRNAs (miRNAs), significantly alter gene expression, particularly of immune-modulatory genes. In the current study, an effort to map the interaction patterns between miRNAs and their target genes was carried out using diverse computational tools. A microarray-based study was retrieved and analysed using GEO2R to identify ubiquitously expressed miRNAs in HPV-associated HNSCC samples, with HPV-negative samples used as controls. Seven miRNAs were identified, namely hsa-miR-150-5p, hsa-miR-142-5p, hsa-miR-142-3p, hsa-miR-1-3p, hsa-miR-133b, hsa-miR-206, and hsa-miR-1260b. Functional annotation using miRNet identified numerous significant signalling pathways dysregulated by the aforementioned miRNAs. miRDB was used to map miRNA target genes, which were visualised in Cytoscape; among these, key immune-modulatory genes were analysed in a comprehensive meta-analysis. Furthermore, the GEPIA2 tool was used to perform survival analysis and generate Kaplan-Meier plots correlating survival percentages in HNSCC patients with gene expression patterns. The viral infectious cycle was dysregulated by miR-1260b expression. DKK1, STC2, SPOCK1, and TP53 were among the genes whose aberrant expression was associated with a significant reduction in survival in HNSCC-affected individuals. This report elucidates the pivotal role of miRNAs in modulating the expression of key immune-modulatory genes, thereby influencing the prognosis of HNSCC and HPV infection. - Source: PubMed
Publication date: 2026/03/31
Datta AnkurMuthu Meenakshi MDaniels SusannaVarshaa BC George Priya Doss - The extracellular matrix (ECM) plays a pivotal role in facilitating tumour development, invasiveness, metastasis, and immunoevasive processes through dynamic ECM remodelling processes. Testican-1 (SPOCK1), an excretory matricellular proteoglycan, is suggested to exert a role in the facilitation of ECM remodelling processes through interacting with matrix metalloproteases (MMPs) and even its less known forms. The structural mechanisms of interactions between testican-1 and MMPs were studied, and their roles in tumour-promotion pathway processes were also examined using a computational approach and immunofluorescence validated by colocalisation technique analysis. A computational analysis using docking, molecular dynamics (MD), and systems biology analysis was employed. HDock and GROMACS were chosen to analyse binding affinity and testican-1 stability with 28 different MMPs. H-bond, free energy, and root mean square fluctuation (RMSF) analyses were performed to confirm the interactions in the testican-1-MMP complexes. The systems biology toolkit implemented in this study consisted of STRING, BioGRID, and Cytoscape, which were employed for testican-1 interaction network and pathway analysis. Kaplan-Meier survival analysis using the GEPIA2 tool was utilised to correlate SPOCK1 gene expression and clinical survival measures for various malignancies. The docking analysis showed robust interactions between testican-1 and MMP23, MMP25, and MMP28. Additionally, testican-1-MMP complexes were confirmed to form stable interfaces based on comprehensive MD analysis, suggesting solid binding interfaces with the MMP-unique domain of testican-1. Our systems biology experiment indicated testican-1 as a central hub for interactions between immunoevasive and ECM remodelling processes. SPOCK expression was also shown to correlate with significant survival measures for different malignancies, revealing clinical implications in cancer. The testican-1-MMP computational analysis suggests testican-1 plays a pivotal role as a therapeutic target for a wide range of malignancies. SPOCK-MMP interactions could be targeted to interrupt tumour-promoting processes by arresting dynamic changes in the ECM, thereby improving patient survival. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/05/15
