ArticleCell proliferation2016
SPOCK1 is upregulated in recurrent glioblastoma and contributes to metastasis and Temozolomide resistance.
Article in Cell proliferation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- SPARC family proteins: matricellular modulators of cancer progression and therapeutic resistance.Cancer gene therapy · 2026Review
- SPOCK1 acts as a negative regulator of ferroptosis in non-small cell lung cancer.NPJ precision oncology · 2026Article
- SPOCK1 overexpression suggests poor prognosis in head and neck squamous cell carcinomas.Pathology oncology research : POR · 2026Article
- Spatial transcriptomics of glioblastoma defines biologically and clinically significant reprogramming patterns across unique spatial microenvironments.bioRxiv : the preprint server for biology · 2025Article
- In vivo generation of CAR macrophages via the enucleated mesenchymal stem cell delivery system for glioblastoma therapy.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- TMBIM1 promotes epithelial mesenchymal transition by accelerating autophagic degradation of E-cadherin in glioblastoma.Scientific reports · 2025Article
- SPOCK: Master regulator of malignant tumors (Review).Molecular medicine reports · 2024Review
- Article
- Potential Effects of Low-Level Toluene Exposure on the Nervous System of Mothers and Infants.International journal of molecular sciences · 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
- Delineating the glioblastoma stemness by genes involved in cytoskeletal rearrangements and metabolic alterations.World journal of stem cells · 2023Review
- Transcriptional Profiling of a Patient-Matched Cohort of Glioblastoma (IDH-Wildtype) for Therapeutic Target and Repurposing Drug Identification.Biomedicines · 2023Article
- Article
- Review
- SPOCK1 Promotes the Development of Hepatocellular Carcinoma.Frontiers in oncology · 2022Article
- Article
- Overview of the molecular mechanisms of migration and invasion in glioblastoma multiforme.Journal of the Chinese Medical Association : JCMA · 2021Article
- Article
- Multiomic analysis of the function ofThe Journal of international medical research · 2021Article
- Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesGlioblastoma multiforme (GBM) is the most aggressive brain tumour type in humans. Its poor prognosis is largely attributed to its invasiveness and high rate of recurrence. Recurring GBM is commonly resistant to chemotherapeutic drugs, making it specially difficult to treat. Recent studies have revealed that matricellular glycoprotein SPOCK1 to be upregulated in several cancer types and to be specifically expressed in invasive GBM, but not in other types of non-invasive brain tumour, which prompted us to study the mechanism of action of SPOCK1 in invasion, recurrence and drug resistance of GBM cells. MATERIALS AND
methodsSPOCK1 expression in GBM tissues was evaluated using qPCR, Western blotting and immunohistochemical staining. Cell migration was tested by the wound healing method and cell invasion was assessed using transwell plates with Matrigel coating. Western blotting was performed for E-cadherin, vimentin, N-cadherin, p-Akt and Akt. Cell viability was examined using the MTT assay.
resultsWe found that the expression of SPOCK1 was significantly upregulated in recurrent GBM. We also demonstrated that SPOCK1 positively regulated migration, invasion and EMT process of GBM cells. Furthermore, SPOCK1 mediated TMZ resistance in GBM, as knockdown of SPOCK1 expression in TMZ-resistant GBM cells substantially sensitized these cells to TMZ.
conclusionSPOCK1 results were positive and it mediated TMZ resistance in GBM. In addition, SPOCK1 regulated invasion and TMZ resistance in GBM cells via the Akt signalling pathway.
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