ArticleJournal of molecular histology2015
Up-regulation of SPOCK1 induces epithelial-mesenchymal transition and promotes migration and invasion in esophageal squamous cell carcinoma.
Article in Journal of molecular histology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- A Genome-Wide Association Study Identifies Genetic Variants Associated with Mathematics Ability.Scientific reports · 2017Pooled it
- Understanding of the characteristics of fibroblasts in ischemic cardiomyopathy using single-nucleus RNA sequencing.Scientific reports · 2025Article
- Association analysis of single nucleotide polymorphisms in the LIFR gene with lambing number in sheep.Frontiers in veterinary science · 2025Article
- SPOCK: Master regulator of malignant tumors (Review).Molecular medicine reports · 2024Review
- scDiffCoAM: A complete framework to identify potential biomarkers for esophageal squamous cell carcinoma using scRNA-Seq data analysis.Journal of biosciences · 2024Article
- SPOCK1, as a potential prognostic and therapeutic biomarker for lung adenocarcinoma, is associated with epithelial-mesenchymal transition and immune evasion.Journal of translational medicine · 2023Article
- Review
- SPOCK1 promotes metastasis in pancreatic cancer via NF-κB-dependent epithelial-mesenchymal transition by interacting with IκB-α.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Proteoglycans and their functions in esophageal squamous cell carcinoma.World journal of clinical oncology · 2021Review
- Article
- MicroRNA-155-5p inhibits the invasion and migration of prostate cancer cells by targeting SPOCK1.Oncology letters · 2020Article
- SPOCK1 overexpression induced by platelet-derived growth factor-BB promotes hepatic stellate cell activation and liver fibrosis through the integrin α5β1/PI3K/Akt signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Article
- SPOCK1 is a novel inducer of epithelial to mesenchymal transition in drug-induced gingival overgrowth.Scientific reports · 2020Article
- SPOCK1 Involvement in Epithelial-to-Mesenchymal Transition: A New Target in Cancer Therapy?Cancer management and research · 2020Review
- SPOCK1: a multi-domain proteoglycan at the crossroads of extracellular matrix remodeling and cancer development.American journal of cancer research · 2020Review
- Targeting the SPOCK1-snail/slug axis-mediated epithelial-to-mesenchymal transition by apigenin contributes to repression of prostate cancer metastasis.Journal of experimental & clinical cancer research : CR · 2019Article
- MiR-139-5p, miR-940 and miR-193a-5p inhibit the growth of hepatocellular carcinoma by targeting SPOCK1.Journal of cellular and molecular medicine · 2019Article
- SPOCK1 promotes the invasion and metastasis of gastric cancer through Slug-induced epithelial-mesenchymal transition.Journal of cellular and molecular medicine · 2018Article
- Regulation of SPOCK1 by dual strands of pre-miR-150 inhibit cancer cell migration and invasion in esophageal squamous cell carcinoma.Journal of human genetics · 2017Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Invasion and metastasis are the major causes of death in patients with esophageal squamous cell carcinoma (ESCC). Recent studies have confirmed that SPARC/osteonectin, cwcv and kazal-like domains proteoglycan 1 (SPOCK1) plays multiple roles in cancer progression. This study aims to explore the clinical characteristics of SPOCK1 in ESCC and its roles in the migration and invasion of ESCC cell lines. In this study, the up-regulation of SPOCK1 expression was frequently detected in primary ESCC tumor tissues compared with those in non-tumor tissues, which was significantly associated with tumor invasion (p = 0.004) and distant metastasis (p = 0.010). SPOCK1 was expressed at higher level in TE13 cells as compared to the low malignant Eca109 and TE1 cells. Overexpression of SPOCK1 in Eca109 cells decreased the expressions of epithelial marker E-cadherin and ZO-1, while increased mesenchymal marker Vimentin and N-cadherin levels. After ectopic expression of SPOCK1, Eca109 cells exhibited a morphological change from an epithelial cobblestone phenotype to an elongated fibroblastic phenotype, concomitant with cytoskeletal rearrangements and increased migration and invasion, suggesting that EMT occurs. While silencing SPOCK1 in TE13 cells had the opposite effects. These results suggest that up-regulation of SPOCK1 in ESCC induces EMT, thus promotes migration and invasion in ESCC cells.
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