Youssefi SepidehSaleki KiarashKadam PrernaMazloomi AmirrezaMukherjee AbhikDekker Lodewijk VNateri Abdolrahman S - Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related morbidity and mortality worldwide. Therefore, there is an urgent need to discover precise diagnostic markers and novel therapeutic strategies. A genome-wide association study (GWAS) was conducted using the Kunshan Elderly Cohort to identify genetic susceptibility factors underlying NSCLC. GWAS results identified that seven single-nucleotide polymorphisms (SNPs) were associated with NSCLC risk, including SPOCK1 (SPARC/osteonectin, CWCV, and Kazal-like domains proteoglycan (1), which emerged as a key candidate oncogene driving NSCLC progression. High expression of SPOCK1 in NSCLC tissues was associated with poor prognosis. Subsequently, using NSCLC cell lines with shRNA-mediated SPOCK1 knockdown (loss of function) and plasmid-mediated SPOCK1 overexpression (gain of function), we demonstrated that SPOCK1 significantly promotes in vitro NSCLC cell proliferation, migration, invasion, and cell cycle progression. Furthermore, in vivo mouse studies demonstrated that xenografted SPOCK1-knockdown NSCLC cells exhibited significantly reduced tumor growth and metastasis, whereas xenografted SPOCK1-overexpressing NSCLC cells enhanced tumor progression and metastasis. Mechanistically, SPOCK1 activates the JAK2/STAT3 signaling pathway by interacting with integrin alpha5 beta1 (α5β1) and subsequently upregulating SLC3A2 expression. This regulatory cascade promotes glutathione (GSH) biosynthesis and mitigates the accumulation of reactive oxygen species (ROS) and lipid peroxidation LPO), thereby suppressing ferroptosis in the NSCLC cells. Furthermore, Heat Shock Factor 1 (HSF1) is a critical upstream transcriptional regulator of SPOCK1. Notably, SPOCK1 acts as a pivotal mediator of the immunosuppressive microenvironment in the NSCLC tumors by inducing T-cell exhaustion and promoting infiltration of regulatory T cells (Tregs). In summary, SPOCK1 drives NSCLC progression by inhibiting ferroptosis and inducing an immunosuppressive microenvironment. Therefore, SPOCK1 is a promising therapeutic target in NSCLC. - Source: PubMed
Publication date: 2026/05/14
Liu NaZhu Xiao-RenLiu YangHan Guo-HuLiu Yuan-YuanZhou Kai-XinChen Min-Bin - The SPARC (secreted protein acidic and rich in cysteine) family represents a unique class of matricellular proteins - including SPARC, SPARCL1, SPOCK1-3, SMOC1-2, and FSTL1 - that regulate extracellular matrix (ECM) dynamics, cell signaling, and tissue homoeostasis. In cancer, their expression is frequently dysregulated, through epigenetic mechanisms, microRNAs, and interactions within the tumor microenvironment (TME). Dysregulation of SPARC family members is most pronounced in aggressive malignancies with SPARC, SPARCL1, SPOCK1, and SPOCK2 most consistently altered. These proteins drive tumor progression through ECM remodeling, epithelial-mesenchymal transition (EMT), maintenance of cancer stemness, immune modulation, and drug resistance acquisition. Their functions are highly context-dependent, exerting either tumor-suppressive or oncogenic effects depending on tissue types and disease stage. While their secreted nature positions family members as promising serum or plasma biomarkers, challenges such as ECM protein undruggability, functional heterogeneity, and the absence of upstream regulators have so far precluded direct therapeutic targeting, with no agents advancing to clinical trials. Nonetheless, indirect strategies leveraging their biology show preclinical promise. This review synthesizes current knowledge on SPARC family structure, regulation, and context-specific functions in cancer-TME interactions, emphasizing their dual roles as modulators of progression and resistance. By integrating mechanistic insights with translational advances, we highlight the emerging utility of SPARC family proteins in precision oncology and underscore the need for deeper understanding to enable effective biomarker development and targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/04/14
Hoe Rachel Huey XuanRamasamy Thamil SelveeSinniah AjanthaAyob Ain Zubaidah - Emerging viral infections can initiate a global pandemic with high mortality. Understanding the immunopathogenesis of these viruses is critical to developing effective strategies for managing/preventing such outbreaks. - Source: PubMed
Publication date: 2025/12/29
Bouzid AmalYusuf Ayesha MMousa MiraVenkatachalam ThenmozhiTay GuanUddin MaimunahAlkaabi NawalAyad Maha SaberAlsafar HabibaHamoudi Rifat